Cases reported "Fatty Liver"

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1/356. Effects of niacin therapy that simulate neoplasia: hepatic steatosis with concurrent hepatic dysfunction.

    niacin, a widely used antihyperlipidemic agent, can produce hepatic steatosis and clinical hepatic abnormalities that together simulate the presentation of hepatobiliary neoplasia. We describe a patient initially suspected of having hepatobiliary neoplasia for whom imaging studies played a pivotal role in reaching the correct diagnosis of niacin-induced hepatotoxicity. Radiologists should become knowledgeable of these niacin-related effects, add niacin effects to the differential diagnosis of hepatic steatosis, and understand the value of correlative imaging in distinguishing these effects from hepatobiliary neoplasia. ( info)

2/356. zidovudine-associated type B lactic acidosis and hepatic steatosis in an hiv-infected patient.

    A 34-year-old obese woman with human immunodeficiency virus (hiv) infection diagnosed a year earlier was seen because of nausea, vomiting, and intermittent diarrhea for 3 weeks. Her current medications included zidovudine. physical examination revealed tachypnea and tender hepatomegaly. Computed tomography of the abdomen showed hepatomegaly with fatty infiltration. Liver enzymes were within normal range except for elevated lactate dehydrogenase (LDH). The serum bicarbonate value was low, with a lactate level three times normal. The tachypnea and dyspnea worsened as lactate concentrations rapidly increased to 15 times normal. Although her Po2 and cardiac index were initially adequate, the patient had acute respiratory failure. She died with multiorgan dysfunction, including hepatic failure, severe lactic acidemia, disseminated intravascular coagulation, and renal failure. autopsy revealed hepatomegaly and massive steatosis. physicians should consider lactic acidosis in patients taking zidovudine and having unexplained tachypnea, dyspnea, and low serum bicarbonate concentrations. ( info)

3/356. Phantom steatosis of the liver: report of a case.

    A patient, referred under a diagnosis of metastatic liver tumors, was found to have multiple areas of focal fatty change (FFC) which, during follow-up, exhibited discordant evolutions. To our knowledge, this phenomenon-regression of a FFC lesion with concurrent appearance or progression of other similar lesions in the same patient, has been reported in only one previous case. FFC can be strongly suggested by clinical, biochemical and radiologic criteria. However, an exact diagnosis can only be made with biopsy. To avoid misdiagnosing a malignancy as FFC and vice versa, biopsy should be performed without hesitation in all patients in whom a change in approach is possible. ( info)

4/356. Successful liver transplantation using an 87 year-old donor.

    The increasing number of patients listed for liver transplantation and the persistent low number of potential donors have led, in recent years, to the expansion of organ availability, as is the case of liver procurement from elderly donors. So far, results reported in the literature are controversial and only a few reports described satisfactory outcomes of transplantation using donors older than 60 years. In the case presented herein, we report the successful elective liver transplantation of a 65 year-old patient, who received a graft from an 87 year-old donor, whose well-preserved hemodynamic conditions, normal hepatic function, absence of parenchymal alterations, as well as short ischemia time, were the key points for this good outcome. Even very old donors can be suitable for liver transplantation. A careful evaluation of all the possible donor-related risk factors, mostly the presence of steatotic changes at liver biopsy, is always mandatory. ( info)

5/356. Late recurrence and rapid evolution of severe hepatopulmonary syndrome after liver transplantation.

    recurrence of hepatopulmonary syndrome (HPS) after orthotopic liver transplantation (OLT) in an adult has never been reported. We describe a 23-year-old woman who initially underwent OLT because of debilitating and severe HPS associated with nonalcoholic steatohepatitis (NASH). Although the clinical resolution of HPS was well documented day 117 post-OLT, the reappearance of NASH was documented by liver biopsy. Severe hypoxemia because of recurrent HPS rapidly evolved beginning approximately day 700 post-OLT. Retransplantation was attempted, but the patient died post-OLT of sepsis and/or multiorgan failure. ( info)

6/356. Microvesicular steatosis, hemosiderosis and rapid development of liver cirrhosis in a patient with Pearson's syndrome.

