Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report on 56 children with sclerosing cholangitis (SC) seen between 1972 and 1992. The first symptoms occurred at a mean age of 3.7 years; 15 infants had neonatal cholestatic jaundice. At diagnosis, cholestatic jaundice was present in 25 children, hepatomegaly in 54, splenomegaly in 41, and ascites in 12. Serum alkaline phosphatase activity was increased in 49 patients and gamma-glutamyltransferase activity in all patients tested. Most often the histopathologic findings were extensive portal fibrosis and neoductular proliferation. Cholangiography showed abnormal intrahepatic bile ducts in all children and abnormal extrahepatic bile ducts in 35 (63%). The children were separated into three groups: (1) those with SC of neonatal onset (27%); (2) those with SC of postneonatal onset associated with another disease (55%)--histiocytosis X in 14 children, immunodeficiency syndromes in 8, chronic inflammatory bowel disease or autoimmune hepatitis in 8, and congenital psoriasis in 1; and (3) those with SC of postneonatal onset without an associated disease (18%). Biliary cirrhosis was present in all but three children after 6 months to 19.3 years of follow-up. Eleven children died of portal hypertension or liver failure, and six died of a complication related to the associated disease. Fifteen children had liver transplantation; 11 of these are alive 6 months to 6 1/2 years later without recurrence of SC. The overall estimated median survival time of children with SC was 10 years from clinical onset. These results indicate that SC should be suspected in all children with a chronic cholestatic disease and increased serum gamma-glutamyl transferase activity, especially when diseases known to be associated with SC are present. The prognosis is poor, but liver transplantation should be considered except in those with severe immunodeficiency syndromes.
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PMID:Sclerosing cholangitis in children. 828 75

Mycoplasma-like organisms (MLO) are non-cultivated intracellular cell-wall deficient pathogenic bacteria with a distinctive ultrastructural appearance. Diagnosis of MLO disease depends on finding the organisms in parasitized cells using a transmission electron microscope. MLO are a well studied cause of transmissible chronic plant disease responsive to antibiotics. MLO have recently been found to cause human chronic uveitis, orbital, and retinal disease with autoimmune features. Ophthalmic leucocytes in these patients display MLO parasitization. Inoculation of human uveitis MLO into mouse eyelids produced chronic uveitis. MLO also disseminated to produce randomly distributed lethal systemic disease including chronic hepatitis. MLO parasitized leucocytes were present in all disease sites. Direct intrahepatic inoculation of human hepatic pathogens is a simple and efficient technique to produce murine hepatitis. This report describes the delayed onset widespread inflammatory liver disease produced by direct intrahepatic inoculation of human chronic uveitis MLO in 12 of 20 mice versus 0 in 40 controls (P < 0.05). The liver disease was accompanied by elevated serum SGOT levels, splenomegaly, and accelerated mortality. All 12 inflamed livers displayed MLO parasitized leucocytes versus 0 of 10 control livers. The resemblance of human chronic active hepatitis, massive hepatic necrosis, and post-necrotic cirrhosis to the MLO induced murine liver disease, the role of molecular biologic techniques in the detection and classification of those bacteria, and in therapy of MLO disease are discussed.
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PMID:Experimental murine chronic hepatitis: results following intrahepatic inoculation of human uveitis mycoplasma-like organisms. 839 4

We report on a tourist returning from Thailand, who presented with classical dengue fever. While in Thailand a 36-year-old Swiss female laboratory assistant suddenly developed fever, devastating headache, retro-ocular pain, myalgia and arthralgia, photophobia, nausea and diarrhea. In addition she suffered from epistaxis, urogenital and skin bleeding, and a morbilliform exanthema. After her return to Switzerland we noted lymphadenopathy and splenomegaly, enanthema and laboratory findings of mild hepatitis, thrombocytopenia and leukopenia. The diagnosis of dengue virus infection was verified serologically. Apart from a long lasting convalescent asthenia we observed restitutio ad integrum within days under symptomatic therapy. Epidemiological clinical and diagnostic aspects of dengue virus infection are discussed.
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PMID:[Imported dengue fever following a stay in the tropics]. 842 57

