Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute liver failure and haemolytic syndrome appeared quite suddenly as the first manifestations of Wilson disease (WD) in five of our patients previously regarded as healthy persons (although an interview showed that 2-4 weeks prior to the illness the patients complained of several non-specific symptoms, such as abdominal pain, headaches, fever, weakness or behavioural changes). All the patients were young women (17-23 years), none of them had any history of liver disease. They were admitted with icterus, nausea, vomiting and symptoms of increasing haemolysis. The diagnosis of WD was given as disturbed copper metabolism. After a short period of observation ascites and anasarca occurred, haemorrhagic diathesis and other symptoms of liver failure increased. Levels of clotting factors decreased rapidly. Despite treatment with D-penicillamine, plasmapheresis, and symptomatic drugs, three of the women died in irreversible liver coma, due to the unavailability of liver transplantation. The fourth woman was carried to the Transplantation Centre, due to aggravation of the symptoms of liver failure, where liver transplantation was performed. Histopathologically micronodular cirrhosis was shown in all these cases. The fifth patient survived having undergone the above treatment without liver transplantation. The main differences between the patient who survived and those who died or underwent transplantation were relatively higher activity of alkaline phosphatase (26 U/l vs. 10-20 U/l), slightly higher levels of clotting factors and prothrombin time, which never fall below 68% of the control (versus 14-44% in other patients). Only in the surviving patient was the Kayser-Fleischer ring present. In four of our patients we found family members who were carriers of WD.
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PMID:Acute haemolytic syndrome and liver failure as the first manifestations of Wilson's disease. 1221 29

In an adult beta-thalassaemic patient admitted on account of the sudden onset of nausea, vomiting and biliary pain, the concomitant jaundice was considered "obstructive" on the basis of ultrasonographic evidence of cholecysto-choledocal stones. However, when the patient was re-evaluated it was found that concomitant Gilbert's disease, hepatitis C virus related cirrhosis and dilated cardiomyopathy had a detrimental effect on clinical and laboratory findings.
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PMID:A puzzling jaundice. 1274 30

BACKGROUND: Hyponatremia is a common electrolyte disorder in hospitalised patients. The distribution of the various causes of hyponatremia has been studied in hospitalised patients in general, but little is known about the distribution in specific departments. We performed a prevalence study on the aetiology of hyponatremia in two departments in our hospital, namely, the Department of Internal Medicine and the Department of Neurosurgery. METHODS: Consecutive adult patients with hyponatremia (serum sodium concentration</=130 mmol/l) who had been admitted to the Departments of Internal Medicine and Neurosurgery were included in the study. The cause of hyponatremia was determined on the basis of information obtained from medical records, estimation of extracellular fluid volume status, water balance and biochemical parameters in blood serum and urine. RESULTS: Out of 41 hyponatremic patients, 12 had hyponatremia due to normovolemic disorders, 10 due to hypervolemic disorders, 11 due to hypovolemic disorders with extrarenal sodium loss and eight due to hypovolemic disorders with renal sodium loss. The most frequent causes of hyponatremia were extrarenal sodium loss due to vomiting or diarrhoea, hepatic cirrhosis, drug-induced hyponatremia and the syndrome of inappropriate ADH secretion. CONCLUSIONS: In the Departments of Internal Medicine and Neurosurgery, certain causes of hyponatremia are more prevalent than others. The use of clinical data, in combination with a few simple laboratory tests, can lead to a correct diagnosis of the principal cause of hyponatremia.
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PMID:Causes of hyponatremia in the Departments of Internal Medicine and Neurosurgery. 1367 55

Hepatic encephalopathy is a frequent complication of cirrhosis. Abnormalities of 5-hydroxytryptamine (5-HT) and its metabolites are recognized and may contribute to its pathogenesis. We therefore studied the effect of an oral tryptophan load (6-18 g) upon psychometric test scores and analyzed EEG's in alcoholic cirrhotic patients. Eight patients had had previous encephalopathic episodes related to variceal bleeds and one patient was awaiting a liver transplant. Five out of the 10 patients had at least one abnormal baseline psychometric test. Following tryptophan challenge there were no changes in blood ammonia but plasma tryptophan levels were elevated approximately 10-fold (p < 0.01 x 10(-7)). Nevertheless, there were no statistically significant changes in psychometric testing or analyzed EEG frequency distribution. All patients reported nausea or vomiting while one patient developed a short-lived serotonin like syndrome. We conclude that in this group of patients, an oral tryptophan load does not induce or worsen subclinical hepatic encephalopathy. If the high blood levels of tryptophan seen in these studies are able to influence cerebral neurotransmitter synthesis, the results do not support a primary role for abnormalities of 5-HT neurotransmission in hepatic encephalopathy.
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PMID:Oral tryptophan challenge studies in cirrhotic patients: no evidence of neuropsychiatric changes. 1456 68

