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)

Significant liver disease developed in 14 patients after renal transplantation. Nine patients had morphologic and functional evidence of chronic active hepatitis. In general, these patients had few symptoms of liver disease, even though the course of chronic active hepatitis was progressive. Despite large doses of prednisone, cirrhosis ultimately developed in five patients. The cause of chronic active hepatitis could not be related to azathioprine or methyldopa therapy because there was no perceptible change in the course of liver disease after treatment with these drugs was stopped. Three patients were persistently positive for hepatitis B surface antigen. Isolated instances of granulomatous hepatitis (Mycobacterium kansasii) and of prolonged intrahepatic cholestasis were encountered in patients with chronic active hepatitis. Two patients had acute cytomegalovirus hepatitis. There was one episode each of fulminant herpes simplex hepatitis and severe fatty metamorphosis.
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PMID:Liver disease in renal transplant recipients. 18 93

Cirrhosis of the liver was provoked in adult rabbits by the administration of CCl4/0,3 ml subcutaneously two times a week during a period of six weeks. It was found that the infection by M. tuberculosis, M. avium and M. kansasii causes a considerably greater dissemination than in the case with the livers of rabbits unaffected by cirrhosis, and that even a non-pathogenic strain (M. intracellulare) is pathogenic, if the liver is affected. Our findings confirm the lowered resistance of a chemically damaged liver to the development of mycobacterial infection.
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PMID:[Pathogenesis of certain mycobacterioses in a chemically damaged liver of the rabbit (author's transl)]. 81 6

Antibodies (type IgG) against the A 60 antigen (Mycobacterium bovis, BCG) and an antigen of Mycobacterium tuberculosis were studied by ELISA in 79 patients with not tuberculous disease: 16 lung carcinoma, 16 hepatic cirrhosis and 47 patients with pulmonary disease. 59.5% and 50.6% of the patients showed antibodies against antigen A 60 and M. tuberculosis antigen respectively; more 25% were strongly positive against antigen A 60; in the patients with lung carcinoma this results were 62.5%. It is concluded than when this methods are use in the serologic diagnostic of tuberculosis the number of cirrhotic and not tuberculous pulmonary disease patients with antibodies against this antigens, obliges a careful study of the individual characteristics of each patient, and it is very important previously to discard a lung neoplastic pathology.
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PMID:[Antibodies against mycobacterial antigens in patients with non-tuberculous pathology]. 162 Sep 20

There are many causes of peritonitis. Primary peritonitis is rare, but may complicate cirrhosis of the liver or may, in developing countries, be caused by Mycobacterium tuberculosis. It is occasionally iatrogenic, particularly as a complication of continuous ambulatory peritoneal dialysis. It is, however, most frequently the result of perforation of a hollow viscus, caused by either trauma or disease. Its most lethal form follows breakdown of an intestinal anastomosis. Primary and iatrogenic peritonitis should be treated with antibiotics, and localized abscesses can sometimes be cured by percutaneous aspiration. Secondary peritonitis requires resuscitation, antibiotics, and operation. When there is gross microbial invasion, it is wise to avoid suture of the hollow viscus. If there is a strong chance of recurrence of intraabdominal abscesses, nonclosure of the abdomen is theoretically desirable and allows frequent reexploration. This is particularly applicable to pancreatic abscesses.
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PMID:Nonoperative antiinfective treatment of intraabdominal infections. 218 86

Clinical and autopsy findings obtained from 15 male patients treated for acquired immunodeficiency syndrome (AIDS) at 3 hospitals in Sao Paulo provided a clearer profile of AIDS cases in Brazil. Of the 12 patients whose sexual orientation was recorded, 9 were homosexual and 3 were bisexual. 75% were between the ages of 22-36 years; 14 were white. The duration of diseases ranged from 14 days-7 months in this series, confirming the rapid evolution of AIDS from 1st symptom to death. The most common clinical manifestations of disease were fever, cough, weight loss, diarrhea, and lymphadenopathy. Organs most frequently involved were the lungs (13 cases) and encephalum (9 cases). Microscopic findings revealed 9 types of microorganisms, fungi, and protozoa, the most common of which was Cytomegalovirus (7 cases). The cause of death was meningoencephalitis in 7 cases and panlobar pneumonia in 3 cases. The incidence of Kaposi's sarcoma (2 cases) was surprisingly low in this series. In addition to lesions produced by microorganisms, there were important associated lesions represented by lymphocytic depletion, acute myocarditis, brown atrophy of neuronia, acute pancreatitis, and liver cirrhosis. Several microorganisms and tumors in these AIDS patients were discovered only at autopsy, confirming the importance of necropsy to the study of the natural history of this disease. An unexpected pathological finding in this series was the absence of cellular reactions to microorganisms, particularly Pneumocystis carinii, Cryptococcus neoformans, and Mycobacterium tuberculosis.
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PMID:Acquired immune deficiency syndrome (AIDS) in Brazil. Necropsy findings. 362 18

The computed tomography (CT) scans of 27 patients with abdominal tuberculosis were reviewed retrospectively to determine the range of abdominal involvement. Most patients had been at increased risk because of intravenous drug abuse, alcoholism, acquired immunodeficiency syndrome (AIDS), cirrhosis, or steroid therapy. The etiologic agent was Mycobacterium tuberculosis in 23 patients and M. avium-intracellulare in four patients with AIDS. In five patients, tuberculosis was limited to the abdomen. CT findings included adenopathy, splenomegaly, hepatomegaly, ascites, bowel involvement, pleural effusion, intrasplenic masses, and intrahepatic masses. Characteristic features were a tendency for adenopathy to prominently involve peripancreatic and mesenteric compartments, low-density centers within enlarged nodes, complex nature of the ascites, and adenopathy adjacent to sites of gastrointestinal tract involvement. Recognition of these manifestations and maintenance of an index of suspicion, especially in patients at risk, should help optimize the correct diagnosis and management of intraabdominal tuberculosis.
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PMID:Abdominal tuberculosis: CT evaluation. 403 67

