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)

Twenty-three clinically normal Beagles were inoculated with North American Trypanosoma cruzi isolates from an opossum (Tc-O), an armadillo (Tc-A), or a dog (Tc-D). The dogs were grouped according to the clinical outcome of inoculation. Group 1 consisted of 7 dogs inoculated with Tc-O or Tc-A that died or were euthanatized during acute stages of disease. Group 2 consisted of 5 dogs inoculated with Tc-O or Tc-A, that also developed acute disease, but survived to develop chronic disease. Group 3 consisted of 7 dogs inoculated with Tc-D neither developed acute nor chronic disease. Group 4 consisted of 4 dogs and served as noninoculated controls. In group 1, the gross lesions were diffusely pale myocardiums with right ventricular enlargement, hepatomegaly, and a moderate amount of modified transudate in the abdominal cavity. Severe diffuse granulomatous myocarditis with large numbers of pseudocysts and minimal fibrosis characterized the tissues from all cardiac chambers and septum. The lesions were most severe in the right atrium and ventricle. Mild multifocal myositis and pseudocysts were observed in skeletal muscles and smooth muscles of the urinary bladder and small intestine. Multifocal encephalitis and pseudocysts were in the cerebral cortex, cerebellum, and brain stem. In group 2, the gross lesions were biventricular enlargement and thinning of the ventricular free walls. The right ventricle contained the most severe microscopic changes. There were mild multifocal interstitial lymphohistocytic cellular infiltrates, perivasculitis, and marked fibrosis in all areas of the myocardium. Mild myositis and multifocal encephalitis were seen in the skeletal muscles and brains. Pseudocysts were not observed in any tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathologic features of dogs inoculated with North American Trypanosoma cruzi isolates. 178 18

Clinical and laboratory manifestations, disease course, outcome, and HLA associations were studied in an inception cohort of 62 subjects with adult Still's disease (ASD) from 5 Canadian universities. Twenty-eight patients (45%) were female and the median age at disease onset was 24 years. In general, the clinical features observed in our patients were identical to those in other published series. However, significantly higher frequencies of sore throat (92%), weight loss (76%), lymphadenopathy (74%), pleuritis (53%), pneumonitis (27%), and abdominal pain (48%) were noted in our patients compared to those in a recent literature review. Liver involvement with hepatomegaly (44%) or abnormal liver function tests (LFTs) (76%) was common and was responsible for the 2 deaths attributed to Still's disease in our series. Severe liver failure always occurred in conjunction with aspirin or NSAID therapy. Therefore, whether or not aspirin or other NSAIDs are used, we recommend close monitoring of LFTs in patients with ASD, especially early in the disease course. Laboratory manifestations were similar to those already reported. Leukocytosis (greater than or equal to 15,000/mm3) was present in 50 patients (81%), a normochromic, normocytic anemia (hemoglobin less than or equal to 10 g/dl) in 42 (68%), and an elevated ESR in all. The mean follow-up of the 62 patients was 70 months (range, 2-163). Twenty-one patients (34%) had a self-limited disease course, 15 (24%) an intermittent course, and 22 (36%) a chronic disease course. Four patients (6%) died, and 2 of these deaths were attributed to Still's disease. For those patients who experienced a recurrence of ASD, the flares were usually of shorter duration and milder in severity than the initial episode. No initiating factor for disease exacerbation was identified in our patients. Although 22 of 62 patients (36%) had a chronic disease course, 52 (90%) were in ARA Functional Class I, and only 4 and 2 patients were in ARA Functional Class II and III, respectively. Patients with Still's disease had higher scores than the controls on the Pain (P less than 0.01) and Physical Disability (P less than 0.05) subscales of Arthritis Impact Measurement Scales health status questionnaire. Joint radiographs performed at the follow-up evaluation disclosed typical carpometacarpal and intercarpal involvement in 16 of 39 patients. In our series, HLA-B17, B18, B35, and DR2 were significantly associated with ASD. Three significant predictors of an unfavorable outcome, either a chronic disease course or a longer time to clinical remission, were identified.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adult Still's disease: manifestations, disease course, and outcome in 62 patients. 200 77

From December 1982 to June 1985, we diagnosed LAV/HTLV-III infection in 16 children of African origin living in Belgium or referred to one of the hospitals participating in this study. Diagnosis was proven in seven of them by isolation of virus of the LAV/HTLV-III group. In the nine others, LAV/HTLV-III infection was highly probable because of the presence of antibodies against the virus (seven subjects) or clinical and immunological evidence of immune deficiency associated with a parental history of LAV/HTLV-III infection (two subjects). Five of these children had a severe illness starting in the first months of life (range 20 days--4 months) and died within 4 months (range 19 days--10 months). Eight children presented later in life (mean age 35 months, range 2-66 months) with a milder and more chronic disease characterized by the presence of generalized lymphadenopathy (6/8), hepatomegaly (5/8), splenomegaly (5/8), interstitial pulmonary infiltration (4/8), parotid swelling (3/8), CSF lymphocytosis (3/5), diarrhoea without pathogen isolated (1/8) and fever (1/8). At least one of the parents of each child was of African origin. At the time of birth of their child two mothers and one father had an AIDS-related complex. After a mean period of 34 months (range 3-87 months) five fathers and six mothers had a symptomatic LAV/HTLV-III infection (AIDS or AIDS-related complex).
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PMID:LAV/HTLV-III infection in children of African origin: experience in Belgium. 294 77

