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Monday, July 27, 2009

Gynecologic Tumor Markers

[Extracted from Emedicine.medscape.com]

Tumor markers are glycoproteins that are usually detected by monoclonal antibodies. Each tumor marker has a variable profile of usefulness for screening, determining diagnosis and prognosis, assessing response to therapy, and monitoring for cancer recurrence. They are produced by tumor cells in response to cancer or certain benign conditions and indicate biological changes that signal the existence of malignancy. These soluble molecules can usually be detected in elevated quantities in the blood, urine, or body tissues of patients with certain types of cancer. They are produced by the tumor itself or by the body in response to the presence of cancer or certain benign conditions. The levels of tumor marker are not altered in all cancer patients, especially in early stage cancer. The level of some tumor markers can be elevated in patients with noncancerous conditions. Following the development of monoclonal antibodies, many new tumor markers have been discovered during the past 2 decades.

Gynecologic malignancies include ovarian cancer, uterine cervical cancer, endometrial cancer, and trophoblastic neoplasms.

Due to the location of ovarian tumors within the abdominal cavity, making a preoperative pathological diagnosis of cancer is difficult without laparotomy. From this point of view, the use of tumor markers that consist of carbohydrate antigens, such as CA-125, in addition to diagnostic imaging are useful in the diagnosis of ovarian cancer. SCC antigen, a marker for squamous cell carcinoma, is clinically useful in the management of advanced cervical cancer. At present, no useful tumor markers exist for endometrial cancer that exhibit both high sensitivity and specificity, although CA-125 is often used in clinical practice. Finally, human chorionic gonadotropin (hCG) serves as an ideal tumor marker for trophoblastic disease; however, the incidence of trophoblastic neoplasms has decreased dramatically with the incorporation of strict clinical management of postmolar disease as well as with the overall decrease in the number of pregnancies.

The use of a tumor marker not only depends on its sensitivity and specificity, but also on its ability to influence decisions between alternative plans for patient management. Use of beta human chorionic gonadotropin (beta-hCG) for monitoring gestational trophoblastic neoplasia has set the standard to which other assays must be compared. Beta-hCG and alpha-fetoprotein have provided useful markers for ovarian germ cell tumors.

Recently, a monoclonal antibody-based immunoassay for CA-125 has been used to monitor the treatment of epithelial ovarian carcinomas. Persistent elevation of CA-125 in serum has generally reflected persistence of disease at second look surveillance procedures. However, CA-125 levels can return to within normal limits and residual disease can be found at laparoscopy or laparotomy. CA-125 shows promise for distinguishing benign from malignant pelvic masses. Several trials are ongoing to determine the potential of CA-125 in combination with other markers to increase earlier detection of occult ovarian cancer.

Tumor markers are glycoproteins that are usually detected by monoclonal antibodies. Each tumor marker has a variable profile of usefulness for screening, determining diagnosis and prognosis, assessing response to therapy, and monitoring for cancer recurrence. They are produced by tumor cells in response to cancer or certain benign conditions and indicate biological changes that signal the existence of malignancy. These soluble molecules can usually be detected in elevated quantities in the blood, urine, or body tissues of patients with certain types of cancer. They are produced by the tumor itself or by the body in response to the presence of cancer or certain benign conditions. The levels of tumor marker are not altered in all cancer patients, especially in early stage cancer. The level of some tumor markers can be elevated in patients with noncancerous conditions. Following the development of monoclonal antibodies, many new tumor markers have been discovered during the past 2 decades.

Gynecologic malignancies include ovarian cancer, uterine cervical cancer, endometrial cancer, and trophoblastic neoplasms.

Due to the location of ovarian tumors within the abdominal cavity, making a preoperative pathological diagnosis of cancer is difficult without laparotomy. From this point of view, the use of tumor markers that consist of carbohydrate antigens, such as CA-125, in addition to diagnostic imaging are useful in the diagnosis of ovarian cancer. SCC antigen, a marker for squamous cell carcinoma, is clinically useful in the management of advanced cervical cancer. At present, no useful tumor markers exist for endometrial cancer that exhibit both high sensitivity and specificity, although CA-125 is often used in clinical practice. Finally, human chorionic gonadotropin (hCG) serves as an ideal tumor marker for trophoblastic disease; however, the incidence of trophoblastic neoplasms has decreased dramatically with the incorporation of strict clinical management of postmolar disease as well as with the overall decrease in the number of pregnancies.

The use of a tumor marker not only depends on its sensitivity and specificity, but also on its ability to influence decisions between alternative plans for patient management. Use of beta human chorionic gonadotropin (beta-hCG) for monitoring gestational trophoblastic neoplasia has set the standard to which other assays must be compared. Beta-hCG and alpha-fetoprotein have provided useful markers for ovarian germ cell tumors.

Recently, a monoclonal antibody-based immunoassay for CA-125 has been used to monitor the treatment of epithelial ovarian carcinomas. Persistent elevation of CA-125 in serum has generally reflected persistence of disease at second look surveillance procedures. However, CA-125 levels can return to within normal limits and residual disease can be found at laparoscopy or laparotomy. CA-125 shows promise for distinguishing benign from malignant pelvic masses. Several trials are ongoing to determine the potential of CA-125 in combination with other markers to increase earlier detection of occult ovarian cancer.1

Tumor markers are glycoproteins that are usually detected by monoclonal antibodies. Each tumor marker has a variable profile of usefulness for screening, determining diagnosis and prognosis, assessing response to therapy, and monitoring for cancer recurrence. They are produced by tumor cells in response to cancer or certain benign conditions and indicate biological changes that signal the existence of malignancy. These soluble molecules can usually be detected in elevated quantities in the blood, urine, or body tissues of patients with certain types of cancer. They are produced by the tumor itself or by the body in response to the presence of cancer or certain benign conditions. The levels of tumor marker are not altered in all cancer patients, especially in early stage cancer. The level of some tumor markers can be elevated in patients with noncancerous conditions. Following the development of monoclonal antibodies, many new tumor markers have been discovered during the past 2 decades.

Gynecologic malignancies include ovarian cancer, uterine cervical cancer, endometrial cancer, and trophoblastic neoplasms.

Due to the location of ovarian tumors within the abdominal cavity, making a preoperative pathological diagnosis of cancer is difficult without laparotomy. From this point of view, the use of tumor markers that consist of carbohydrate antigens, such as CA-125, in addition to diagnostic imaging are useful in the diagnosis of ovarian cancer. SCC antigen, a marker for squamous cell carcinoma, is clinically useful in the management of advanced cervical cancer. At present, no useful tumor markers exist for endometrial cancer that exhibit both high sensitivity and specificity, although CA-125 is often used in clinical practice. Finally, human chorionic gonadotropin (hCG) serves as an ideal tumor marker for trophoblastic disease; however, the incidence of trophoblastic neoplasms has decreased dramatically with the incorporation of strict clinical management of postmolar disease as well as with the overall decrease in the number of pregnancies.

The use of a tumor marker not only depends on its sensitivity and specificity, but also on its ability to influence decisions between alternative plans for patient management. Use of beta human chorionic gonadotropin (beta-hCG) for monitoring gestational trophoblastic neoplasia has set the standard to which other assays must be compared. Beta-hCG and alpha-fetoprotein have provided useful markers for ovarian germ cell tumors.

Recently, a monoclonal antibody-based immunoassay for CA-125 has been used to monitor the treatment of epithelial ovarian carcinomas. Persistent elevation of CA-125 in serum has generally reflected persistence of disease at second look surveillance procedures. However, CA-125 levels can return to within normal limits and residual disease can be found at laparoscopy or laparotomy. CA-125 shows promise for distinguishing benign from malignant pelvic masses. Several trials are ongoing to determine the potential of CA-125 in combination with other markers to increase earlier detection of occult ovarian cancer.1

Some tumor markers can be used for screening, diagnosis, management, determining response, and recurrence. Some markers show promise as prognostic indicators.

The following are important gynecologic tumor markers :

a) Cancer antigen 125 (CA-125)

b) Beta chorionic gonadotropin (beta-hCG)

c) Alpha-fetoprotein (AFP)

d) Inhibin

e) Estradiol

f) Müllerian inhibiting substance (MIS)

g) Carbohydrate antigen 19-9

h) Ferritin

i) Topoisomerase II

j) Urinary gonadotropin fragment

k) Carcinoembryonic antigen (CEA)

m) Human telomerase reverse transcriptase (hTERT)

n) Others :

1) Tumor-associated trypsin inhibitor

2) Cyclin E

3) Lysophosphatidic acid (a lipid found to be elevated in serum and ascites fluid)

4) Mesothelin

5) HE4

6) Osteopontin

7) Vascular endothelial growth factor (VEGF)

8) Interleukin 8

9) Macrophage colony-stimulating factor

10) Insulinlike growth factor–binding protein-3

11) OVX1

No marker is completely specific; therefore, diagnostic immunohistochemistry testing must be used in conjunction with morphologic and clinical findings.

Cancer Antigen 125

After its initial discovery in the early 1980s, the serum CA-125 level has been widely used as a marker for a possible epithelial ovarian cancer in the primary assessment of a pelvic mass. In this setting, false-positive results may derive from several conditions, especially those associated with peritoneal inflammation, such as endometriosis, adenomyosis, pelvic inflammatory disease, menstruation, uterine fibroids, or benign cysts. Malignancies other than ovarian cancer can also increase CA-125 levels, but the most marked elevations (>1500 U/mL) are generally seen with ovarian cancer.

The primary use of CA-125 measurement is to monitor the disease status of patients with ovarian cancer, such as detecting early recurrence or assessing chemoresponse during chemotherapy. Serum CA-125 levels are also included in the American College of Obstetricians and Gynecologists and Society of Gynecologic Oncologists guidelines for referring patients to a gynecologic oncologist.

Postmenopausal women with serum levels of CA-125 higher than 35 U/mL or premenopausal women with CA-125 levels higher than 200 U/mL should be referred to a gynecologic oncologist. In an attempt to improve CA-125 measurement for the detection of epithelial ovarian cancers, especially at an early stage, recent studies have identified several new candidates for markers. Examples include lysophosphatidic acid (a lipid found to be elevated in serum and ascites fluid), mesothelin, HE4, osteopontin, vascular endothelial growth factor (VEGF) and interleukin 8, macrophage colony-stimulating factor, and different kallikreins. Interestingly, among these potential markers, HE4 has sensitivity similar to CA-125 in detecting late-stage disease but greater specificity than CA-125 in diagnosing early ovarian cancer. Validation of HE4 as a diagnostic biomarker in detecting ovarian cancer at early stages is currently ongoing.

