![]() Though encouraging, normal imaging does not rule out cirrhosis. Because the liver's condition is not homogenous, surface contour can belie existing fibrosis within the interior liver parynchema. ![]() Cirrhosis CAN be present even if the liver is 'normal sized and has a smooth surface contour' - unfortunately, imaging, be it MRI, ultrasound, or CT Scan, does not have a high specificity or sensitivity in detecting early cirrhosis. I agree with my friend Hector that the results you posted make it unlikely your husband has frank cirrhosis, but there are some points on which we have differing opinions. Though there is no clear absolute signal showing that your husband has cirrhosis, I don't think the doctor's "gut" should be ignored either. Since your husband's physician is a Transplant doctor, the expectation would be that he is sufficiently experienced to make good estimations based on his knowledge and your husband's history. The elastography results do not indicate cirrhosis, nor for the most part do his other results, but the 'gold standard' for measuring liver fibrosis is still via liver biopsy, though even biopsies are not without error. " - Exactly what I did and how I felt when I happened on the forum. "I have been a stealth reader here for many months & finally got my nerve up to ask this question. ![]() I do appreciate all the expertise based on everyone's own experiences and would like to get your input on if you think he could have cirrhosis and therefore should continued the extra months of treatment of pegasys & ribavirin following the completion of the incivek. I realize that not even my husband's doctor can definitely say whether he has cirrhosis. 2011 Labs (Before triple tx) Protime 14.6 INR 1.16 Platelets 195 Alk Phos131 ALT 76 AST 49 AFP 1.9 Many thanks if you have made it this far in my ramblings. Calculated mean hepatic shear stiffness is elevated at 5.50 kPascals. ![]() Liver normal sized and with smooth surface contour. 2011 MRI Abd & Elastography - Borderline spleen. Mildly enlarged peripancratic & periportal lymphnodes. Esophageal varices identified (EGD done in response to this found no varicies). No reason identified 2007 Biopsy grade 1 stCT - Spleen normal size. So the doctor is considering him a relasper. Genotype 1 subgroup not identified Il28B CC Previous tx: 1996 Intron-A 3xweek x 5 months non responder 1998 Interferon & ribavirin daily for 28 days non responder 2008 Pegasys & Copegus x 11 months und 12 wks & till end of tx but virus came back 6mth after tx completed. Last August 2011, he started triple tx (Incivek) und at 4, 8, & 12 week and he is trying to decide if there is any evidence to support the 48 week treatment? Exposed to Hep C in 1981. The doc did not want to do a biopsy prior to triple treatment with Incivek as he feels the biopsies can be very inaccurate & feels the elastography is more reliable. The doc keeps referring to a "borderline spleen" and platelets being low (though still in the normal range) and stiffness from the elastography. MD is hepatologist at major transplant hospital. My husband's doctor's "gut" thinks that he may be borderline cirrhosis. This stuff is so hard to understand and I have been trying to make sense of it for months. Large conglomerations of eggs in the bladder wall produce masses known as bilharzioma, which may also eventually calcify.I have been a stealth reader here for many months & finally got my nerve up to ask this question. The granulomas calcify, causing linear streaks of calcium in the bladder wall. From there, millions of eggs enter the urine, or are trapped in the bladder walls where they die, producing a severe granulomatous reaction. They eventually reach the smallest venules in the wall of the bladder, probably through the hemorrhoidal plexus. They develop into adolescent flukes in the portal blood and then migrate against the flow in the portal system using two suckers, which they alternately attach to the wall of a vein. The cercariae that survive enter the mesenteric arteries and, hence, pass through the portal venous system. After the skin is penetrated, they enter peripheral capillaries, drain to the lung, squeeze through the alveolar capillaries, and enter the systemic circulation. These cercariae infect humans directly through the skin, when humans are wading into or swimming in infested waters. These eggs, when deposited in fresh water, hatch into miricidia, which infest snails, develop, and emerge as cercariae. Because the disease typically involves the intestines and bladder, eggs escape the human host in the feces and urine. The definitive host is a human, and the intermediate host is a freshwater snail. Only Schistosoma hematobium affects the urinary tract. ![]() Schistosomiasis (Bilharzia) is one of the most common parasitic infections in the world, but is especially prevalent in the Nile Valley. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |