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)

Diacerein is a drug for the treatment of patients with osteoarthritis. This drug is administered orally as 50 mg twice daily. Diacerein is entirely converted into rhein before reaching the systemic circulation. Rhein itself is either eliminated by the renal route (20%) or conjugated in the liver to rhein glucuronide (60%) and rhein sulfate (20%); these metabolites are mainly eliminated by the kidney. The pharmacokinetics characteristics of diacerein are about the same in young healthy volunteers and elderly people with normal renal function, both after a single dose (50 mg) or repeated doses (25 to 75 mg twice daily). Rhein kinetics after single oral doses of diacerein are linear in the range 50 to 200 mg. However, rhein kinetics are time-dependent, since the nonrenal clearance decreases with repeated doses. This results in a moderate increase in maximum plasma concentration, area under the plasma concentration-time curve and elimination half-life. Nevertheless, the steady-state is reached by the third administration and the mean elimination half-life is then around 7 to 8 hours. Taking diacerein with a standard meal delays systemic absorption, but is associated with a 25% increase in the amount absorbed. Mild-to-severe (Child Pugh's grade B to C) liver cirrhosis does not change the kinetics of diacerein, whereas mild-to-severe renal insufficiency (creatinine clearance < 2.4 L/h) is followed by accumulation of rhein which justifies a 50% reduction of the standard daily dosage. Rhein is highly bound to plasma proteins (about 99%), but this binding is not saturable so that no drug interactions are likely to occur, in contrast to those widely reported with nonsteroidal anti-inflammatory drugs. Except for moderate and transient digestive disturbances (soft stools, diarrhoea), diacerein is well tolerated and seems neither responsible for gastrointestinal bleeding nor for renal, liver or haematological toxicity.
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PMID:Clinical pharmacokinetics of diacerein. 983 88

A 66-year old man was admitted to our hospital because of vomiting, diarrhea and progressive dyspnea. Acute respiratory distress syndrome (ARDS) due to bilateral pneumonia was diagnosed and he was also in septic shock. The patient had a history of partial hepatectomy for hepatoma, and suffered from liver cirrhosis. Emergency bronchoalveolar lavage (BAL) revealed abundant gram-positive cocci and polymorphonuclear leukocytes in the collected sample. Blood culture revealed corynebacterium. Treatment consisted of mechanical ventilation and administration of fluids, effective antibiotics, and high-dose methylprednisolone (MPS). MPS was administered from the onset of ARDS with a starting dose of 1,000 mg, which was gradually reduced to 60 mg over 8 days. Pulmonary infiltrates shown on the chest X-ray film were alleviated, and arterial blood gas data rapidly improved. The patient was successfully extubated on the 10th hospital day, and discharged on the 30th hospital day. Serial BAL and plasma levels of inflammatory cytokines decreased rapidly in parallel with the improvement of the patient's clinical condition. This is a case report of severe bacterial pneumonia that was successfully treated with effective antibiotics and high-dose MPS for several days from the onset of ARDS.
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PMID:[Successfully treated acute respiratory distress syndrome with serial plasma and bronchoalveolar measurement of inflammatory cytokines]. 984 90

Excessive consumption of alcoholic beverages may be associated with gastrointestinal symptoms, including dyspepsia and diarrhoea. It is not clear whether or not chronic alcohol ingestion damages the mucosa of the small intestine. We investigated the effect of chronic alcohol abuse on the duodenal mucosa, and particularly on its extracellular matrix (ECM) network. Duodenal biopsy specimens were obtained during upper gastrointestinal endoscopy from 50 chronic alcoholics without cirrhosis and 10 healthy subjects. Morphological studies were performed by routine histology, immunohistochemistry and electron microscopy. Morphometry of duodenal tissues was performed with a computerized image analyser. No significant duodenal epithelial changes were found in alcoholics, despite an evident reduction in the enterocyte turnover. Myofibroblast-like cells were significantly increased in the villus stroma of alcoholics in comparison to controls. These cells stained positively for desmin, alpha-smooth muscle actin and for several ECM components. In alcohol abusers the thickness of the mucosal basement membrane was greater and the staining for collagen I and III was enhanced both in the basement membrane and in the villus stroma. A higher expression of tenascin was also seen at the base of villi of alcoholics. Chronic alcohol abuse may induce fibrosis of duodenal villi which is associated with a transformation of villus juxta-parenchymal cells into active subepithelial myofibroblast-like cells able to produce different ECM components.
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PMID:Ethanol-induced alterations of matrix network in the duodenal mucosa of chronic alcohol abusers. 1007 Dec 47