The treatment and early diagnosis of choledochal cyst are very important to prevent complications of the disease. Delay in treatment can cause lethal complications like biliary cirrhosis and increased morbidity in patients. We studied 26 children with choledochal cyst retrospectively for their clinical presentation, and for the diagnostic tools and treatment modalities, used. The most common findings of choledochal cyst in our series were abdominal pain, vomiting, and ictures in contrast to the classical triad of the disease of jaundice, mass and pain. The most useful diagnostic tool was abdominal ultrasonography. For the treatment, we preferred Roux-en-Y hepaticojejunostomy to the internal drainage procedures, and the results were excellent with minimal mortality and morbidity. We underline prompt diagnosis and treatment to prevent late complications of the disease.
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PMID:A retrospective study of choledochal cyst: clinical presentation, diagnosis and treatment. 1476 97

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer death in Taiwan. In order to delineate the unique demographic features and clinical profile of terminal HCC, we conducted a retrospective study in a hospital-based hospice in Taiwan. Of a total of 991 terminally ill cancer patients (654 men and 337 women, mean age 66.1 years) admitted to our palliative care unit during a three-year period, 110 patients (11.1%) were diagnosed as having HCC (93 men and 17 women, mean age 60.5 years). The most common metastatic sites were bone and lung. Eighty-five HCC patients (77.3%) also had associated liver cirrhosis. The most common symptoms of HCC patients upon admission to the hospice ward were pain, fatigue or weakness, anorexia/vomiting, peripheral edema, cachexia, and ascites. Hypoalbuminemia, anemia, hyponatremia and jaundice were common laboratory abnormalities. Eighty-four patients (76.4%) required opiates for pain management. Upper gastrointestinal bleeding or varices bleeding developed in 76 patients (69.1%). Ninety-four patients (85.5%) died at the hospital, and the overall median survival time at hospice ward was 12 days. Because of more severe underlying portal hypertension and deteriorated liver function, terminal HCC patients with decompensated liver cirrhosis (Child-Pugh class C) had a significantly higher prevalence of peripheral edema, ascites, dyspnea, jaundice, thrombocytopenia, and stage III-IV hepatic encephalopathy than noncirrhotic or Child-Pugh class A and B terminal HCC patients. Symptoms and signs resulting from these portal hypertensions frequently complicated the symptomatic management of terminal HCC patients in the hospice ward. The treatment of these complications is mostly empirical in hospice ward, where intensive laboratory or diagnostic tests are usually not performed. In conclusion, symptoms and signs of terminally ill HCC patients in hospice are unique and should be managed appropriately.
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PMID:Hospice palliative care for patients with hepatocellular carcinoma in Taiwan. 1504 5

We report a 67-yr-old woman with hepatitis C-related liver cirrhosis and hepatoma who had developed severe bone marrow suppression after taking Cantharanthus roseus as an alternative anticancer treatment. The patient developed severe pancytopenia with initial presentations of vomiting, diarrhea, oral ulcer, and fever about 1 week after taking 5-days' course of Cantharanthus roseus. Bone marrow biopsy showed autolysis, which indicated massive necrosis of the hematopoietic cells. There was no malignant cell infiltration. The patient also had severe gastrointestinal disturbances, bacteremia, urinary tract infection, and impaired renal and liver function. Supportive care with broad-spectrum antibiotics, granulocyte colony-stimulating factor, repeated blood transfusions, and albumin supplement was given. She recovered and was discharged after 48 days hospitalization. Coadministration of Cantharanthus roseus and cisapride was noted, and these two drugs are both substrates of cytochrome P450 3A4 enzymes (CYP 3A4). Because the vinca alkaloids are extensively metabolized by the liver cytochrome P450 enzymes, poor hepatic function and drug-herb interaction might predispose the patient to develop the bone marrow toxicity. This case report demonstrated possible effect of oral dose of vinca alkaloids and also hinted that all the substrates and inhibitors of CYP 3A4 have propensity to interfere with metabolism of vinca alkaloids.
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PMID:Severe bone marrow depression induced by an anticancer herb Cantharanthus roseus. 1546 62