Pleural effusion (PE) has been increasingly diagnosed over the last eight years in the Department of Internal Medicine of the Centre Hospitalier of Kigali, Rwanda. To determine the etiology of PE and to examine its possible association with HIV-1 infection and tuberculosis (TB), the authors performed an etiological work-up, including thoracocentesis and pleural punch biopsy, of all new patients with PE of undetermined etiology referred to the Division of Pulmonary Diseases at the hospital between September 14, 1988, and October 16, 1989. 81 men and 46 women of mean age 34 years were enrolled in the study. Pleural TB was diagnosed in 86% and confirmed histologically and/or bacteriologically in 82%. 82 of the 98 pleural TB patients tested for antibody to HIV-1 were HIV-1-seropositive. Metastatic cancer was responsible for PE in six patients, Kaposi's sarcoma in three, lymphoma in one, anaplastic carcinoma in one, and adenocarcinoma in one. Non-TB pneumonia was documented in five patients and was associated with HIV-1 infection in four. Other causes of PE were congestive heart failure, decompensated cirrhosis, constrictive pericarditis, or undetermined; only one of these latter patients was HIV-seropositive. The authors therefore found TB to be the predominant cause of PE and it is strongly associated with HIV-1 infection. In an African area highly endemic for HIV-1 and Mycobacterium tuberculosis co-infection, PE should therefore be considered a good marker of TB as well as HIV-1 infection.
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PMID:Pleural effusion, tuberculosis and HIV-1 infection in Kigali, Rwanda. 844 20

We report a case of tuberculous peritonitis in a patient with concomitant HIV infection and liver cirrhosis. A 50-year-old man with viral B and delta liver cirrhosis and AIDS was diagnosed with spontaneous Escherichia coli peritonitis and successfully treated with beta-lactamins. Three months later, ascites reappeared and Mycobacterium tuberculosis was identified in peritoneal fluid cultures. The triple antituberculosis regimen was adjusted to his level of liver failure but the patient died of hepatic encephalopathy. Concomitant HIV infection and liver cirrhosis favour tuberculous peritonitis but they also make its diagnosis extremely difficult. Considering the poor prognosis of this infection when untreated, tuberculous peritonitis should be systematically suspected in such patients.
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PMID:Unusual presentation of a tuberculous peritonitis in a patient with concomitant AIDS and liver cirrhosis. 893 May 71

Abnormalities in iron metabolism have been reported in patients with acquired immunodeficiency syndrome (AIDS). To assess the frequency of abnormal hepatic iron deposition in these patients and to examine potential causes of iron overload, we analyzed the amount of iron at different cellular sites in liver sections obtained at autopsy of 78 patients with AIDS. Quantitation of serum iron and transferrin levels and estimation of total iron binding capacity was obtained using serum from 63 patients. The number of whole blood/packed red blood cell transfusions and opportunistic infections was recorded. Of the 78 patients, 25 (32%) showed a Grade 3 or 4 (0-4 scale) iron level, distributed in three patterns, i.e., in hepatocytes only, in hepatocytes and Kupffer cells, and in Kupffer cells only. In these 25 livers, 4 had cirrhosis, with no documented cause; the mean number of transfusions was 12.5; and 16 (64%) had Mycobacterium avium-Mycobacterium intracellulare infection. In the 53 livers with little or no iron, 5 had cirrhosis, with 3 of those 5 listing alcoholic liver disease or hepatitis as the cause; the mean number of transfusions was 1.4; and 18 (34%) had Mycobacterium avium-Mycobacterium intracellulare infection. Transferrin saturation was more than 50% in 6 (29%) of 21 cases with increased hepatic iron levels and in 6 (14%) of 42 cases with little or no hepatic iron. These results indicate that hepatic iron overload in patients with AIDS is associated with blood transfusions, an elevated transferrin saturation, and Mycobacterium avium-Mycobacterium intracellulare infection. Significant hepatic iron deposition in patients with AIDS with no other apparent cause of cirrhosis suggests an etiologic role for iron in hepatic injury. The increase in hepatic iron levels in these patients has potentially adverse clinical effects related to the use of transfusions, iron supplements, and iron-containing drugs.
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PMID:Increased hepatic iron in the acquired immunodeficiency syndrome: an autopsy study. 938 70

In a study to determine the prevalence of urinary tract infections (UTI) in primary biliary cirrhosis, midstream specimens of urine from 97 females with primary biliary cirrhosis and 85 females with other chronic liver diseases were investigated prospectively for urinary pathogens and Mycobacterium gordonae. No significant differences between primary biliary cirrhosis and the two groups were observed in the prevalence of significant bacteriuria (11.3% vs. 7.1%), the prevalence of Escherichia coli UTI (9.3% vs. 7.1%) or the colony morphology of Escherichia coli. No mycobacterial species were grown from any sample. In both groups, the prevalence of UTI was higher in patients with cirrhosis (20% in both) than in those without.
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PMID:Urinary tract infections in primary biliary cirrhosis and other chronic liver diseases. 940 45


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