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yxfbbiedtj · Wysłany: Pon 15:40, 07 Mar 2011

Dubin-Johnson syndrome in 1 case report and literature review

No family history and similar genetic diseases. Admission examination: T36.7 ℃, P78 times / min, R18 times / rain, BP105 / '70mmlqg. Manchu language and interests of God, the body yellowish discoloration of skin, no spider angioma, liver palms, scleral jaundice, heart and lungs were normal, abdomen soft, no tenderness, liver and spleen not palpable,[link widoczny dla zalogowanych], knocking drum sound, shifting dullness negative, bowel sounds normal,[link widoczny dla zalogowanych], no edema of both lower extremities. Laboratory examination: liver: TBiL71.8 ~ mol / L, DBiL53.4tanol / L, indirect bilirubin mainly,, AST,[link widoczny dla zalogowanych], GGT normal, AKP163.3u / L. Blood, urine, then routine, reticulocyte count, tumor markers were normal. B-and CT abdomen showed normal liver morphology, density, slightly larger size,[link widoczny dla zalogowanych], portal vein, hepatic vein Traveling normal. Chest radiograph, colonoscopy was normal. 1 = I served gallbladder gallbladder angiography showed delayed development. Liver puncture biopsy showed normal liver structure and no inflammatory changes in liver cell necrosis,[link widoczny dla zalogowanych], bile capillary no expansion of the cytoplasm of liver cells in a large number of brown pigment granules composed, in line with Dubin-Johnson syndrome in performance. Discharged after diagnosis. The chromosome 10q24 in patients with a variety of often specific organic anion transporter (CMOAT) gene mutation in codon 1066. The mutation leads to four transmembrane domains and the first two ATP binding sites in all the missing, and thus the loss of fungal esophagitis diagnosis and treatment of 17 cases of non-bile acid organic anion transport function, bilirubin into the blood and anti- cause jaundice. ... Clinical manifestations: chronic persistent or intermittent jaundice, patients occasionally liver pain, fatigue, nausea, vomiting, loss of appetite symptoms. Drinking, infection, pregnancy or birth control pills can precipitate or aggravate jaundice. Some patients have no obvious symptoms. Main aspects are signs of jaundice, liver and spleen may have mild swelling of Russia, soft, may have light tenderness. Laboratory and other auxiliary examinations: serum bilirubin increased to varying degrees, mainly direct bilirubin; AL 『r, AST, AKP were normal. Positive for urinary bilirubin, urobilinogen increased. Fecal porphyrin in urine l-isomers exclude the increase in l2J. Early course of the patients were mainly indirect bilirubin, direct bilirubin late mainly still rare. Not develop oral gallbladder contrast. Laparoscopy: the liver was significantly better color, showed a Pathological examination: prominent lesions are a large number of liver cell cytoplasm of brown pigment granules composed. Uneven particle size and distribution throughout the lobule to the central lobular majority, especially in the liver cell cord on both sides of the adjacent surface of liver cells significantly. After staining and immunohistochemistry, confirmed that such a melanin pigment lipofuscin may be complex L3J. Differential Diagnosis: The disease to be with Gilbert syndrome, viral hepatitis, drug-induced hepatitis, autoimmune hepatitis and other identification. Treatment and prognosis: no special treatment of this disease, the prognosis is good. But to avoid the result of various incentives exacerbations.