The liver and spleen volume ratio (S/L ratio) was estimated with X-ray computed tomography and evaluated by comparison with the prognosis in 10 patients with fulminant hepatitis. S/L ratio of control group (n = 10) was 0.122 +/- 0.026 (mean +/- SD), that of the alive group with fulminant hepatitis (n = 5) was 0.112 +/- 0.021, and that of the dead group (n = 5) was 0.308 +/- 0.136. There is a significant difference between S/L ratio of control group and that of the dead group with fulminant hepatitis. The rise of S/L ratio on the patients with fulminant hepatitis reflects the liver atrophy or splenomegaly and the prognosis was poor. The prognosis of the patients with fulminant hepatitis, whose S/L ratio indicated the near value of control group, was good. The measurement of S/L ratio by computed tomography was considered to be useful to evaluate the prognosis of fulminant hepatitis.
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PMID:[Prognostic judgment of fulminant hepatitis by measurement of hepatosplenic volume ratio by computed tomography]. 846 12

Toxoplasmosis was diagnosed in a free-ranging wild turkey (Meleagris gallopavo) from West Virginia (USA) in June 1993. Gross findings included emaciation, splenomegaly, multifocal necrotizing hepatitis and splenitis, and crusting dermatitis on the head and neck. Histologically, multifocal necrosis with mononuclear inflammation was present in kidney, liver, spleen, heart, lungs, and pancreas. Toxoplasma gondii was confirmed in sections of liver by avidin-biotin immunohistochemical analysis. Subsequently, a retrospective serosurvey of wild turkeys for T. gondii antibodies was conducted using turkey sera collected between 1984 and 1989. An antibody prevalence of 10% was detected in 130 birds from 21 locations in the southeastern United States. While wild turkeys in the Southeast have T. gondii antibodies, this is only the second natural case of fatal toxoplasmosis reported; it appears that wild turkeys infrequently develop clinical disease when infected with T. gondii.
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PMID:Toxoplasmosis in wild turkeys: a case report and serologic survey. 858 48

Idiopathic neonatal hepatitis (INH) is a syndrome characterized clinically and histologically but there is little information concerning the relationship between the clinical features and histological findings. In the present study, sixty-two patients clinically diagnosed as non-familial INH were histologically classified into four groups according to a provisional definition based on predominant lesions and examination of their clinical features. Patients of cholestasis (n = 23) and giant cell hepatitis (GCH, n = 21) were most frequent (37% and 33%, respectively), and patients of fatty liver (n = 10) and hepatitis (n = 8) were less common (16% and 13%). The GCH group showed a dominance of male, low birthweight, older and breast-fed babies. The cholestasis group demonstrated a dominance of male, low birthweight, younger and bottle-fed babies. The hepatitis group had the highest frequencies of high-grade hepatomegaly and splenomegaly. Fifty six cases completely recovered. Two died of hepatic failure in early infancy and four had chronic liver diseases at the age of 12 months. The fatty liver group had the worst outcome. Histological features in non-familial INH were variable and typical giant cell hepatitis was seen in only one-third of patients. Characteristic clinical features in each histologically classified group may suggest heterogenous etiologies underlying non-familial INH.
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PMID:Relationships between clinical and histological profiles of non-familial idiopathic neonatal hepatitis. 874 14

In an attempt to assess concepts of disease, we questioned 33 Ethiopian Jews (Falashas) in Ethiopia about 13 diseases: 8 western and 5 cultural syndromes (in the Amharic language): birrd (cold), wugat (stabbing chest pain), moygnbagegn (neurologic disorder), mitch (sunstroke), and attent hono kere (retained fetus becoming bone). Disease causation was often attributed to spirits and the sun. None of the interviewees understood the cause of: a) epilepsy, most attributing it to spirits and recommending smelling match smoke as treatment, b) prolonged labor, attributed by most to the evil kole spirit and is managed by traditional birth attendants; and c) abortion, believed to be caused by exposure to sun or cold. Less than 20% linked malaria to mosquitoes. Most correlated splenomegaly with malaria. Hepatitis was believed to be caused by a bird or bat flying around the affected person. Multiple factors were linked to diarrhea, including a journey in the sun. Moygnbagegn is the only condition treated by venisection from brachial veins; wugat is treated by "cupping". Modern medicine was recommended by < 30% of those questioned for epilepsy, splenomegaly, hepatitis, and Ethiopian cultural diseases. It was recommended most for malaria (52%), sexually transmitted diseases (55%), and diarrhea (69%).
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PMID:Traditional beliefs and disease practices of Ethiopian Jews. 875 85