Approximately 90% of ovarian cancers are celomic epithelial carcinomas and contain a celomic epithelium–related glycoprotein-designated CA-125. CA-125 can be localized in most serous, endometrioid, and clear cell ovarian carcinomas; mucinous tumors express this antigen less frequently. CA-125 is also found in the epithelium of the fallopian tubes, endometrium, and uterine cervix.

Ovarian carcinoma is the leading cause of death from gynecologic malignancies. CA-125 is an important tumor marker for the diagnosis, treatment, and follow-up care of patients with epithelial ovarian cancer and has been recommended for screening; however, CA-125 may not lead to early diagnosis because it is not perfectly sensitive or specific for ovarian cancer. CA-125 can be used clinically to determine response to treatment, relapse, and survival.

Although CA-125 is most consistently elevated in patients with epithelial ovarian cancer, it can be expressed in a number of gynecologic (eg, endometrium, fallopian tube) and nongynecologic (eg, pancreas, breast, colon, lung) cancers. CA-125 levels are frequently elevated with tumor spread beyond the uterus and have been found highly sensitive in detecting extrauterine disease.

Serum CA-125 markers are primarily used to monitor the progress of ovarian cancer. An increase in CA-125 levels during or after treatment is a strong predictor of future disease progression. A rapid decrease in CA-125 levels during initial treatment correlates with longer progression-free intervals and survival. A CA-125 level less than 15 U/mL after a standard 6-course treatment generally correlates with longer progression-free intervals, although it does not predict whether microscopic disease is present. A CA-125 value greater than 35 U/mL after a standard 6-course chemotherapy treatment predicts the presence of disease. Disease progression may also occur when CA-125 values are stable.

Standardized CA-125 definitions have the potential of complementing or, in some cases, replacing current response definitions in a cost-effective way. The rate of CA-125 decline during primary chemotherapy is an important independent prognostic factor. Persistent elevation of CA-125 levels at the time of a second-look surgical surveillance procedure predicts residual disease with at least a 95% specificity. Rising CA-125 values have preceded clinical detection of recurrent disease by at least 3 months. Given the modest activity of salvage chemotherapy, this information has not yet influenced survival rates. Rising CA-125 level during subsequent chemotherapy is associated with progressive disease in at least 90% of cases. CA-125 may serve as an effective surrogate marker for clinical response in clinical trials of new drugs.

The measurement of CA-125 levels, usually in combination with other modalities (eg, bimanual pelvic examination, transvaginal ultrasonography) is a proposed method of early detection of ovarian cancer, which is the most promising application of this tumor marker. CA-125 levels can help distinguish malignant and benign pelvic masses, which permits effective triage of patients for primary surgery. In addition, an algorithm has been developed that estimates the risk of ovarian cancer based on the level and trend of CA-125 values.

Screening using CA-125

Early-stage ovarian cancer has excellent prognosis after definitive therapy. Therefore, early detection is vital in reducing mortality due to this disease. However, no screening program for ovarian cancer has achieved this goal. Several studies have been launched to identify the best strategy for detecting early-stage disease and reducing mortality by using either CA-125 or ultrasonography as the primary screening test. In a cohort of roughly 15,500 women, the positive predictive value for ultrasonography screening ranged from 1.5% when abdominal ultrasonography was used to close to the screening-recommended 10% when transvaginal ultrasonography was used. This low positive predictive value is due to the commonality of benign pelvic lesions, even in postmenopausal women.

High specificity is important in screening strategies for ovarian cancer because a positive test result generally requires definitive surgical assessment. Given the relatively low prevalence of ovarian cancer, a test with 95% specificity would result in 50 surgical procedures for every ovarian cancer detected. Einhorn and colleagues screened 5550 women with CA-125 alone and this screening approach resulted in an unacceptable 29 surgeries for every cancer detected. Another major limitation of CA-125 screening is that serum levels are elevated in only about 50% of patients with stage I disease.

Because several gynecologic and nongynecologic conditions can elevate CA-125 levels, combination test strategies have been tried to improve the predictive value of CA-125. Jacobs and colleagues randomized 22,000 postmenopausal women to be screened with 3 annual CA-125 measurements or no screening. Those patients with CA-125 levels higher than 30 U/mL underwent transvaginal ultrasonography. Twenty-nine women were referred for surgical exploration, and 6 women were diagnosed as having ovarian cancer (3 of whom had stage I). The positive predictive value was 20.7%. Ten additional women in the screening arm developed ovarian cancer during follow-up. Twenty women in the control arm developed ovarian cancer. The investigators were able to show a median survival benefit (73 months in the screened arm vs 42 months in the control group; P =.01)

Two large randomized studies are currently ongoing. The NIH Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial4 enrolled 75,000 women aged 55-74 years from 1992-2001. The study randomly assigned women to screening (ie, annual pelvic examination, transvaginal ultrasonography, and CA-125 assay) or no screening. The recently published prevalence data from this study revealed familiar findings: 31 women operated on for every invasive cancer detected and a high proportion of advanced-stage cancers. However, these initial results are affected greatly by the benign and malignant conditions prevalent at a woman’s first screening evaluation. The true effectiveness of the screening strategy will now be tested by its ability to detect new cancers during the next several years.

The second study, started in 2001, called the UK Collaborative Trial of Ovarian Cancer Screening, has completed randomization of 200,000 postmenopausal women to transvaginal ultrasonography, multimodality screening, or a control group. These studies will answer the question of whether ultrasonography with or without CA-125–based screening in women with ovarian cancer can reduce mortality due to ovarian cancer.

Currently new screening approaches are being studied including high-throughput techniques using microarray technology and proteomic screening to identify panels of novel markers that may be altered early in the disease.

Ovarian epithelial tumors are histologically classified into serous tumors, mucinous tumors, endometrioid tumors, clear cell tumors, Brenner tumors, undifferentiated tumors, mixed epithelial tumors (composed of ≥2 of the 5 major cell types of common epithelial tumors), and intraperitoneal cancer (the ovaries appear to be incidentally involved and not the primary origin, which should be classified as extraovarian peritoneal cancer).

Serous tumors are the most common type, accounting for almost half of all epithelial ovarian cancers. These cells histologically resemble cells that line the fallopian tube. They tend to be high grade and are the cancers most often seen in BRCA mutation carriers. Endometrioid cancers resemble the cells that line the endometrium. These cancers are sometimes associated with endometriosis. Clear cell tumors are relatively uncommon, occurring most often in women in their 40s. Approximately 50% of women with clear cell tumors have associated endometriosis. Although most clear cell cancers are diagnosed at an early stage, these tumors are aggressive. The cells of mucinous tumors resemble those of the cervix or intestine. Mucinous tumors are more likely to be found in younger women, and 75-80% are benign and develop in only 1 ovary. Cancerous mucinous tumors are more common in older women and do not produce CA-125.

Epithelial tumors of the ovary are also subclassified by grading: Gx, grade cannot be assessed; G1, well differentiated; G2, moderately differentiated; and G3, poorly differentiated. Grade is related to prognosis in ovarian cancer, with patients with low-grade cancers doing better. Grade information is considered in treatment decisions for women with stage I disease.

Borderline ovarian tumors, or tumors of low malignant potential, also develop in the epithelial cells that cover the surface of the ovaries. Although borderline tumors have some malignant features, such as malignant-appearing histologic features and excess proliferation, they generally behave in an indolent manner. One important feature of borderline tumors is that they do not invade the stroma of the ovary. Borderline tumors make up 10-15% of all epithelial ovarian tumors. Approximately 3000 women in the United States are diagnosed with borderline tumors every year. Although these tumors can occur in women of all ages, they commonly occur in younger woman compared to epithelial ovarian cancers, and they have the same risk factors as epithelial ovarian cancer.

At diagnosis, approximately 20% of borderline tumors have spread beyond the ovary via peritoneal implants, but unlike epithelial ovarian cancer implants, these borderline peritoneal implants are noninvasive. However, in less than 5% of borderline tumors, so-called invasive implants can be found that invade below the peritoneal surface layer. A borderline tumor with invasive implants behaves more aggressively than does a borderline tumor with noninvasive implants. Surgery is the mainstay of treatment for women with borderline tumors of the ovary. Chemotherapy can be given to those patients that have more aggressive features, such as invasive implants or rapid recurrence after surgery.

CA-125 can be elevated up to 3% more than normal postmenopausal women. Therefore, screening using the CA-125 test has not been effective enough for widespread use. For ovarian cancer to be detected in 1 additional patient using CA-125 as the primary screening tool, another 100-150 women would have to receive evaluation and approximately 30 diagnostic operations be performed. To enhance the use of CA-125 for ovarian cancer screening, the change in CA-125 concentration in the bloodstream over time is being investigated as compared to just depending upon the absolute value.

Ovarian cancer screening is not recommended for women with no risk factors (RR≤3). For women with increase risk (RR=3-6 times), after evaluating risks and benefits, ovarian cancer screening with CA-125 and/or transvaginal ultrasonography can be done, usually by clinical trials. In women at inherited risk (RR>6 times), usually with mutations in ovarian cancer susceptibility genes, should receive screening by a combination of transvaginal ultrasonography and CA-125. For patients with mutations in BRCA1 or the mismatch repair genes, MLH1, MSH2, and MSH6, screening should begin around 30-35 years of age. For patients with mutations in BRCA2, ovarian cancer screening should be performed around 35-40 years of age.

The Gynecologic Cancer Intergroup uses the Rustin definition to define a rise in CA-125. If the CA-125 level becomes normal after surgery, a subsequent level twice the upper limit of normal is consistent with progression. If the CA-125 level is not normal after surgery, then a subsequent level twice the patient's nadir value signifies progressive disease.

