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)

Brucella infection is a systemic disease, but the microorganism rarely causes infections in the gastrointestinal system such as hepatitis, cholecystitis, colitis and pancreatitis. Spontaneous bacterial peritonitis due to Brucella is extremely rare. Herein, we report a case of cirrhosis complicated with nongranulomatous hepatitis and peritonitis, both due to Brucella. A 63 year-old man with diabetes mellitus was admitted to hospital with complaints of weakness, backache, abdominal pain and abdominal swelling. On the basis of physical examination and laboratory findings, cryptogenic cirrhosis and spontaneous bacterial peritonitis were diagnosed. Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture. Liver biopsy findings revealed cirrhosis and a nongranulomatous hepatitis which was thought might be due to Brucella infection. Doxycycline and rifampicin, in addition to diuretics were administered for spontaneous ascites infection due to Brucella. A week later, the patient's condition improved and he became afebrile. After two months of therapy, the ascites had almost disappeared.
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PMID:Spontaneous bacterial peritonitis due to Brucella infection. 1461 44

EPIDEMIOLOGY ADN PHYSIOPATHOLOGY: Hereditary haemochromatosis is the most common genetic disease in France. Its frequency is on average 1 out of 300 French individuals. It is due to excessive dietary iron absorption, leading to accumulation of iron in the body. Mutations of the HFE1 gene are responsible for the majority of the case of haemochromatosis. FROM A CLINICAL POINT OF VIEW: The first clinical manifestations (weakness, sexual dysfunction, arthralgia, cardiac symptoms, dyspnoea on effort) can occur after the age of 30 years in men and 35 years in women (protected for longer by menstruation, pregnancy and delivery). In the absence of diagnosis, severe complications can develop during the 5th decade: nervous breakdown, arthropathy, heart failure, diabetes mellitus, cirrhosis with risk of progression towards carcinoma, responsible for handicaps and premature death. DIAGNOSTIC ELEMENTS: The diagnosis is evoked in the case of an increase in transferrine saturation (>45%), associated or not with excessive ferritin plasma levels. It is confirmed by the genetic test, showing homozygotes for the C282Y mutation or compound heterozygotes for the C282Y and H63D mutations on the HFE1 gene. RMI quantifies hepatic iron loading and generally avoids the need for a liver biopsy. The differential diagnosis must exclude secondary iron overload due to chronic transfusions in congenital or acquired blood diseases, a polymetabolic syndrome, chronic viral or alcoholic hepatic diseases and porphyria cutanea tarda. EFFICIENT TREATMENT: Today, haemochromatosis is still treated by phlebotomy. This consists in withdrawing 400 to 500ml of blood every week at the initial depletion stage and subsequently a maintenance therapy in order to maintain ferritin levels below 50 ng/ml. Paradoxically and through ignorance, hereditary haemochromatosis remains a serious disease, although its diagnosis is easy and the treatment simple and effective.
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PMID:[Hereditary haemochromatosis]. 1579 37

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

Six patients infected with Cyclospora cayetanensis who sought medical care at three different hospitals in Turkey are herein presented. Four patients were male and the others were female and their ages ranged from 7 to 62 years. The first patient was HIV-positive and presented with watery diarrhea with a frequency of up to 18 times a day for more than ten months and diagnosed as cyclosporiosis in Kayseri, 1996. The second patient was also HIV positive and diagnosed as cyclosporiosis in Kayseri, 2000. The third patient was an acute myeloblastic leukemia (AML) patient and diagnosed in Istanbul, 2000. The fourth patient was idiopathic hepatic cirrhosis complaining of diarrhea and weakness and diagnosed in Kayseri, 2001. The fifth and sixth patients were immunocompetent patients complaining of diarrhea and diagnosed in Izmir and Kayseri, 2002. Diarrhea occurring from one to ten times a day continued for 7 to 70 d in the last 5 patients. Treatment with a trimethoprim/sulfamethoxazole compound was done for all patients. Both symptomatic and parasitologic improvements were quickly observed. In summary, C. cayetanensis infection is rare in Turkey and most patients infected with this pathogen tend to be immunosuppressive individuals at present.
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PMID:Human cyclosporiosis in Turkey. 1518 22

Patients with liver cirrhosis have protein-energy malnutrition (PEM) and run short of proteins and energy. Protein deficiency leads to hypoalbuminemia, which induces peritoneal effusion and edema. Energy deficiency decreases fat and muscle mass and causes muscle weakness, which decreases the QOL of these patients. A decrease in triceps skinfold thickness (TSF) and arm muscle circumference (AMC), which are indicators of hypoalbuminemia and energy deficiency, and a decrease in respiratory quotient (RQ) affect the prognosis of these patients. Therefore, appropriate nutritional assessment should be performed in order to detect PEM in these patients, and necessary proteins or energy should be supplied. TSF, AMC and RQ are improved by increasing the energy supply to correct its deficiency and by dividing daily food intake (in some cases, adding nocturnal supplementation). Serum albumin levels increase when branched-chain amino acids (BCAAs) are administered after every meal or at bedtime. Consequently, nutritional assessment on PEM, and nutritional therapy based on this assessment are essential for improving the QOL and prognosis of patients with liver cirrhosis.
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PMID:Nocturnal energy and BCAA supplementation in patients with liver cirrhosis. 1560 41

