Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The characteristics of liver damage associated with the use of diclofenac, a popular nonsteroidal anti-inflammatory drug, were investigated by reviewing adverse drug reaction reports for Australia. Twenty six patients were reported for whom diclofenac was the sole suspected drug cause of their liver damage. The average age of the patients was 64 years (range 37-84 years); 19 (70%) were women. The most common clinical features were jaundice, hepatomegaly, anorexia, and nausea. Features of drug hypersensitivity were not reported. Duration of treatment with diclofenac before the onset of the illness ranged from 6-417 days (median 76 days). The most prominent biochemical abnormalities were raised serum aspartate transaminase and alanine transaminase activity of up to 30 to 40 times the upper limit of the normal range. Recovery generally started soon after withdrawal of diclofenac and the decrease in aspartate transaminase and alanine transaminase for the group was exponential, with half lives of around 13 days. The average total dose taken by 18 patients for whom accurate data were available was 8.7 g (range 1.4-63.5 g) and, unexpectedly, there was a significant relation between the logarithm of the dose of diclofenac and the logarithms of the peak and mean transaminase levels. Hepatocellular damage during treatment with diclofenac seems to be a rare event. From this analysis of Australian reports it seems that in a small subgroup of patients liver injury may be a direct toxic effect of diclofenac or a metabolite.
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PMID:Diclofenac hepatitis. 175 73

The clinical and pathological associations of hepatic granulomas in patients who presented to the Royal Adelaide Hospital between January 1, 1968 and February 29, 1984 were reviewed retrospectively. Cases of primary biliary cirrhosis were excluded. Of 59 patients with hepatic granulomas, clear associations with diseases were identified in 42 (71%) patients. These were sarcoidosis (seven cases), chronic liver disease (12 cases), biliary tract disease (three cases), tuberculosis (four cases), Q-fever (three cases), other infections (four cases), drug hypersensitivity (four cases) and neoplasms (five cases). Ten patients had multiple associations and five other patients presented without any clearly defined cause for granulomas. Three of these latter patients presented with an acute febrile illness, showed hepatomegaly and had abnormal results of liver function tests. These cases may represent the entity that is labeled "idiopathic granulomatous hepatitis". Two other patients abused alcohol. Granulomas were categorized morphologically as microgranulomas, macrogranulomas and lipogranulomas according to their size, organization and the presence of fat droplets. Microgranulomas were associated with diseases of short duration and less architectural disturbance of the liver parenchyma. The presence of granulomas did not confer any prognostic implication over and above that of the associated disease.
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PMID:Hepatic granulomas: a 15-year experience in the Royal Adelaide Hospital. 333 38

The term lymphogranulomatosis X (LgX) designates a clinicopathological entity of unknown etiology ("X"), which was first described by Forster and Moeschlin in 1954. LgX includes the "immunoblastic lymphadenopathy" of Lukes and to a large extent the "angioimmunoblastic lymphadenopathy" of Rappaport (except for the cases with active germinal centers), but in LgX there is another morphologic variant not mentioned either by Lukes or by Rappaport. To establish the morphologic diagnosis of LgX three typical changes of the affected lymph nodes are needed: effacement of the nodal architecture, absence of active germinal centers, and markedly increased proliferation of epithelioid venules. Cases with only partial effacement of nodal architecture, and especially with active germinal centers, were considered hyperimmune reactions (HR). This "hyperimmune reaction" may be an early stage of LgX: 4 of 39 cases showed later transformation into LgX. Based on cytologic aspects, five different variants of LgX are distinguished: immunoblastic predominance, plasma cell predominance, mixed cell type, epithelioid cell predominance and lymphocytic predominance. Case history and clinical picture of the five variants of LgX (172 patients) are reported and compared with HR (37 patients). In LgX the age peak is in the 7th decade; the youngest patient was 16 years old. HR are seen in children as well as in elderly people, the mean age being 49 years. In LgX males predominate and in HR females. In LgX the disorder is usually more generalized than in HR (80% versus 46% with generalized lymph node enlargement, 69% versus 24% with hepatomegaly and 62% versus 27% with splenomegaly). Skin involvement and high sedimentation rate are less frequent in HR. In LgX a Coombs-positive anemia is occasionally found; its origin is "aplastic" rather than hemolytic. Based on the data presented, some reflections relative to the etiology and pathogenesis of LgX are presented. Rubella virus should be considered a possible etiologic agent. In most cases with drug hypersensitivity, allergic reactions to drugs appear only in the course of the illness; in these cases drugs are ruled out as an etiologic factor. Occasionally, an augmented number of azurophil granulated lymphocytes (suppressor T-cells?) is observed in the blood, a fact that could be a pointer to the pathogenesis of LgX and possibly explain the high incidence of infections seen in this disorder.
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PMID:[History and clinical picture of lymphogranulomatosis X (including (angio)immunoblastic lymphadenopathy]. 726 65