Serum CA-125 level has been widely used as a marker for a possible epithelial ovarian cancer in the primary assessment of a pelvic mass. The predominant use of CA-125 measurement is to monitor disease status of patients with ovarian cancer, such as detecting early recurrence or assessing response during chemotherapy. CA-125 has provided a useful first-generation marker for monitoring ovarian cancer and triaging patients with pelvic masses, despite limitations in sensitivity and specificity. In the next decade, the challenge will be to identify new markers that will complement CA-125 in monitoring ovarian cancer and facilitate screening for occult early-stage disease. The expression of growth factors and their receptors and application of monoclonal antibodies to immunohistochemistry and radionuclide imaging may also provide new areas of diagnostic application for monoclonal antibodies in gynecologic oncology.

Other Gynecologic Tumor Markers

human chorionic gonadotropin

Beta-hCG is expressed in human fetal tissue and cancer cells of various histologic types. It is degraded to the beta-core fragment, which is concentrated in urine and is also known as urinary gonadotropin peptide. Urinary gonadotropin fragment and lipid-associated sialic acid levels are elevated in up to 60% of patients with endometrial cancer.

Increased levels of beta-hCG occur in patients with choriocarcinoma of the uterus, embryonal carcinomas, polyembryomas, mixed cell tumors, and, less commonly, dysgerminomas. Both beta-hCG and human placental lactogen (hPL) are the most useful markers for trophoblastic disease and can be localized in syncytiotrophoblasts of partial and complete hydatidiform moles. The intensity and pattern of reactivity for these antigens differ in partial and complete moles. Gestational choriocarcinomas demonstrate variable but positive staining results for beta-hCG and hPL. The hPL immunostaining differentiates placental-site trophoblastic tumors from choriocarcinomas. The use of beta-hCG is not limited to trophoblastic diseases because it has been localized in a wide array of nontrophoblastic gynecologic neoplasms.

The following diagnostic criteria is commonly used for malignant gestational trophoblastic disease :

a) lateauing of beta-hCG levels over at least 3 weeks
b) 10% or greater rise in beta-hCG for 3 or more values over at least 2 weeks
c) Persistence of beta-hCG 6 months after molar evacuation
d) Histologic identification of choriocarcinoma

Patients who have undergone molar pregnancy evacuation should undergo weekly beta-hCG monitoring until normal levels are achieved, then monthly monitoring until 6-12 months of normal values have been achieved. About 20% patients undergoing evacuation of molar pregnancy will develop postmolar gestational trophoblastic disease, usually manifesting as failure to normalize the postevacuation beta-hCG levels. A 10% rise in beta-hCG over 3 or more weekly titers or a beta-hCG titer of 40,000 mIU/L 4-5 months after uterine evacuation constitutes a serological diagnosis of postmolar trophoblastic disease.

For metastatic malignant trophoblastic disease, beta-hCG monitoring is recommended every 6 months for an indefinite period of time because late recurrence is a possibility.

The beta subunit of human chorionic gonadotropin (beta-hCG) is normally produced by the placenta. Elevated b-hCG levels are most commonly associated with pregnancy, germ cell tumors, and gestational trophoblastic disease. False-positive levels occur in hypogonadal states and with marijuana use.

Both AFP and beta-hCG play crucial roles in the management of patients with nonseminomatous germ cell tumors. The AFP or beta-hCG level is elevated in 85% of patients with these tumors but in only 20% of patients with stage I disease. Hence, these markers have no role in screening.

In patients with extragonadal disease or metastasis at the time of diagnosis, highly elevated AFP or beta-hCG values can be used in place of biopsy to establish a diagnosis of nonseminomatous germ cell tumor. AFP values in excess of 10,000 ng/mL or beta-hCG levels above 50,000 mIU/mL at initial diagnosis portend a poor prognosis, with a 5-year survival rate of 50%. Similarly staged patients with lower AFP and beta-hCG levels have a cure rate above 90%.

Following AFP and beta-hCG levels is imperative in monitoring response to treatment in patients who have nonseminomatous germ cell tumors. Patients with AFP and beta-hCG levels that do not decline as expected after treatment have a significantly worse prognosis, and changes in therapy should be considered. Because curative salvage therapy is possible, the tumor markers are followed every 1-2 months for 1 year after treatment, then quarterly for 1 year, and less frequently thereafter. AFP or beta-hCG level elevation is frequently the first evidence of germ cell tumor recurrence; a confirmed elevation should prompt reinstitution of therapy.

In spite of complete clinical response after chemotherapy, almost 50% of patients with stage III/IV disease have residual tumor. Among patients with persistent elevation of CA-125, about 90-95% will have residual tumor. The beta-hCG level is used for monitoring response to therapy and detecting early relapse. Testing for the beta-hCG is an integral part of the diagnosis, management, and response to treatment for gestational trophoblastic disease and in selected patients with epithelial carcinomas of the ovary. Combined AFP and beta-hCG testing is an essential adjunct in the evaluation and treatment of nonseminomatous germ cell tumors, and in monitoring the response to therapy. AFP and beta-hCG may also be useful in evaluating potential origins of poorly differentiated metastatic cancer.

Human telomerase reverse transcriptase (hTERT)

Human telomerase reverse transcriptase (hTERT) is a novel and newly available biomarker for patients with ovarian and uterine cancers. The hTERT mRNA level has a significant correlation with CA-125 and with histological findings in ovarian cancer. Serum hTERT mRNA is useful for diagnosing gynecologic cancer and is superior to conventional tumor markers. Upregulation of hTERT may play an important role in the development of cervical intraepithelial neoplasia (CIN) and cervical cancer; hTERT could be used as an early diagnostic biomarker for cervical cancer in the future.

Inhibin

Inhibin is a peptide hormone normally produced by ovarian granulosa cells. It inhibits the secretion of follicle-stimulating hormone (FSH) by the anterior pituitary gland. It reaches a peak of 772 +/- 38 U/L in the follicular phase of the menstrual cycle and is normally undetectable in the serum of menopausal women. Granulosa-cell tumors produce inhibin and its serum levels reflect the the tumor burden. Measurement of inhibin can be used as a marker for primary as well as recurrent granulosa cell tumor.

The recent availability of markers of ovarian stroma, including melan-A and inhibin-alpha, has provided a means for the positive identification of ovarian stromal tumors, which can manifest in a myriad of histological appearances.

The hormonal activity of granulosa cell tumors permits the use of a variety of serum tumor markers in the diagnostic evaluation. Clinically, the most useful serum marker for granulosa cell tumors is inhibin. Inhibin exists in 2 different isoforms, inhibin A and inhibin B. Both isoforms consist of a dimer of 2 subunits, the alpha and beta subunits. The alpha subunit is the same for both isoforms, while the beta subunits differ (beta A and beta B) and show about 64% homology. The 3 subunits (alpha, beta A, beta B) are produced on separate genes located on chromosomes 2 (alpha and beta B) and 7 (beta A).

Inhibin usually becomes nondetectable after menopause. However, certain ovarian tumors, mostly mucinous epithelial ovarian carcinomas and granulosa cell tumors, produce inhibin. An elevated inhibin level in a postmenopausal woman or a premenopausal woman presenting with amenorrhea and infertility is suggestive of the presence of a granulosa cell tumor, but not specific. Inhibin levels can also be used for tumor surveillance after treatment to assess for residual or recurrent disease. Although most commercial laboratories only provide assays for inhibin A, serum levels of inhibin B seem to be more frequently elevated. Whenever available, the use of assays is suggested that detect both isoforms. The free alpha subunit can also be measured.

Estradiol

Estradiol was one of the first markers identified in the serum of patients with granulosa cell tumors. In general, estradiol is not a sensitive marker for the presence of a granulosa cell tumor. About 30% of tumors do not produce estradiol due to lack of theca cells, which produce androstendione, a necessary precursor for estradiol synthesis. However, following serum estradiol levels postoperatively may be useful for detecting recurrence of an estradiol-secreting tumor.

Müllerian inhibiting substance

Müllerian inhibiting substance (MIS) is produced by granulosa cells in the developing follicles. It has emerged as a potential tumor marker for granulosa cell tumors. As with inhibin, MIS is typically undetectable in postmenopausal women. The elevated MIS level is highly specific for ovarian granulosa cell tumors; however, this test is not commercially available for clinical use.

Topoisomerase II

Topoisomerase II expression is detected in tumor samples by immunohistochemistry and has emerged as a promising, clinically relevant biomarker for survival in patients with advanced epithelial ovarian cancer.

Carbohydrate antigen 19-9

Serum carbohydrate antigen 19-9 levels are elevated in up to 35% of patients with endometrial cancer and can be used in a follow-up evaluation of patients with mucinous borderline ovarian tumors. Measurement of serum tumor markers in the follow-up care of these patients may lead to earlier detection of recurrence in only a very small proportion of patients; the clinical value of earlier detection of recurrence remains to be established. Carbohydrate antigen is not specific for ovarian cancer.

Cancer antigen 27-29

Elevated cancer antigen 27-29 levels are associated with cancers of the colon, stomach, kidney, lung, ovary, pancreas, uterus, and liver. First-trimester pregnancy, endometriosis, ovarian cysts, benign breast disease, kidney disease, and liver disease are noncancerous conditions that are also associated with increased cancer antigen 27-29 levels.

Markers for Response to Therapy and Relapse

The following tumor markers are helpful in assessing response to chemotherapy and in determining relapse when monitoring patients with complete remission.

Squamous cell carcinoma antigen

The squamous cell carcinoma antigen level can be increased in patients with epidermoid carcinoma of the cervix, benign tumors of epithelial origin, and benign skin disorders.

Carcinoembryonic antigen

Most sweat gland tumors of the vulva stain positively for carcinoembryonic antigen (CEA). In most instances, the reaction for CEA occurs in cells that line cysts, form glands, or are arranged around a lumen. The reaction for CEA does not differentiate eccrine from apocrine adnexal tumors. In patients with vaginal adenosis, both surface columnar epithelium and glands may show focal cytoplasmic membrane staining for CEA. As the columnar cells are gradually replaced by the process of squamous metaplasia, CEA positivity may be observed in the cytoplasm of metaplastic cells. Malignant vulvar tumors of sweat gland origin stain positively for CEA. Both in situ and invasive adenocarcinomas underlying extramammary Paget disease of the anogenital area express CEA. CEA is also demonstrable in Paget cells at metastatic sites such as lymph nodes. CEA is present in most urothelial adenocarcinomas of the female urethra.