Copper can induce acute and chronic intoxications in humans. Copper in tap water has caused a series of severe systemic diseases in Germany in recent years (copper induced liver cirrhosis). Besides cirrhosis, another type of disease with predominantly gastrointestinal symptoms has occurred which likewise appeared to be induced by copper in tap water. - In a retrospective investigation we looked for additional indications and proof that chronic copper poisoning has been the cause of the observed gastrointestinal diseases. All patients suffering from this type of disease had copper plumbing in their houses. - The patients (children and adults) suffered from nausea, vomiting, colic, and diarrhoea. In the group of infants, one refused formula milk (prepared with tap water) and the others suffered from persistent restlessness, unexplainable screaming (especially at night) and/or long lasting diaper rash. - We accept the diagnosis of chronic copper intoxication as the cause of the gastrointestinal symptoms when at least one of the following criteria were fulfilled: 1. first manifestation, remission and relapse of the disease depend on intake and a non-intake of water containing copper, respectively. 2. hypercupric state of the patients (i.e. pathological high concentrations of the non-ceruloplasmin-bound copper in serum and/or elevated copper levels in urine) 3. signs of systemic copper intoxication in the same patient 4. signs of systemic copper intoxication or hypercupric states in members of the patient s family or in his neighbourhood (non-relatives) - We found that the disease can even be caused by copper concentrations below the allowed concentration given by the German Guidelines for Drinking Water (Trinkwasserverordnung). - The data prove that copper in drinking water can cause gastrointestinal diseases and not only the better known systemic diseases (i.e. copper induced liver cirrhosis). Copper poisoning must be considered as a possible cause of chronic gastrointestinal diseases in those countries in which copper plumbing is common.
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PMID:Chronic poisoning by copper in tap water: I. Copper intoxications with predominantly gastointestinal symptoms. 1057 26

A 6 year-old boy with autoimmune hepatitis accompanied with cirrhosis was reported. He was admitted to our hospital because of abdominal distention, high fever, and diarrhea. Laboratory examination revealed abnormalities in hepatic function, cholestasis, anemia, thrombocytopenia, hypoalbuminemia, hypocomplementemia, and low concentration of coagulation factors. Abdominal MRI, and asialoglycoprotein receptor-mediated liver scintigraphy strongly indicated liver cirrhosis. Viral hepatitis, Wilson's disease, and antitrypsin deficiency were excluded serologically. Instead, hypergammaglobulinemia, and positive antinuclear antibody suggested autoimmune hepatitis, and the survey of anti-mitochondrial antibody, anti-smooth muscle antibody, and anti-LKM-1 antibody was negative, indicating type I autoimmune hepatitis. Finally, the histology of liver biopsy specimen indicating the destruction of hepatic lobular architecture, dense mononuclear cell infiltrates, and severe fibrosis confirmed the diagnosis. He was treated firstly with methylprednisolone pulses, and then prednisolone p.o. + azathioprine p.o. All of the abnormal laboratory parameters improved to normal levels, indicating that the immunosuppressive therapy will be effective for the severe AIH with cirrhosis.
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PMID:[An infant of autoimmune hepatitis (type I) with cirrhosis]. 1053 82

Acute graft-versus-host disease (GVHD) is a frequent complication of bone marrow transplantation but is only rarely observed after solid organ transplantation. We describe a 68-year-old man who developed a maculopapular eruption 7 days following orthotopic liver transplantation for cirrhosis with malignant transformation due to haemochromatosis. At day 20, the patient complained of nausea, vomiting, diarrhoea and fever. Skin biopsy revealed a lymphocytic infiltrate at the dermoepidermal interface, vacuolization of basal cells and epidermal dyskeratosis. Immunohistochemistry showed HLA-DR and intercellular adhesion molecule-1 expression of lesional keratinocytes. HLA-typing of peripheral blood lymphocytes demonstrated circulating lymphocytes of donor origin. Endoscopy revealed extensive erosions of the oesophagus, stomach and duodenum that on histology disclosed multifocal loss of crypts, lymphocytic infiltrates and epithelial cell death. A diagnosis of acute GVHD was made, and high-dose immunosuppressive therapy with azathioprine and methylprednisolone was instituted. The skin and gastrointestinal symptoms subsided within 4 weeks, but the patient died from severe infectious complications 105 days after transplantation. We conclude that acute GVHD is a rare but potentially fatal complication of liver transplantation. Skin lesions are an early sign of acute GVHD and thus represent an important tool for early diagnosis.
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PMID:Cutaneous lesions as the presenting sign of acute graft-versus-host disease following liver transplantation. 1058 55