In this study, Babesia microti (ATCC30222) from mice was adapted to golden hamsters. The parasite was passaged to immunosuppressed and then adapted to normal hamsters. When 30 normal hamsters were inoculated with this strain, parasitaemia increased to 74% of erythrocytes by day 7 and 70% of the hamsters died. By day 12, parasitaemia extended to 90%, with 97% mortality. Hearts and kidneys from infected animals were enlarged. Histopathology revealed acute myocarditis, hepatitis, pneumonitis, glomerulonephritis and splenomegaly. Giemsa, Acridine Orange and Rhodamine staining of the parasite were compared. Scanning electron microscopy of blood from infected hamsters revealed from 1 to 5 intra-erythrocytic parasites.
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PMID:Acute fulminating babesiosis in hamsters infected with Babesia microti. 887 13

In 28 children, with bacteriologically and/or serologically diagnosed typhoid fever treated at KEM Hospital, Bombay in 1991, initially one of the three recommended drugs (viz. chloramphenicol, amoxycillin or co-trimoxazole) was given for 7 days for defervescence to occur. In those who failed to respond, a second trial of therapy with one of the other two drugs was initiated, after omitting the first drug. A second failure of therapy was taken as an indication to use ciprofloxacin singly. Eventually, 18 (64.3%) cases responded to chloramphenicol or amoxycillin or co-trimoxazole. Ciprofloxacin was used in 19(35.7%) cases. the failure rate of treatment with chloramphenicol was 50%, with amoxycillin 71.4%, with co-trimoxazole 75% and 0% with ciprofloxacin. An analysis of the 28 cases revealed that apart from fever (in 100%), splenomegaly (in 82.1%) was the most important clinical pointer to diagnosis, along with absolute eosinopenia (in 71.4%). There were no major complications, except 2 cases with typhoid hepatitis who responded to choramphenicol and co-trimoxazole, respectively. Blood culture grew Salmonella typhi in 7 cases, of which 5 (72%) were multidrug resistant S. typhi. There were no characteristic clinical features to identify multi-drug resistant typhoid fever.
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PMID:An analysis of children with typhoid fever admitted in 1991. 913 40

Fatal disseminated toxoplasmosis was diagnosed in seven captive slender-tailed meerkats (Suricata suricatta) according to clinicopathologic findings and immunohistochemistry. Five of nine meerkats died during an outbreak in late 1994. These included four kits (2.5 to 4.5 months old) and a 4-year-old meerkat. Two other meerkats, both adults, died in 1992 and 1995. Respiratory insufficiency (4/7) and incoordination (3/7) were the most consistent clinical signs. although two of seven meerkats died unexpectedly. At necropsy, the lungs were reddened and noncollapsed (6/7), and had multiple pale round foci (4/7). Yellow foci of necrosis in mesenteric lymph nodes (4/7), splenomegaly (3/7), and hydropericardium (3/7) were other common gross findings. Microscopically, interstitial pneumonia was present in all seven meerkats, being acute to subacute in six of them. Type 2 pneumocyte hyperplasia, aggregates of foamy macrophages, and giant cells were consistently seen. Multifocal to locally extensive necrosis of mesenteric lymph nodes (4/7), mild to severe multifocal necrotizing hepatitis (5/6), and mild nonsuppurative encephalitis (4/6) were also seen. Toxoplasma-like organisms were consistently associated with these lesions and were stained by the avidin biotin peroxidase procedure with an antiserum that does not cross-react with Neospora caninum. Meerkats were most likely infected after an oral, primary exposure to Toxoplasma. Several observations indicate that meerkats may be highly susceptible to toxoplasmosis.
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PMID:Epizootic disseminated toxoplasmosis in captive slender-tailed meerkats (Suricata suricatta). 915 May 39


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