CEA levels are elevated in up to 35% of patients with endometrial cancer. CEA immunohistochemistry cannot distinguish between benign and malignant glandular proliferations of the uterine cervix; therefore, CEA staining is of no value in the differential diagnosis of endocervical and endometrial adenocarcinomas.

Most epithelial neoplasms of the ovary also express CEA. The neoplasms include, with decreasing intensity and frequency, Brenner, endometrioid, clear cell, and serous tumors. CEA is frequently present in patients with cancer that has metastasized to the ovary because the primary cancer is generally mammary or gastrointestinal in origin and these tumors frequently contain CEA.

Alpha-fetoprotein

Alpha-fetoprotein (AFP) is a normal fetal serum protein synthesized by the liver, yolk sac, and gastrointestinal tract that shares sequence homology with albumin. AFP is a major component of fetal plasma, reaching a peak concentration of 3 mg/mL at 12 weeks of gestation. Following birth, AFP rapidly clears from the circulation because its half-life is 3.5 days. AFP concentration in adult serum is less than 20 ng/mL.

Most endodermal sinus tumors of the ovary express AFP. AFP is present within the cytoplasm of tumor cells and in the characteristic hyalin globules observed in the endodermal sinus tumor. AFP is also expressed by ovarian embryonal cell carcinoma, immature teratomas, and polyembryomas.

Lysophosphatidic acid

Lysophosphatidic acid stimulates cancer cell proliferation, intracellular calcium release, and tyrosine phosphorylation, including mitogen-activated protein kinase activation. Lysophosphatidic acid has been shown to be a multifunctional signaling molecule in fibroblasts and other cells. It has been found in the ascitic fluid of patients with ovarian cancer and is associated with ovarian cancer cell proliferation. Further studies are needed to determine the role of these markers.

MIB1-determined tumor growth fraction has recently been studied as an additional tool for the decision of adjuvant therapy in patients with very early stages of ovarian carcinomas. In one study, MIB1 predicted tumor recurrences in 84% of the ovarian cancers.

L1 (CAM)

According to Daponte et al, L1 (CAM) immunoreactivity correlates with stage and grade of ovarian cancer. It increases from benign tumors to early carcinomas and to advanced stage carcinomas progressively and significantly. L1 (CAM) expression represents a novel diagnostic marker in serous ovarian neoplasms that shows characteristics of tumor progression. L1 expression is associated with chemotherapy response.6

Normalization of tumor markers

Normalization of tumor marker values may indicate cure despite radiographic evidence of persistent disease. In this situation, the residual tumor is frequently nonviable. Sometimes, tumor marker levels may rise after effective treatment (due to cell lysis), but the increase may not portend treatment failure. A consistent increase in tumor marker levels, combined with lack of clinical improvement, may indicate treatment failure. Residual elevation after definitive treatment usually indicates persistent disease.

Screening

Screening tests require high sensitivity to detect early-stage disease. These tests also must have sufficient specificity to protect patients with false-positive results from unnecessary diagnostic work up.

So far, no tumor marker has demonstrated a survival benefit in randomized controlled trials of screening in the general population. However, these tumor markers can play a crucial role in detecting disease, assessing response to therapy, and monitoring for disease recurrence.

The NCI is currently conducting the Prostate, Lung, Colorectal, and Ovarian Cancer (PLCO) screening trial to determine if certain screening tests, including CA-125 to screen for ovarian cancer, reduce the number of deaths from these cancers.

Proteomics are being investigated for developing better cancer screening and treatment options. Proteomics may also help to identify new proteins that serve as tumor markers in early stages and to predict the effectiveness of treatment and probability of recurrence.

Saturday, July 18, 2009

What is Henoch-Schonlein Purpura (HSP) ?



[Extracted from MedicineNet.Com]

Henoch-Schonlein purpura (HSP) is a form of blood vessel inflammation or vasculitis. There are many different conditions that feature vasculitis. Each of the forms of vasculitis tends to involve certain characteristic blood vessels. HSP affects the small vessels called capillaries in the skin and frequently the kidneys. HSP results in skin rash (most prominent over the buttocks and behind the lower extremities) associated with joint inflammation (arthritis) and sometimes cramping pain in the abdomen. Henoch-Schonlein purpura is also referred to as anaphylactoid purpura.

What causes HSP ?

HSP occurs most often in the spring and frequently follows an infection of the throat or breathing passages. HSP seems to represent an unusual reaction of the body's immune system that is in response to this infection (either bacteria or virus). Aside from infection, drugs can also trigger the condition. HSP occurs most commonly in children, but people of all age groups can be affected.



What are symptoms of HSP ?

Classically, HSP causes skin rash, pain in the abdomen, and joint inflammation (arthritis). Not all features need be present for the diagnosis. The rash of skin lesions appears in gravity-dependent areas, such as the legs. The joints most frequently affected with pain and swelling are the ankles and the knees. Patients with HSP can develop fever. Inflammation of the blood vessels in the kidneys can cause blood and/or protein in the urine. Serious kidney complications are infrequent but can occur.

Symptoms usually last approximately a month. Recurrences are not frequent but do occur.

How is HSP diagnosed ?

HSP is usually diagnosed based on the typical skin, joint, and kidney findings. Throat culture, urinalysis, and blood tests for inflammation and kidney function are used to suggest the diagnosis. A biopsy of the skin, and less commonly kidneys, can be used to demonstrate vasculitis. Special staining techniques (direct immunofluorescence) of the biopsy specimen can be used to document antibody deposits of IgA in the blood vessels of involved tissue.

What is the treatment for HSP ?

While HSP is generally a mild illness that resolves spontaneously, it can cause serious problems in the kidneys and bowels. The rash can be very prominent, especially on the lower extremities.

The treatment of HSP is directed toward the most significant area of involvement. Joint pain can be relieved by antiinflammatory medications such as aspirin or ibuprofen (Motrin). Some patients can require cortisone medications, such as prednisone or prednisolone, especially those with significant abdominal pain or kidney disease. With more severe kidney disease, involvement called glomerulonephritis or nephritis, cyclophosphamide (Cytoxan), azathioprine (Imuran), or mycophenolate mofetil (Cellcept) have been used to suppress the immune system. Infection, if present, can require antibiotics.



What is the prognosis for patients with HSP ?

The prognosis for patients with HSP is generally excellent. Nearly all patients have no long-term problems. The kidney is the most serious organ involved when it is affected. Rarely, patients can have serious long-term kidney damage or an abnormal bowel folding called intussusception. Some patients have recurrences of symptoms, particularly skin rash, for months to a year after the onset of the illness.

Recent data show that HSP in adults is generally more severe than in children. Adults have more severe kidney involvement and can require more aggressive treatment. The ultimate outcome, however, is usually very good for both adults and children.

Henoch-Schonlein Purpura At A Glance

* Henoch-Schonlein purpura is a particular form of blood vessel inflammation called vasculitis.

* Henoch-Schonlein purpura frequently follows an infection of the throat or breathing passages, but it can be induced by certain medications.

* Henoch-Schonlein purpura causes skin rash, pain in the abdomen, and joint inflammation (arthritis).

* The treatment of Henoch-Schonlein purpura is directed toward the most significant area of involvement.

* The prognosis for patients with Henoch-Schonlein purpura is generally excellent.

Friday, July 17, 2009

What is Lung Cancer ?



This article is posted for every friend to know what is this type of Cancer all about. Smokers especially, do take care of yourself and if you don't..always remember that there are others around, who does

[Extraced from MedicineNet.Com]

What is cancer of the lung ?

Cancer of the lung, like all cancers, results from an abnormality in the body's basic unit of life, the cell. Normally, the body maintains a system of checks and balances on cell growth so that cells divide to produce new cells only when needed. Disruption of this system of checks and balances on cell growth results in an uncontrolled division and proliferation of cells that eventually forms a mass known as a tumor.

Tumors can be benign or malignant; when we speak of "cancer," we refer to those tumors that are considered malignant. Benign tumors can usually be removed and do not spread to other parts of the body. Malignant tumors, on the other hand, grow aggressively and invade other tissues of the body, allowing entry of tumor cells into the bloodstream or lymphatic system and then to other sites in the body. This process of spread is termed metastasis; the areas of tumor growth at these distant sites are called metastases. Since lung cancer tends to spread or metastasize very early in its course, it is a very life-threatening cancer and one of the most difficult cancers to treat. While lung cancer can spread to any organ in the body, certain organs -- particularly the adrenal glands, liver, brain, and bone -- are the most common sites for lung-cancer metastasis.

The lung is also a very common site for metastasis from tumors in other parts of the body. Tumor metastases are made up of the same type of cells as the original, or primary, tumor. For example, if prostate cancer spreads via the bloodstream to the lungs, it is metastatic prostate cancer in the lung and is not lung cancer.

Lung Cancer Picture



The principal function of the lungs is the exchange of gases between the air we breathe and the blood. Through the lung, carbon dioxide is removed from the bloodstream and oxygen from inspired air enters the bloodstream. The right lung has three lobes, while the left lung is divided into two lobes and a small structure called the lingula that is the equivalent of the middle lobe. The major airways entering the lungs are the bronchi, which arise from the trachea. The bronchi branch into progressively smaller airways called bronchioles that end in tiny sacs known as alveoli where gas exchange occurs. The lungs and chest wall are covered with a thin layer of tissue called the pleura.

Lung cancers can arise in any part of the lung, but 90%-95% of cancers of the lung are thought to arise from the epithelial, or lining cells of the larger and smaller airways (bronchi and bronchioles); for this reason, lung cancers are sometimes called bronchogenic carcinomas or bronchogenic cancers. Cancers can also arise from the pleura (the thin layer of tissue that surrounds the lungs), called mesotheliomas, or rarely from supporting tissues within the lungs, for example, blood vessels.

How common is lung cancer ?

Lung cancer is responsible for the most cancer deaths in both men and women throughout the world. The American Cancer Society estimates that 215,020 new cases of lung cancer in the U.S. will be diagnosed and 161,840 deaths due to lung cancer will occur in 2008. According to the U.S. National Cancer Institute, approximately one out of every 14 men and women in the U.S. will be diagnosed with cancer of the lung or airways at some point in their lifetime.