Seventeen cases of dapsone syndrome were seen in five years from 1992 onwards. Their mean age was 27.8 years (range 11 to 60 years). Male to female ratio was 1.1:1. Of these cases, seven had confirmed leprosy, nine were cases of suspected leprosy and one case had lichen planus. On an average, they developed the symptoms 27 days after the intake of dapsone. The cutaneous lesions were in the form of erythematous papules and plaques (13 cases), eczematous lesions (four cases) and associated bullous lesions (two cases). The other manifestations were: fever (16 cases), pruritus (15 cases), lymphadenopathy (14 cases), hepatomegaly (10 cases), icterus and oral erosions (five cases each), photosensitivity (four cases) and splenomegaly (two cases). Previous drug allergy was present in four cases. Elevated ESR and liver enzyme levels were invariable findings. Raised bilirubin levels and hemolytic anaemia were seen in eight cases. Apart from one case with hepatic encephalopathy, all other cases had a favourable outcome either on conservative management (eight cases) or on oral corticosteroids (eight cases). Oral provocation test was done in two cases with positive response while intradermal test was not very reliable.
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PMID:Dapsone syndrome--a five year retrospective analysis. 980 99

Five weeks after the start of treatment with an association of sulfasalazopyridine and piroxicam, a 30-year-old woman presented with an eczematous eruption in light-exposed areas, hepatomegaly and fever (38 degrees C). Laboratory studies showed leukocytosis, eosinophilia and hepatic cytolysis. Treatment consisted of withdrawing the two drugs and topical steroids. The clinical signs regressed in 6 days. An increase in eosinophilia and hepatic cytolysis was observed until the tenth day, after which the trend reversed. Laboratory parameters were normal on the twentieth day. One month later, photopatch testing was performed. A patch test with sulfanilamide irradiated with UVA was positive. Clinical and laboratory findings were highly suggestive of drug hypersensitivity syndrome. The positive result from the UVA photopatch test with sulfanilamide suggests that sulfasalazopyridine was involved in the occurrence of hypersensitivity syndrome in our patient. We conclude that photodistributed eruptions can be observed in drug hypersensitivity syndrome with photosensitizing drugs.
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PMID:Photosensitivity with sulfasalazopyridine hypersensitivity syndrome. 1044 39

Erythroderma is a clinical manifestation of dermatoses from different causes. Our objective was to determine its incidence, causes and clinicopathological features. Clinical, laboratory, and biopsy materials of 49 patients diagnosed as having erythroderma were reviewed. They were treated in our department over a 10-year period (1985 through 1994). The male-female ratio was 2:1. The mean age at diagnosis was 51.7 years. The most common causative factors were drugs (38.77%) and preexisting dermatoses (26.5%). Hepatomegaly, jaundice and abnormal liver function tests were found more commonly in the drug allergy group, while in cases with preexisting dermatoses nail involvement was a common finding. Clinicopathologic correlation in our study did not inform the etiology because it showed chronic nonspecific dermatitis or psoriasiform dermatitis, without any clue as to its origin. Drug-induced-erythroderma had an acute onset and a good prognosis with rapid resolution when the causative drug was withdrawn, while histopathology and laboratory findings were largely unrewarding.
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PMID:Erythroderma in Thai patients. 1051 79

Drug hypersensitivity with myocarditis is known to occur with many drugs especially with antiepileptics, sulpha-compounds and daposne. Dapsone (4, 4 diaminodiphenyl sulphone) induced hypersensitivity is known to occur in about 2% of leprosy patients on treatment and an incidence of 1.66% in non-leprosy patients. We report this rare case of dapsone hypersensitivity syndrome in a girl on dapsone who presented with fever, anaemia, jaundice, skin rash, lymphadenopathy, and hepatomegaly and later developed myocarditis. The drug was withdrawn and the patient was treated with steroids. She improved and was discharged. She relapsed after the corticosteroids were discontinued at home.
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PMID:Dapsone hypersensitivity syndrome with myocarditis. 2585 47