Glycogen storage disease type III (GSD III) was diagnosed in 4 Inuit children (3 confirmed, 1 suspected case) at our institution over the last decade. This rare autosomal recessive disease, which results from a deficiency of the debranching enzyme required for complete degradation of the glycogen molecule, has not been previously described in this population. The possible clinical presentations are heterogeneous, as is the spectrum of severity of this disease. The long-term sequelae can be severe, including recurrent hypoglycemia, hepatic cirrhosis and progressive muscle weakness. These 4 cases would suggest an increased prevalence of GSD III in the Inuit population. Therefore, it is important for health care providers caring for this population to consider and recognize this rare but serious disease.
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PMID:Glycogen storage disease type III in Inuit children. 1568 18

Fenoverine is a derivative of phenothiazine. It is commonly used in the treatment of gastrointestinal and gynecological spasmodic disorders. Myalgia is a common side effect, but rhabdomyolysis has only been scarcely reported before. A 77-year-old patient without previous history of liver diseases received fenoverine therapy for four days due to abdominal pain. Acute onset of myalgia, proximal muscle weakness and high creatinine phosphokinase (CK) occurred. The foregoing symptoms and signs and abnormal biochemistry improved gradually after discontinuation of fenoverine use. The pathophysiology of fenoverine-induced rhabdomyolysis is unclear. Some predisposing factors, especially liver cirrhosis, had been reported. However, our patient had none of the well-known precipitating factors. Physicians should be aware of the possibility of rhabdomyolysis in patients receiving fenoverine, whether they are healthy or have musculoskeletal or liver dysfunction.
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PMID:Rhabdomyolysis induced by fenoverine: a case report and literature review. 1625 17

Risks persists during liver resection in the patients with cirrhosis. Routine examinations usually are unable to predict the morbidity and mortality following surgery. Evaluation approaches of liver function, including aminotransferase, bilirubin, albumin, prothrombin time, Child-Pugh classification, and indocyanine green (ICG) test, currently remain the most important method to determine the prognosis of liver resection, especially in cirrhotic patients. However, all these approaches have their weakness. Some new methods, including non-invasive ICG test, liver function evaluation by hepatic imaging, and remnant hepatic function test, are awaiting further investigation. This article reviews the current status and future prospect in the assessment of liver functions.
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PMID:[Approaches of preoperative assessment of liver function in cirrhotic patient: current status and future prospects]. 1726 Apr 81

To analyze the clinical features of hepatocellular carcinoma (HCC) in patients with signs and symptoms of nervous system involvement as the initial presentation. Over a period of 11 years (January 1993 to December 2003), 15,008 HCC patients were identified at the Chang Gung Memorial Hospital in Kaohsiung, Taiwan. Amongst them, 42 cases had nervous system involvement, of which six had nervous system involvement as their initial presentation. These six cases were enrolled in this study and their clinical and laboratory data were analyzed. The clinical features of the other 36 HCC cases with nervous system involvement were also analyzed for comparison. The six cases were all males, aged 36-68 years old. The involved parts of the nervous system were the cerebellar hemisphere (one), the frontal lobe (one), the sphenoid sinus, sellar turcica, and cavernous sinus (one), the cervical spine (one), and the thoracic spine (two). Their corresponding neurologic presentations were back pain, headache, consciousness disturbance, visual disturbance, and limb weakness. Whilst three out of six patients presenting with nervous system manifestations were found to have concurrent systemic metastases in other expected sites (lung, bone), three had isolated nervous system involvement even after extensive work up. The associated medical conditions of the six cases included hepatitis B (three), hepatitis C (one), liver cirrhosis (two), portal vein thrombosis (three), and diabetes mellitus (two). All the six died within 9 months after the detection of nervous system involvement. The prevalence of nervous system involvement in HCC patients is 0.28% (42/15,088), with 0.04% (6/15,088) having this as their initial presentation. The prognosis of HCC with nervous system involvement is grave. Their clinical and laboratory data are not unique but the diagnosis could only be confirmed by hepatic and nervous system imaging studies, histopathologic examination, and serum alpha-fetoprotein detection. This consideration should be emphasized especially in areas that are hyperendemic for HCC and if the original focus of metastatic lesion is obscure.
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PMID:Hepatocellular carcinoma presenting as nervous system involvement. 1738 89

Amiodarone chlorhydrate is a diiodated benzofuran derivative, and it is used to treat cardiac rhythm abnormalities. Hepatotoxicity is a relatively uncommon side effect of amiodarone, and symptomatic hepatic dysfunction occurs in fewer than 1% of the patients taking amiodarone. Cirrhosis is a rare complication that's been confirmed in 12 cases. Peripheral neuropathy occurs in 10% of patients taking aminodarone. We report here on an unusual case of amiodarone-induced hepatotoxicity and peripheral neurotoxicity. A 75 year old man with normal liver function was given amiodarone for treating his atrial fibrillation and heart failure. He developed nausea, vomiting, muscle weakness and wasting after 17.8 months therapy with amiodarone (400 mg orally once per day). Liver biopsy showed the presence of foam cells in the hepatic sinusoids and Mallory bodies in the periportal hepatocytes on light microscopy. Sural nerve biopsy showed demyelination, and nerve conduction studies showed mixed sensorimotor polyneuropathy. These observations show the necessity of monitoring the hepatic function and conducting neurologic examination of the patients treated with amiodarone.
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PMID:Amiodarone-induced hepatitis and polyneuropathy. 1793 44


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