Lung cancer is predominantly a disease of the elderly; almost 70% of people diagnosed with the condition are over 65 years of age, while less than 3% of cases occur in people under age 45.

Lung cancer was not common prior to the 1930s but increased dramatically over the following decades as tobacco smoking increased. In many developing countries, the incidence of lung cancer is beginning to fall following public education about the dangers of cigarette smoking and effective smoking-cessation programs. Nevertheless, lung cancer remains among the most common types of cancers in both men and women worldwide.

Lung cancer has also surpassed breast cancer in causing the most cancer-related deaths in women in the United States.

What causes lung cancer ?

Smoking

The incidence of lung cancer is strongly correlated with cigarette smoking, with about 90% of lung cancers arising as a result of tobacco use. The risk of lung cancer increases with the number of cigarettes smoked over time; doctors refer to this risk in terms of pack-years of smoking history (the number of packs of cigarettes smoked per day multiplied by the number of years smoked). For example, a person who has smoked two packs of cigarettes per day for 10 years has a 20 pack-year smoking history. While the risk of lung cancer is increased with even a 10-pack-year smoking history, those with 30-pack-year histories or more are considered to have the greatest risk for the development of lung cancer. Among those who smoke two or more packs of cigarettes per day, one in seven will die of lung cancer.

Pipe and cigar smoking can also cause lung cancer, although the risk is not as high as with cigarette smoking. While someone who smokes one pack of cigarettes per day has a risk for the development of lung cancer that is 25 times higher than a nonsmoker, pipe and cigar smokers have a risk of lung cancer that is about five times that of a nonsmoker.

Tobacco smoke contains over 4,000 chemical compounds, many of which have been shown to be cancer-causing, or carcinogenic. The two primary carcinogens in tobacco smoke are chemicals known as nitrosamines and polycyclic aromatic hydrocarbons. The risk of developing lung cancer decreases each year following smoking cessation as normal cells grow and replace damaged cells in the lung. In former smokers, the risk of developing lung cancer begins to approach that of a nonsmoker about 15 years after cessation of smoking.

Passive smoking

Passive smoking, or the inhalation of tobacco smoke from other smokers sharing living or working quarters, is also an established risk factor for the development of lung cancer. Research has shown that nonsmokers who reside with a smoker have a 24% increase in risk for developing lung cancer when compared with other nonsmokers. An estimated 3,000 lung cancer deaths occur each year in the U.S. that are attributable to passive smoking.

Asbestos fibers

Asbestos fibers are silicate fibers that can persist for a lifetime in lung tissue following exposure to asbestos. The workplace is a common source of exposure to asbestos fibers, as asbestos was widely used in the past as both thermal and acoustic insulation. Today, asbestos use is limited or banned in many countries, including the U.S. Both lung cancer and mesothelioma (cancer of the pleura of the lung as well as of the lining of the abdominal cavity called the peritoneum) are associated with exposure to asbestos. Cigarette smoking drastically increases the chance of developing an asbestos-related lung cancer in exposed workers. Asbestos workers who do not smoke have a fivefold greater risk of developing lung cancer than nonsmokers, and those asbestos workers who smoke have a risk that is 50 to 90 times greater than nonsmokers.

Radon gas

Radon gas is a natural, chemically inert gas that is a natural decay product of uranium. Uranium decays to form products, including radon, that emit a type of ionizing radiation. Radon gas is a known cause of lung cancer, with an estimated 12% of lung-cancer deaths attributable to radon gas, or 15,000-22,000 lung-cancer-related deaths annually in the U.S., making radon the second leading cause of lung cancer in the U.S. As with asbestos exposure, concomitant smoking greatly increases the risk of lung cancer with radon exposure. Radon gas can travel up through soil and enter homes through gaps in the foundation, pipes, drains, or other openings. The U.S. Environmental Protection Agency estimates that one out of every 15 homes in the U.S. contains dangerous levels of radon gas. Radon gas is invisible and odorless, but it can be detected with simple test kits.

Familial predisposition

While the majority of lung cancers are associated with tobacco smoking, the fact that not all smokers eventually develop lung cancer suggests that other factors, such as individual genetic susceptibility, may play a role in the causation of lung cancer. Numerous studies have shown that lung cancer is more likely to occur in both smoking and nonsmoking relatives of those who have had lung cancer than in the general population. Recent research has localized a region on the long (q) arm of human chromosome number 6 that is likely to contain a gene that confers an increased susceptibility to the development of lung cancer in smokers.

Lung diseases

The presence of certain diseases of the lung, notably chronic obstructive pulmonary disease (COPD), is associated with an increased risk (four to six times the risk of a nonsmoker) for the development of lung cancer even after the effects of concomitant cigarette smoking are excluded.

Prior history of lung cancer

Survivors of lung cancer have a greater risk than the general population of developing a second lung cancer. Survivors of non-small cell lung cancers (NSCLCs, see below) have an additive risk of 1%-2% per year for developing a second lung cancer. In survivors of small cell lung cancers (SCLCs, see below), the risk for development of second cancers approaches 6% per year.

Air pollution

Air pollution from vehicles, industry, and power plants can raise the likelihood of developing lung cancer in exposed individuals. Up to 1% of lung cancer deaths are attributable to breathing polluted air, and experts believe that prolonged exposure to highly polluted air can carry a risk for the development of lung cancer similar to that of passive smoking.

What are the types of lung cancer ?

Lung cancers, also known as bronchogenic carcinomas (carcinoma is another term for cancer), are broadly classified into two types: small cell lung cancers (SCLC) and non-small cell lung cancers (NSCLC). This classification is based upon the microscopic appearance of the tumor cells themselves. These two types of cancers grow and spread in different ways and may have different treatment options, so a distinction between these two types is important.

SCLC comprise about 20% of lung cancers and are the most aggressive and rapidly growing of all lung cancers. SCLC are strongly related to cigarette smoking, with only 1% of these tumors occurring in nonsmokers. SCLC metastasize rapidly to many sites within the body and are most often discovered after they have spread extensively. Referring to a specific cell appearance often seen when examining samples of SCLC under the microscope, these cancers are sometimes called oat cell carcinomas.

NSCLC are the most common lung cancers, accounting for about 80% of all lung cancers. NSCLC can be divided into three main types that are named based upon the type of cells found in the tumor :

* Adenocarcinomas are the most commonly seen type of NSCLC in the U.S. and comprise up to 50% of NSCLC . While adenocarcinomas are associated with smoking like other lung cancers, this type is observed as well in nonsmokers who develop lung cancer. Most adenocarcinomas arise in the outer, or peripheral, areas of the lungs. Bronchioloalveolar carcinoma is a subtype of adenocarcinoma that frequently develops at multiple sites in the lungs and spreads along the preexisting alveolar walls.

* Squamous cell carcinomas were formerly more common than adenocarcinomas; at present, they account for about 30% of NSCLC. Also known as epidermoid carcinomas, squamous cell cancers arise most frequently in the central chest area in the bronchi.

* Large cell carcinomas, sometimes referred to as undifferentiated carcinomas, are the least common type of NSCLC.

* Mixtures of different types of NSCLC are also seen.

Other types of cancers can arise in the lung; these types are much less common than NSCLC and SCLC and together comprise only 5%-10% of lung cancers:

* Bronchial carcinoids account for up to 5% of lung cancers. These tumors are generally small (3-4 cm or less) when diagnosed and occur most commonly in people under 40 years of age. Unrelated to cigarette smoking, carcinoid tumors can metastasize, and a small proportion of these tumors secrete hormone-like substances that may cause specific symptoms related to the hormone being produced. Carcinoids generally grow and spread more slowly than bronchogenic cancers, and many are detected early enough to be amenable to surgical resection.

* Cancers of supporting lung tissue such as smooth muscle, blood vessels, or cells involved in the immune response can rarely occur in the lung.

As discussed previously, metastatic cancers from other primary tumors in the body are often found in the lung. Tumors from anywhere in the body may spread to the lungs either through the bloodstream, through the lymphatic system, or directly from nearby organs. Metastatic tumors are most often multiple, scattered throughout the lung, and concentrated in the peripheral rather than central areas of the lung.

What are the signs and symptoms of lung cancer ?

Symptoms of lung cancer are varied depending upon where and how widespread the tumor is. Warning signs of lung cancer are not always present or easy to identify. A person with lung cancer may have the following kinds of symptoms:

* No symptoms: In up to 25% of people who get lung cancer, the cancer is first discovered on a routine chest X-ray or CT scan as a solitary small mass sometimes called a coin lesion, since on a two-dimensional X-ray or CT scan, the round tumor looks like a coin. These patients with small, single masses often report no symptoms at the time the cancer is discovered.

* Symptoms related to the cancer: The growth of the cancer and invasion of lung tissues and surrounding tissue may interfere with breathing, leading to symptoms such as cough, shortness of breath, wheezing, chest pain, and coughing up blood (hemoptysis). If the cancer has invaded nerves, for example, it may cause shoulder pain that travels down the outside of the arm (called Pancoast's syndrome) or paralysis of the vocal cords leading to hoarseness. Invasion of the esophagus may lead to difficulty swallowing (dysphagia). If a large airway is obstructed, collapse of a portion of the lung may occur and cause infections (abscesses, pneumonia) in the obstructed area.

* Symptoms related to metastasis: Lung cancer that has spread to the bones may produce excruciating pain at the sites of bone involvement. Cancer that has spread to the brain may cause a number of neurologic symptoms that may include blurred vision, headaches, seizures, or symptoms of stroke such as weakness or loss of sensation in parts of the body.

* Paraneoplastic symptoms: Lung cancers frequently are accompanied by symptoms that result from production of hormone-like substances by the tumor cells. These paraneoplastic syndromes occur most commonly with SCLC but may be seen with any tumor type. A common paraneoplastic syndrome associated with SCLC is the production of a hormone called adrenocorticotrophic hormone (ACTH) by the cancer cells, leading to oversecretion of the hormone cortisol by the adrenal glands (Cushing's syndrome). The most frequent paraneoplastic syndrome seen with NSCLC is the production of a substance similar to parathyroid hormone, resulting in elevated levels of calcium in the bloodstream.

* Nonspecific symptoms: Nonspecific symptoms seen with many cancers, including lung cancers, include weight loss, weakness, and fatigue. Psychological symptoms such as depression and mood changes are also common.