    BACKGROUND/AIMS: Pearson's marrow-pancreas syndrome consists of refractory sideroblastic anemia with vacuolization of marrow precursors and exocrine pancreas dysfunction. patients with this disease usually have large deletions of the mitochondrial genome. We report a patient with Pearson's syndrome who had predominantly hepatic manifestations such as microvesicular steatosis, hemosiderosis and rapidly developing cirrhosis. methods: Analysis of the mitochondrial and nuclear genomes, determination of enzyme activities and of the hepatic iron content were performed using standard techniques of molecular biology and biochemistry. RESULTS: The patient had typical ringed sideroblasts in a bone marrow smear and a 7436-bp deletion of the mitochondrial genome in all tissues investigated, compatible with Pearson's syndrome. He died within 3 months after birth due to liver failure. Histopathological analysis of the liver revealed complete cirrhosis with signs of chronic cholestasis, microvesicular steatosis and massive hemosiderosis. In addition, the patient was heterozygous for the C282Y and H63D mutations of the hemochromatosis gene. CONCLUSIONS: Pearson's syndrome should be added to the list of neonatal diseases which can cause microvesicular steatosis, hepatic accumulation of iron and liver cirrhosis. ( info)

7/356. lymph loss in the bowel and severe nutritional disturbances in Crohn's disease.

    A severe nutritional deficiency status is described in a 22-year-old patient with Crohn's disease. The clinical picture on admission was dominated by an episode of gastrointestinal bleeding secondary to clotting disturbances (vitamin k deficiency) and severe cachexia due to a protein energy malnutrition. The mechanisms of severe nutritional disturbances in Crohn's disease are multifactorial. In this patient, lymphatic leakage into the intestinal lumen was a major contributing factor in the pathogenesis of protein-losing enteropathy, fat malabsorption, and lymphocytopenia. The authors were able to demonstrate this intestinal lymph loss by nuclear imaging. ( info)

8/356. Long-chain 3-hydroxyacyl-coa dehydrogenase deficiency: variable expressivity of maternal illness during pregnancy and unusual presentation with infantile cholestasis and hypocalcaemia.

    patients with long-chain 3-hydroxyacyl-coa dehydrogenase (LCHAD) deficiency present with a Reye-like syndrome, cardiomyopathy, or sudden unexpected death. We describe an unusual presentation in a patient with unsuspected LCHAD deficiency. The proband presented at 2 months of age with an acute infantile hypocalcaemia and vitamin d deficiency associated with occult, unexplained cholestatic liver disease. Sudden, unexpected death occurred at 8 months. Molecular analysis revealed homozygosity for the prevalent LCHAD (1528G > C, E474Q) mutation. The mother had pre-eclampsia during the third trimester of her pregnancy. In a subsequent pregnancy, she developed severe acute fatty liver of pregnancy (AFLP) and intrauterine fetal death at 33 weeks of gestation. In conclusion, infantile hypocalcaemia is an unusual phenotype associated with LCHAD deficiency. The maternal pregnancy history documents that fetal LCHAD deficiency is associated with a spectrum of maternal illnesses ranging from pre-eclampsia to life-threatening AFLP. ( info)

9/356. Cytogenetic studies in a patient with acute granulocytic leukemia of seven and one-half years duration.

    During a 7 1/2-yr period we monitored a chromosomally aberrant cell line in a woman with acute granulocytic leukemia (AGL) whose disease followed a rather unusual course. Her initial remission induced with 6-mercaptopurine (6-MP) and prednisone was maintained for 52 mo with biweekly doses of methotrexate (MTX) given orally. Because signs of liver dysfunction occurred, maintenance therapy was stopped. After 15 mo without chemotherapy, she suffered her first relapse (5 yr 7 mo after the initial diagnosis). A second remission, again induced with 6-MP and prednisone, was maintained for 1 yr, after which a second relapse occurred. Another remission lasting for only 4 mo was followed by a relapse of the leukemic process which led to her death. Cytogenetic studies of marrow cells and peripheral blood at the time of her initial diagnosis showed abnormal stem lines with characteristic chromosome markers. A small percentage of malignant cells bearing these markers persisted in her marrow during the years of her prolonged remission. At the time of her first relapse, 75% of her marrow cells had the marker karyotype, and at the time of her death (7 1/2 yr after the leukemia was diagnosed) all analyzable marrow metaphases had the characteristic chromosome changes. ( info)

10/356. pancreatitis following intestinal bypass for obesity.

    Three out of 24 patients undergoing intestinal bypass in the treatment of morbid obesity have developed acute pancreatitis in the postoperative period. All three had undergone end-to-end jejunoileal bypass. This serious postoperative complication has been infrequently recorded. Its significance and possible aetiological factors are discussed. ( info)
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