Vibrio parahemolyticus (V. parahemolyticus) is a halophilic gram-negative bacillus that lives in the ocean. It is the leading cause of infectious diarrhea in Taiwan and sometimes produces soft tissue infections, but it is rarely a cause of bacteremia. There have been only 11 cases reported in the literature. Most of the cases involved a history of ingestion of seafood or exposure to seawater. In addition, those patients were all immunosuppressed, especially with leukemia and cirrhosis. We report a 60-year-old male patient with chronic hepatitis C and adrenal insufficiency. He developed V. parahemolyticus bacteremia following ingestion of seafood one week prior to admission. His condition was complicated with neck and right lower leg soft tissue infection, as well as multiple organ failure. The patient survived after intravenous ceftazidime, oral doxycycline, and surgical debridement. To our knowledge, this is the 12th reported cases on Medline, and the second bacteremic case in Taiwan. After reviewing the literature, we suggest that all patients with immunosuppressed conditions or adrenal insufficiency should eat foods that are well cooked and avoid raw seafood. Moreover, when patients who are at risk to develop fever, diarrhea, and soft tissue infection after ingestion of seafood, V. parahemolyticus infection should be suspected. All culture specimens should be inoculated on Vibrios selective media.
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PMID:Vibrio parahemolyticus bacteremia: case report. 1058 27

We describe the case of a 18-year-old male patient who first presented with decompensated cirrhosis, fever and generalized lymphadenopathy. He had abnormal results for liver biochemical tests, with a hepatitic-like picture and high titre of antinuclear antibodies. According to the scoring system proposed by the International Autoimmune Hepatitis Group he had 'definite' autoimmune hepatitis and responded well to immunosuppressive treatment. One year later he developed pyoderma gangrenosum which was successfully treated with cyclosporine. Two years later he experienced bloody diarrhoea as a first presentation of ulcerative colitis. At that time both the cholestatic biochemical picture and the cholangiographic appearances of the biliary tree were consistent with primary sclerosing cholangitis. Despite the addition of azathioprine and ursodeoxycholic acid to his treatment regime he developed recurrent episodes of cholangitis and intractable pruritus for which he underwent successful liver transplantation.
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PMID:Overlapping syndrome of autoimmune hepatitis and primary sclerosing cholangitis associated with pyoderma gangrenosum and ulcerative colitis. 1065 5

Isolates of Vibrio cholerae other than O1 and O139 (non O1 Vibrio cholerae) are associated with sporadic diarrheal disorders, and limited outbreaks of diarrhea, and have often been reported in association with extraintestinal infections. The majority of cases of non O1 Vibrio cholerae infection involve immunocompromised patients with hematologic malignancies or cirrhosis. In Italy, very few cases of gastrointestinal and extraintestinal infections due to non O1 Vibrio cholerae have been described in the past years. We describe a case of non O1 Vibrio cholerae infection with cutaneous bullous lesions in a tourist returning from Tunisia.
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PMID:Vibrio cholerae O2 as a cause of a skin lesion in a tourist returning from Tunisia. 1075 77

The study compares the cause of death profile in a rural area of South Africa (Agincourt), with that in a rural area of West Africa (Niakhar), and in a developed country with the same life expectancy (France, 1951) in order to determine causes with high and low mortality and priorities for future health interventions. In the two African sites, causes of death were assessed by verbal autopsies, whereas they were derived from regular cause of death registration in France. Age-standardized death rates were used to compare cause-specific mortality in the three studies. Life expectancy in Agincourt was estimated at 66 years, similar to that of France in 1951, and much higher than that of Niakhar. Causes of death with outstandingly high mortality in Agincourt were violent deaths (homicide and suicide), accidents (road traffic accidents and household accidents), certain infectious diseases (HIV/AIDS, tuberculosis, diarrhea and dysentery), certain chronic diseases (cancer of genital organs, liver cirrhosis, gastrointestinal hemorrhage, maternal mortality, epilepsy, acute rheumatic fever, and pneumoconiosis) and malnutrition of young children (kwashiorkor). Causes of death with lower mortality than expected were primarily respiratory diseases (pneumonia, bronchitis, influenza, lung cancer), other cancers, vaccine preventable diseases (measles, whooping cough, tetanus), and marasmus. Verbal autopsies could be used in a rural area of a developing country without formal cause of death registration to identify the most salient health problems of the population, and could be compared with a formal cause of death registration system of a developed country.
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PMID:Causes of death in a rural area of South Africa: an international perspective. 1089 26


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