When should one consult a doctor ?

One should consult a health-care provider if he or she develops the symptoms associated with lung cancer, in particular, if they have

* a new persistent cough or worsening of an existing chronic cough

* blood in the sputum,

* persistent bronchitis or repeated respiratory infections

* chest pain

* unexplained weight loss and/or fatigue and/or

* breathing difficulties such as shortness of breath or wheezing

How is lung cancer diagnosed ?

Doctors use a wide range of diagnostic procedures and tests to diagnose lung cancer. These include...

* The history and physical examination may reveal the presence of symptoms or signs that are suspicious for lung cancer. In addition to asking about symptoms and risk factors for cancer development such as smoking, doctors may detect signs of breathing difficulties, airway obstruction, or infections in the lungs. Cyanosis, a bluish color of the skin and the mucous membranes due to insufficient oxygen in the blood, that suggests compromised function of the lung. Likewise, changes in the tissue of the nail beds, known as clubbing, may also indicate lung disease.

* The chest X-ray is the most common first diagnostic step when any new symptoms of lung cancer are present. The chest X-ray procedure often involves a view from the back to the front of the chest as well as a view from the side. Like any X-ray procedure, chest X-rays expose the patient briefly to a minimum amount of radiation. Chest X-rays may reveal suspicious areas in the lungs but are unable to determine if these areas are cancerous. In particular, calcified nodules in the lungs or benign tumors called hamartomas may be identified on a chest X-ray and mimic lung cancer.

* CT (computerized axial tomography scan, or CAT scan) scans may be performed on the chest, abdomen, and/or brain to examine for both metastatic and primary tumor. A CT scan of the chest may be ordered when X-rays are do not show an abnormality or do not yield sufficient information about the extent or location of a tumor. CT scans are X-ray procedures that combine multiple images with the aid of a computer to generate cross-sectional views of the body. The images are taken by a large donut-shaped X-ray machine at different angles around the body. One advantage of CT scans is that they are more sensitive than standard chest X-rays in the detection of lung nodules. Sometimes intravenous contrast material is given prior to the procedure to help delineate the organs and their positions. A CT scan exposes the patient to a minimal amount of radiation. The most common side effect is an adverse reaction to intravenous contrast material that may have been given prior to the procedure. There may be resulting itching, a rash, or hives that generally disappear rather quickly. Severe anaphylactic reactions (life-threatening allergic reactions with breathing difficulties) to contrast material are rare. CT scans of the abdomen may identify metastatic cancer in the liver or adrenal glands, and CT scans of the head may be ordered to reveal the presence and extent of metastatic cancer in the brain.

* A technique called a low-dose helical CT scan (or spiral CT scan) is sometimes used in screening for lung cancers. This procedure requires a special type of CT scanner and has been shown to be an effective tool for the identification of small lung cancers in smokers and former smokers. However, it has not yet been proven whether the use of this technique actually saves lives or lowers the risk of death from lung cancer. The heightened sensitivity of this method is actually one of the sources of its drawbacks, since lung nodules requiring further evaluation will be seen in approximately 20% of people with this technique. Of the nodules identified by low-dose helical screening CTs, 90% are not cancerous but require up to two years of costly and often uncomfortable follow-up and testing. Trials are underway to further determine the utility of spiral CT scans in screening for lung cancer.

* Magnetic resonance imaging (MRI) scans may be appropriate when precise detail about a tumor's location is required. The MRI technique uses magnetism, radio waves, and a computer to produce images of body structures. As with CT scanning, the patient is placed on a moveable bed which is inserted into the MRI scanner. There are no known side effects of MRI scanning, and there is no exposure to radiation. The image and resolution produced by MRI is quite detailed and can detect tiny changes of structures within the body. People with heart pacemakers, metal implants, artificial heart valves, and other surgically implanted structures cannot be scanned with an MRI because of the risk that the magnet may move the metal parts of these structures.

* Positron emission tomography (PET) scanning is a specialized imaging technique that uses short-lived radioactive drugs to produce three-dimensional colored images of those substances in the tissues within the body. While CT scans and MRI scans look at anatomical structures, PET scans measure metabolic activity and functioning of tissue. PET scans can determine whether a tumor tissue is actively growing and can aid in determining the type of cells within a particular tumor. In PET scanning, the patient receives a short half-lived radioactive drug and receives approximately the amount of radiation exposure as two chest X-rays. The drug discharges particles known as positrons from wherever they are taken up and used in the body. As the positrons encounter electrons within the body, a reaction producing gamma rays occurs. A scanner records these gamma rays and maps the area where the radioactive drug is located. For example, combining glucose (a common energy source in the body) with a radioactive substance will show where glucose is rapidly being used, for example, in a growing tumor.

* Bone scans are used to create images of bones on a computer screen or on film. Doctors may order a bone scan to determine whether a lung cancer has metastasized to the bones. In a bone scan, a small amount of radioactive material is injected into the bloodstream and collects in the bones, especially in abnormal areas such as those involved by metastatic tumors. The radioactive material is detected by a scanner, and the image of the bones is recorded on a special film for permanent viewing.

* Sputum cytology: The diagnosis of lung cancer always requires confirmation of malignant cells by a pathologist, even when symptoms and X-ray studies are suspicious for lung cancer. The simplest method to establish the diagnosis is the examination of sputum under a microscope. If a tumor is centrally located and has invaded the airways, this procedure, known as a sputum cytology examination, may allow visualization of tumor cells for diagnosis. This is the most risk-free and inexpensive tissue diagnostic procedure, but its value is limited since tumor cells will not always be present in sputum even if a cancer is present. Also, noncancerous cells may occasionally undergo changes in reaction to inflammation or injury that makes them look like cancer cells.

* Bronchoscopy: Examination of the airways by bronchoscopy (visualizing the airways through a thin, fiberoptic probe inserted through the nose or mouth) may reveal areas of tumor that can be sampled (biopsied) for diagnosis by a pathologist. A tumor in the central areas of the lung or arising from the larger airways is accessible to sampling using this technique. Bronchoscopy may be performed using a rigid or a flexible, fiberoptic bronchoscope and can be performed in a same-day outpatient bronchoscopy suite, an operating room, or on a hospital ward. The procedure can be uncomfortable, and it requires sedation or anesthesia. While bronchoscopy is relatively safe, it must be carried out by a lung specialist (pulmonologist or surgeon) experienced in the procedure. When a tumor is visualized and adequately sampled, an accurate cancer diagnosis usually is possible. Some patients may cough up dark-brown blood for one to two days after the procedure. More serious but rare complications include a greater amount of bleeding, decreased levels of oxygen in the blood, and heart arrhythmias as well as complications from sedative medications and anesthesia.

* Needle biopsy: Fine needle aspiration (FNA) through the skin, most commonly performed with radiological imaging for guidance, may be useful in retrieving cells for diagnosis from tumor nodules in the lungs. Needle biopsies are particularly useful when the lung tumor is peripherally located in the lung and not accessible to sampling by bronchoscopy. A small amount of local anesthetic is given prior to insertion of a thin needle through the chest wall into the abnormal area in the lung. Cells are suctioned into the syringe and are examined under the microscope for tumor cells. This procedure is generally accurate when the tissue from the affected area is adequately sampled, but in some cases, adjacent or uninvolved areas of the lung may be mistakenly sampled. A small risk (3%-5%) of an air leak from the lungs (called a pneumothorax, which can easily be treated) accompanies the procedure.

* Thoracentesis: Sometimes lung cancers involve the lining tissue of the lungs (pleura) and lead to an accumulation of fluid in the space between the lungs and chest wall (called a pleural effusion). Aspiration of a sample of this fluid with a thin needle (thoracentesis) may reveal the cancer cells and establish the diagnosis. As with the needle biopsy, a small risk of a pneumothorax is associated with this procedure.

* Major surgical procedures: If none of the aforementioned methods yields a diagnosis, surgical methods must be employed to obtain tumor tissue for diagnosis. These can include mediastinoscopy (examining the chest cavity between the lungs through a surgically inserted probe with biopsy of tumor masses or lymph nodes that may contain metastases) or thoracotomy (surgical opening of the chest wall for removal or biopsy of a tumor). With a thoracotomy, it is rare to be able to completely remove a lung cancer, and both mediastinoscopy and thoracotomy carry the risks of major surgical procedures (complications such as bleeding, infection, and risks from anesthesia and medications). These procedures are performed in an operating room, and the patient must be hospitalized.

* Blood tests: While routine blood tests alone cannot diagnose lung cancer, they may reveal biochemical or metabolic abnormalities in the body that accompany cancer. For example, elevated levels of calcium or of the enzyme alkaline phosphatase may accompany cancer that is metastatic to the bones. Likewise, elevated levels of certain enzymes normally present within liver cells, including aspartate aminotransferase (AST or SGOT) and alanine aminotransferase (ALT or SGPT), signal liver damage, possibly through the presence of metastatic tumor.

What is staging of lung cancer ?

The stage of a cancer refers to the extent to which a cancer has spread in the body. Staging involves both evaluation of a cancer's size as well as the presence or absence of metastases in the lymph nodes or in other organs. Staging is important for determining how a particular cancer should be treated, since lung-cancer therapies are geared toward specific stages. Staging of a cancer is also critical in estimating the prognosis of a given patient, with higher-stage cancers generally having a worse prognosis than lower-stage cancers.

Doctors may use several tests to accurately stage a lung cancer, including laboratory (blood chemistry) tests, X-rays, CT scans, bone scans, and MRI scans. Abnormal blood chemistry tests may signal the presence of metastases in bone or liver, and radiological procedures can document the size of a cancer as well as possible spread to other organs.

NSCLC are assigned a stage from I to IV in order of severity :

* In stage I, the cancer is confined to the lung.

* In stages II and III, the cancer is confined to the chest (with larger and more invasive tumors classified as stage III).

* Stage IV cancer has spread from the chest to other parts of the body.

SCLC are staged using a two-tiered system :

* Limited-stage SCLC refers to cancer that is confined to its area of origin in the chest.

* In extensive-stage SCLC, the cancer has spread beyond the chest to other parts of the body.

How is lung cancer treated ?

Treatment for lung cancer can involve surgical removal of the cancer, chemotherapy, or radiation therapy, as well as combinations of these treatments. The decision about which treatments will be appropriate for a given individual must take into account the localization and extent of the tumor as well as the overall health status of the patient.