A 2-year-old, castrated, male European Shorthair cat was presented with inappetence, vomiting, and fever. Ascites and an irregularly nodular liver were observed on laparotomy; in view of the poor prognosis, the animal was euthanatized. Histopathologic examination of the liver showed a chronic hepatitis with cirrhosis associated with massive accumulation of copper in hepatocytes and macrophages, particularly in the fibrotic areas between the regenerative nodules. Electron microscopy and energy-dispersive X-ray analysis revealed lysosomal accumulation of copper in the hepatocytes. Analytical determination showed very high copper concentrations in the liver. No evidence for increased dietary or environmental copper could be found. This and the pattern of hepatic copper storage, the associated inflammation and fibrosis, strongly suggest a primary copper storage disorder.
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PMID:Copper-associated chronic hepatitis and cirrhosis in a European Shorthair cat. 1565 81

On May 19, 2004, azacitidine (5-azacytidine; Vidaza(trade mark); Pharmion Corporation, Boulder, CO, http://www.pharmion.com) for injectable suspension received regular approval by the U.S. Food and Drug Administration (FDA) for the treatment of all subtypes of myelodysplastic syndrome (MDS). This report summarizes the basis for this approval. Effectiveness was demonstrated in one randomized, controlled trial comparing azacitidine administered s.c. with best supportive care (observation group) and in two single-arm studies, one in which azacitidine was administered s.c. and in the other in which it was administered i.v. The dose of azacitidine, 75 mg/m2/day for 7 days every 28 days, was the same in all three studies. In the randomized trial, study participants were well matched with respect to age, sex, race, performance status, MDS subtype, and use of transfusion during the 3 months before study entry. Patients in the observation arm were permitted by protocol to cross over to azacitidine treatment if their disease progressed according to prespecified criteria. During the course of the study, more than half of the patients in the observation arm did cross over to the azacitidine treatment arm. The primary efficacy end point was the overall response rate. Response consisted of complete or partial normalization of blood cell counts and of bone marrow morphology. The response rate in the azacitidine arm was about 16%; there were no responses in the observation arm. The response rates in the two single-arm studies were similar (13% and 19%). The responses were sustained, with median durations of 11 months and 17 months respectively. Responding patients who were transfusion dependent at study entry lost the need for transfusions. In addition, about 19% of patients had less than partial responses (termed improvement), and two-thirds of them became transfusion independent. Common adverse events associated with azacitidine treatment were gastrointestinal (nausea, vomiting, diarrhea, constipation, and anorexia), hematologic (neutropenia, thrombocytopenia), fevers, rigors, ecchymoses, petechiae, injection site events, arthralgia, headache, and dizziness. Liver function abnormalities occurred in 16% of patients with intercurrent hepatobiliary disorders and in two patients with previously diagnosed liver cirrhosis. Renal failure occurred in patients during sepsis and hypotension. There were no deaths attributed to azacitidine. Azacitidine, the first drug approved by the U.S. FDA for MDS, has a favorable safety profile and provides a clinical benefit of eliminating transfusion dependence and complete or partial normalization of blood counts and bone marrow blast percentages in responding patients.
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PMID:FDA drug approval summary: azacitidine (5-azacytidine, Vidaza) for injectable suspension. 1579 20

Amifostine is a broad-spectrum cytoprotective agent approved for protection against cisplatin toxicities and radiation-induced xerostomia; strong clinical evidence exists that amifostine protects normal mucosa and lung from radiation damage. Hypotension, nausea/vomiting, fatigue and fever/rash are the main side-effects associated with amifostine administration. The present study summarizes our experience on daily amifostine administration to cancer patients with various coexisting medical conditions and diseases. The tolerance and the eventual interference of amifostine with the course of the coexisting diseases is reported, providing a core list of medical conditions met in radiotherapy practice, their compatibility with amifostine administration and recommendations on how to deal with these patients. This list comprises genetic diseases (xeroderma pigmentosum, glucose-6-phosphate dehydrogenase deficiency), autoimmune disorders (vitiligo, scleroderma, thyroiditis, perforating collagenosis), metabolic diseases (diabetes mellitus), cardiovascular diseases, neuro/psychiatric diseases and other medical conditions (hypoglycemia, hepatic cirrhosis, alcoholism). A high incidence of fever/rash was noted in patients with autoimmune diseases, while all other conditions did not alter the patterns of side-effects expected following amifostine administration.
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PMID:Amifostine administration during radiotherapy for cancer patients with genetic, autoimmune, metabolic and other diseases. 1642 30


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