As with other cancers, therapy may be prescribed that is intended to be curative (removal or eradication of a cancer) or palliative (measures that are unable to cure a cancer but can reduce pain and suffering). More than one type of therapy may be prescribed. In such cases, the therapy that is added to enhance the effects of the primary therapy is referred to as adjuvant therapy. An example of adjuvant therapy is chemotherapy or radiotherapy administered after surgical removal of a tumor in order to be certain that all tumor cells are killed.

Surgery : Surgical removal of the tumor is generally performed for limited-stage (stage I or sometimes stage II) NSCLC and is the treatment of choice for cancer that has not spread beyond the lung. About 10%-35% of lung cancers can be removed surgically, but removal does not always result in a cure, since the tumors may already have spread and can recur at a later time. Among people who have an isolated, slow-growing lung cancer removed, 25%-40% are still alive five years after diagnosis. Surgery may not be possible if the cancer is too close to the trachea or if the person has other serious conditions (such as severe heart or lung disease) that would limit their ability to tolerate an operation. Surgery is less often performed with SCLC because these tumors are less likely to be localized to one area that can be removed.

The surgical procedure chosen depends upon the size and location of the tumor. Surgeons must open the chest wall and may perform a wedge resection of the lung (removal of a portion of one lobe), a lobectomy (removal of one lobe), or a pneumonectomy (removal of an entire lung). Sometimes lymph nodes in the region of the lungs are also removed (lymphadenectomy). Surgery for lung cancer is a major surgical procedure that requires general anesthesia, hospitalization, and follow-up care for weeks to months. Following the surgical procedure, patients may experience difficulty breathing, shortness of breath, pain, and weakness. The risks of surgery include complications due to bleeding, infection, and complications of general anesthesia.

Radiation : Radiation therapy may be employed as a treatment for both NSCLC and SCLC. Radiation therapy uses high-energy X-rays or other types of radiation to kill dividing cancer cells. Radiation therapy may be given as curative therapy, palliative therapy (using lower doses of radiation than with curative regimens), or as adjuvant therapy in combination with surgery or chemotherapy. The radiation is either delivered externally, by using a machine that directs radiation toward the cancer, or internally through placement of radioactive substances in sealed containers within the area of the body where the tumor is localized. Brachytherapy is a term used to describe the use of a small pellet of radioactive material placed directly into the cancer or into the airway next to the cancer. This is usually done through a bronchoscope.

Radiation therapy can be given if a person refuses surgery, if a tumor has spread to areas such as the lymph nodes or trachea making surgical removal impossible, or if a person has other conditions that make them too ill to undergo major surgery. Radiation therapy generally only shrinks a tumor or limits its growth when given as a sole therapy, yet in 10%-15% of people it leads to long-term remission and palliation of the cancer. Combining radiation therapy with chemotherapy can further increase the chances of survival when chemotherapy is administered. External radiation therapy can generally be carried out on an outpatient basis, while internal radiation therapy requires a brief hospitalization. A person who has severe lung disease in addition to a lung cancer may not be able to receive radiotherapy to the lung. A type of external radiation therapy called the "gamma knife" is sometimes used to treat single brain metastases. In this procedure, multiple beams of radiation are focused on the tumor over a few minutes to hours while the head is held in place by a rigid frame.

For external radiation therapy, a process called simulation is necessary prior to treatment. Using CT scans, computers, and precise measurements, simulation maps out the exact location where the radiation will be delivered, called the treatment field or port. This process usually takes 30 minutes to two hours. The external radiation treatment itself generally is done over four or five days a week for several weeks.

Radiation therapy does not carry the risks of major surgery, but it can have unpleasant side effects including fatigue and lack of energy. A reduced white blood cell count (rendering a person more susceptible to infection) and low blood platelet levels (making blood clotting more difficult) can also occur with radiation therapy. If the digestive organs are in the field exposed to radiation, patients may experience nausea, vomiting, or diarrhea. Radiation therapy can irritate the skin in the area that is treated, but this irritation generally improves with time after treatment has ended.

Chemotherapy : Both NSCLC and SCLC may be treated with chemotherapy. Chemotherapy refers to the administration of drugs that stop the growth of cancer cells by killing them or preventing them from dividing. Chemotherapy may be given alone, as an adjuvant to surgical therapy, or in combination with radiotherapy. While a number of chemotherapeutic drugs have been developed, the class of drugs known as the platinum-based drugs have been the most effective in treatment of lung cancers.

Chemotherapy is the treatment of choice for most SCLC, since these tumors are generally widespread in the body when they are diagnosed. Only half of people who have SCLC survive for four months without chemotherapy. With chemotherapy, their survival time is increased up to four- to fivefold. Chemotherapy alone is not particularly effective in treating NSCLC, but when NSCLC have metastasized, it can prolong survival in many cases.

Chemotherapy may be given as pills, as an intravenous infusion, or as a combination of the two. Chemotherapy treatments are usually given in an outpatient setting. A combination of drugs is given in a series of treatments, called cycles, over a period of weeks to months, with breaks in between cycles. Unfortunately, the drugs used in chemotherapy also kill normally dividing cells in the body, resulting in unpleasant side effects. Damage to blood cells can result in increased susceptibility to infections and difficulties with blood clotting (bleeding or bruising easily). Other side effects include fatigue, weight loss, hair loss, nausea, vomiting, diarrhea, and mouth sores. The side effects of chemotherapy vary according to the dosage and combination of drugs used and may also vary from individual to individual. Medications have been developed that can treat or prevent many of the side effects of chemotherapy. The side effects generally disappear during the recovery phase of the treatment or after its completion.

Brain prophylactic radiation: SCLC often spreads to the brain. Sometimes people with SCLC that is responding well to treatment are treated with radiation therapy to the head to treat very early spread to the brain (called micrometastasis) that is not yet detectable with CT or MRI scans and has not yet produced symptoms. Brain radiation therapy can cause short-term memory problems, fatigue, nausea, and other side effects.

Treatment of recurrence : Lung cancer that has returned following treatment with surgery, chemotherapy, and/or radiation therapy is called recurrent or relapsed. If a recurrent cancer is confined to one site in the lung, it may be treated with surgery. Relapsed tumors generally do not respond to the chemotherapeutic drugs that were previously administered. Since platinum-based drugs are generally used in initial chemotherapy of lung cancers, these agents are not useful in most cases of recurrence. A type of chemotherapy referred to as second-line chemotherapy is used to treat recurrent cancers that have previously been treated with chemotherapy, and a number of second-line chemotherapeutic regimens have been proven effective at prolonging survival. People with recurrent lung cancer who are well enough to tolerate therapy are also good candidates for experimental therapies (see below), including clinical trials.

Targeted therapy : One alternative to standard chemotherapy is the drug erlotinib (Tarceva) which may be used in patients with NSCLC who are no longer responding to chemotherapy. It is a so-called targeted drug, a drug that more specifically targets cancer cells, resulting in less damage to normal cells. Erlotinib targets a protein called the epidermal growth factor receptor (EGFR) that helps cells to divide. This protein is found at abnormally high levels on the surface of some types of cancer cells, including many cases of non-small cell lung cancer. Erlotinib is taken by mouth in pill form.

Other attempts at targeted therapy include drugs known as antiangiogenesis drugs, which block the development of new blood vessels within a cancer. Without adequate blood vessels to supply oxygenated blood, the cancer cells will die. The antiangiogenic drug bevacizumab (Avastin) has recently been found to prolong survival in advanced lung cancer when it is added to the standard chemotherapy regimen. Bevacizumab is given intravenously every two to three weeks. However, since this drug may cause bleeding, it is not appropriate for use in patients who are coughing up blood, if the lung cancer has spread to the brain, or in people who are receiving anticoagulation therapy ("blood thinner" medications). Bevacizumab is also not used in cases of squamous cell cancer, because it leads to bleeding from this type of lung cancer.

Photodynamic therapy (PDT): One newer therapy used for different types and stages of lung cancer (as well as some other cancers) is photodynamic therapy. In photodynamic treatment, a photosynthesizing agent (such as a porphyrin, a naturally occurring substance in the body) is injected into the bloodstream a few hours prior to surgery. During this time, the agent deposits itself selectively in rapidly growing cells such as cancer cells. A procedure then follows in which the physician applies a certain wavelength of light through a handheld wand directly to the site of the cancer and surrounding tissues. The energy from the light activates the photosensitizing agent, causing the production of a toxin that destroys the tumor cells. PDT has the advantages that it can precisely target the location of the cancer, is less invasive than surgery, and can be repeated at the same site if necessary. The drawbacks of PDT are that it is only useful in treating cancers that can be reached with a light source and is not suitable for treatment of extensive cancers. Research is ongoing to further determine the effectiveness of PDT in lung cancer.

Radiofrequency ablation (RFA): Radiofrequency ablation is being studied as an alternative to surgery, particularly in cases of early stage lung cancer. In this newer type of treatment, a needle is inserted through the skin into the cancer, usually under guidance by CT scanning. Radiofrequency (electrical) energy is then transmitted to the tip of the needle where it produces heat in the tissues, killing the cancerous tissue and closing small blood vessels that supply the cancer. RFA usually is not painful and has been approved by the U.S. Food and Drug Administration for the treatment of certain cancers including lung cancers. Studies have shown that this treatment can prolong survival similarly to surgery, when used to treat early stages of lung cancer, but without the risks of major surgery and the prolonged recovery time associated with major surgical procedures.

Experimental therapies : Since no therapy is currently available that is absolutely effective in treating lung cancer, patients may be offered a number of new therapies that are still in the experimental stage, meaning that doctors do not yet have enough information to decide whether these therapies should become accepted forms of treatment for lung cancer. New drugs or new combinations of drugs are tested in so-called clinical trials, which are studies that evaluate the effectiveness of new medications in comparison with those treatments already in widespread use. Experimental treatments known as immunotherapies are being studied that involve the use of vaccine-related therapies or other therapies that attempt to utilize the body's immune system to fight cancer cells.

What is the prognosis (outcome) of lung cancer ?

The prognosis of lung cancer refers to the chance for cure or prolongation of life (survival) and is dependent upon where the cancer is localized the size of the cancer, the presence of symptoms, the type of lung cancer, and the overall health status of the patient.

SCLC has the most aggressive growth of all lung cancers, with a median survival time of only two to four months after diagnosis when untreated. (That is, by two to four months, half of all patients have died.) However, SCLC is also the type of lung cancer most responsive to radiation therapy and chemotherapy. Because SCLC spreads rapidly and is usually disseminated at the time of diagnosis, methods such as surgical removal or localized radiation therapy are less effective in treating this tumor type. However, when chemotherapy is used alone or in combination with other methods, survival time can be prolonged four- to fivefold; however, of all patients with SCLC, only 5%-10% are still alive five years after diagnosis. Most of those who survive have limited-stage SCLC.

In non-small cell lung cancer (NSCLC), results of standard treatment are generally poor in all but the most localized cancers that can be surgically removed. However, in stage I cancers that can be completely removed, five-year survival approaches 75%. Radiation therapy can produce a cure in a small minority of patients with NSCLC and leads to relief of symptoms in most patients. In advanced-stage disease, chemotherapy offers modest improvements in survival time, although overall survival rates are poor.

The overall prognosis for lung cancer is poor when compared with some other cancers. Survival rates for lung cancer are generally lower than those for most cancers, with an overall five-year survival rate for lung cancer of about 16% compared to 65% for colon cancer, 89% for breast cancer, and over 99% for prostate cancer.

How can lung cancer be prevented ?

Smoking cessation is the most important measure that can prevent lung cancer. Many products, such as nicotine gum, nicotine sprays, or nicotine inhalers, may be helpful to people trying to quit smoking. Minimizing exposure to passive smoking is also an effective preventive measure. Using a home radon test kit can identify and allow correction of increased radon levels in the home, which can also cause lung cancers. Methods that allow early detection of cancers, such as the helical low-dose CT scan, may also be of value in the identification of small cancers that can be cured by surgical resection and prevention of widespread, incurable metastatic cancer.

Lung Cancer At A Glance

* Lung cancer is the number-one cause of cancer deaths in both men and women in the U.S. and worldwide.

* Cigarette smoking is the principal risk factor for development of lung cancer.

* Passive exposure to tobacco smoke can also cause lung cancer.

* The two types of lung cancer, which grow and spread differently, are the small cell lung cancers (SCLC) and non-small cell lung cancers (NSCLC).

* The stage of lung cancer refers to the extent to which the cancer has spread in the body.

* Treatment of lung cancer can involve a combination of surgery, chemotherapy, and radiation therapy as well as newer experimental methods.

* The general prognosis of lung cancer is poor, with overall survival rates of about 16% at five years.

* Smoking cessation is the most important measure that can prevent the development of lung cancer.

What is a Hernia ?

[Extracted from Medicine.Net.Com]

What is a hernia ?

A hernia is an opening or weakness in the muscular structure of the wall of the abdomen. This defect causes a bulging of the abdominal wall. This bulging is usually more noticeable when the abdominal muscles are tightened, thereby increasing the pressure in the abdomen. Any activities that increase intra-abdominal pressure can worsen a hernia; examples of such activities are lifting, coughing, or even straining to have a bowel movement. Imagine a barrel with a hole in its side and a balloon that is blown up inside the barrel. Part of the inflated balloon would bulge out through the hole. The balloon going through the hole is like the tissues of the abdomen bulging through a hernia.

Serious complications from a hernia result from the trapping of tissues in the hernia—a process called incarceration. Trapped tissues may have their blood supply cut off, leading to damage or death of the tissue. The treatment of an incarceration usually involves surgery.

Where are hernias located ?

The most common location for hernias is the groin (or inguinal) area. There are several reasons for this tendency. First, there is a natural anatomical weakness in the groin region which results from incomplete muscle coverage. Second, the upright position of human posture results in a greater force occurring at the bottom of the abdomen, thereby increasing the stress on these weaker tissues. The combination of these factors over time breaks down the support tissues enlarging any preexisting hole or leads to a tear resulting in a new hole.

Several different types of hernia may occur, and frequently coexist, in the groin area. These include indirect, direct, and femoral hernias, which are defined by the location of the opening of the hernia from the abdomen to the groin. Another type of hernia, called a ventral hernia, occurs in the midline of the abdomen, usually above the navel (umbilicus). This type of hernia is usually painless. Hernias can also occur within the navel (umbilical hernia).

What are the symptoms of a hernia ?

Symptoms of a hernia include pain or discomfort and a localized swelling somewhere on the surface of the abdomen or in the groin area.

What other types of hernias are there ?

Epigastric, umbilical, incisional, lumbar, internal, and Spigelian hernias all occur at different sites over the abdomen in areas that are prone to anatomical or structural weakness. With the exception of internal hernias (within the abdomen), these hernias are commonly recognized as a lump or swelling and are often associated with pain or discomfort at the site. Internal hernias can be extremely difficult to diagnose until the intestine (bowel) has become trapped and obstructed because there is usually no external evidence of a lump.

How is a hernia repaired ?

A hernia repair requires surgery. There are several different procedures that can be used for fixing any specific type of hernia. In a standard repair, following appropriate anesthesia and sterilization of the surgical site, an incision is made over the area of the hernia and carried down carefully through the sequential tissue layers. The goal is to separate away all the normal tissue and define the margins of the hole or weakness. Once this has been achieved, the hole is then closed, usually by some combination of suture and a plastic mesh. When a repair is done by suture alone, the edges of the defect are pulled together, much like sewing a hole together in a piece of cloth. One of the problems with this approach is that it can put excessive strain on the surrounding tissues through which the sutures are passed. Over time, with normal bodily exertion, this strain can lead to the tearing of these stressed tissues and the formation of another hernia. The frequency of such recurrent hernias, especially in the groin region, has led to the development of many different methods of suturing the deep tissue layers in an attempt to provide better results.

In order to provide a secure repair and avoid the stress on the adjacent tissue caused by pulling the hole closed, an alternative technique was developed which bridges the hole or weakness with a piece of plastic-like mesh or screen material. The mesh is a permanent material and, when sewn to the margins of the defect, it allows the body's normal healing process to incorporate it into the local structures. This has proved to be a very effective means of repair.

After the hernia repair is completed, the overlying tissues and skin are surgically closed, usually with absorbable sutures. More and more of hernia repairs are now being done using laparoscopic techniques

What is laparoscopic hernia repair ?

A number of factors have led to the recent development of a new method of repair called laparoscopic hernia repair. This technique is really an extension of a traditional mesh repair method that was used in patients who had already experienced several hernia recurrences at the same site. Previously, this mesh repair approach had required a separate incision somewhat removed from the target area. However, with the progressive development of the instruments and techniques for laparoscopic surgery, the same procedure can now be done with several relatively small incisions. This allows the surgeon to enter the space behind the hernia defect and place the mesh with minimal injury to the surface of the abdomen. The advantages of this method include coverage of all the potential sites of groin hernia, which reduces the risks of recurrence while also decreasing the amount of postsurgical pain.

What about the use of a laser in hernia repair ?

This is a relatively common question. It arises because, for a time, there were some surgeons marketing "laser hernia repair." While a laser may have been used to make the incision and to separate the tissues, the laser has no application in the repair of a hernia. It is impossible to perform the necessary structural repair with a laser, which functions essentially as a cutting tool. Hopes that somehow an incision made with a laser would significantly reduce pain have not been confirmed.

What kind of anesthesia is used for hernia surgery ?

Most hernia repairs (except in children) can be done with a variety of anesthetic methods. With modern general anesthetic techniques and monitoring, general anesthesia (inducing "sleep") can be very safe. However the surgery can also be performed under local anesthesia or regional anesthetics, often at the same time using sedation medications to help relax the patient. The specific type of anesthetic for an individual patient is selected after careful evaluation of the patient's general health and individual concerns.

Can strengthening the muscles make a hernia go away ?

Unfortunately, exercising to improve a hernia is likely to aggravate the condition. The hernia exists because of a localized absence of muscle and supporting structure. Exercise can strengthen the surrounding muscles, thereby worsening the localized weakness and increasing the pressures inside the abdomen. The result is that more tissue can be forced through the defect and enlarge the hernia.

What can be done to prevent a hernia ?

Most of the factors that lead to the development of hernias are beyond the control of the individual. Some of those factors are inherited and develop as the individual grows. The arrangement of the local tissues and their thickness and strength may greatly affect the relative risk of developing a hernia over a lifetime. However, that risk can be increased by failure to use good body mechanics when lifting, poor abdominal support posture, and weight-control problems.

Are hernias inherited ?

Since genetics dictate inherited features and structure, there is a significant risk of inheriting the anatomical features that may predispose to a hernia. There may also be inherited factors that result in tissue weakness, which ultimately allows the deterioration of the supporting structures and leads to the formation of a hernia. However, this does not necessarily imply that the offspring of an individual with a hernia will ultimately develop the problem.

Do hernias usually develop on both sides of the body ?

Groin hernias are somewhat more likely to develop on both sides. This is probably because the structural elements develop symmetrically, and the stresses on the body that occur over time are similar on both sides. When a patient becomes aware of a groin swelling on one side, examination by a doctor will often identify a small hernia on the opposite side.

Should all hernias be repaired ?

In general, hernias that are at risk for complications, that cause pain, or that limit activity should be repaired. If they are not repaired, there is a risk that an emergency surgical procedure may be required at a later date.

Sometimes, a hernia can be temporarily controlled by wearing a belt-like device that applies external compression, which pushes the tissues back into the abdomen and holds them there. This device is called a truss. The truss must be carefully applied on a daily basis. It should only be used for selected situations following careful evaluation by a doctor.

How can I tell if a lump or swelling is a hernia ?

Not all lumps or swellings on the abdominal wall or in the groin are hernias. A doctor should evaluate any such swelling. Other possible causes include growths or enlarged lymph nodes. These problems require entirely different types of evaluation and treatment.

Hernia At A Glance :

* Symptoms of a hernia include pain or discomfort and a localized swelling somewhere on the surface of the abdomen or in the groin area.

* There are many different types of hernias.

* Serious complications from a hernia result from the trapping of tissues in the hernia (incarceration), which can result in the damage of death of the tissue.

* Hernia repair and the treatment of hernia complications require surgery.