Hepatic vein occlusion causes morphologic changes that can be demonstrated by computed tomography (CT) and ultrasound. In this study the imaging findings of acute, subacute, and chronic occlusion of the hepatic veins were analyzed retrospectively in 9 patients and correlated with the histopathologic changes. The CT findings were focal or scattered hypodense parenchymal lesions of the liver before and a patchy enhancement after intravenous bolus injection of contrast material. In none of the cases could the hepatic veins be identified. Hepatomegaly with relative enlargement of the caudate lobe was almost always observed. Ultrasonography demonstrated solid material within the major hepatic veins, intrahepatic venous collaterals, and focal parenchymal lesions, which varied with the stage of the disease: a hypoechogenic area was observed in acute hepatic vein thrombosis with subsequent hemorrhagic infarction; hyperechogenic lesions corresponded with fibrotic zones in chronic disease. Ascites was shown by both methods in all patients.
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PMID:Hepatic vein occlusion: morphologic features on computed tomography and ultrasonography. 353 89

The clinico-pathological features of 42 children with autoimmune haemolysis are described. Over 65% of cases were seen before their 5th birthday. In this group males predominated by the ratio of 2.5:1, but in the older children both sexes were equally affected. The incidence decreased from 1 in 188 X 10(3) in young males to 1 in 1,780 X 10(3) in children over 10. Cases were classified serologically. Of particular note was the frequency of Donath-Landsteiner haemolysis which equalled that due to warm autoantibodies; together these groups made up 79% of the total cases. Most haemolytic episodes followed an acute infection. This was frequently mild and often involved the upper respiratory tract; in only 2 patients was haemolysis associated with underlying collagenosis. Typically there was a sudden onset of pallor and malaise; jaundice, splenomegaly and hepatomegaly were found in about half the subjects. Haemoglobinuria was characteristic of Donath-Landsteiner haemolysis. The illness was severe, with Hb levels falling below 6.0 g/dl in 28 patients. Prednisolone, blood transfusion and, where indicated, antibiotics were usually effective in treating the illness, with splenectomy reserved for cases where this treatment was unsatisfactory. In several individuals no treatment was required. Recovery was rapid, and complete recovery occurred in 83% of patients, usually within 6 months. Although 2 patients died, a generally optimistic prognosis can be given, particularly in the absence of an underlying chronic disorder.
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PMID:Autoimmune haemolysis in childhood and adolescence. 643 92

Previous attempts to assess the health impact of schistosomiasis control programs on community morbidity have been limited by a lack of a theoretical framework that describes the dynamic relationships between infection and morbidity. In this paper, a model of schistosomal morbidity is developed and parameterized. Morbidity is divided into that due to current heavy infection, and early and late stages of chronic disease. The model was parameterized using data showing resolution of disease after treatment, correlations between prevalence of disease and intensity of infection and using age-morbidity profiles. The fitted parameters suggest that early manifestations of disease such as hepatomegaly in Schistosoma mansoni and S. japonicum infections would resolve relatively quickly following treatment whereas later forms of disease such as liver fibrosis resolve very slowly or not at all. Similar general conclusions were obtained with data on early and late forms of urinary tract morbidity in S. haematobium.
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PMID:Dynamic models of schistosomiasis morbidity. 870 23

Hereditary hemochromatosis (HHC) is one of the most common inherited disorders in the Caucasian population. Diagnosis usually made after an elevation in ferritin and serum transferrin saturation is noted, often accompanied by asymptomatic hepatomegaly. Diagnosis is confirmed by genetic testing or liver biopsy. Damage to organs is due to excessive intestinal iron, which is transported to and then deposited in the liver parenchyma, and the heart, skin, and endocrine organs, causing skin pigmentation, development of cirrhosis and hepatic carcinoma, diabetes and endocrine failure, and heart failure. Bony changes can be manifested by arthritis, often in non-weight-bearing joints. The treatment of HHC is phlebotomy, which depletes iron stores. When diagnosis is made before organ damage occurs, treatment can prevent manifestations of the disease. Skin pigmentation and some cardiac damage may reverse on depletion of iron stores, but liver and endocrine damage is rarely reversible. Arthropathy is also not reversible, and often continues to progress even with effective treatment. When hemochromatosis is diagnosed, all first degree relatives of the patient should undergo genetic testing. With early detection and treatment this can be a manageable chronic disease. If undetected, it is potentially fatal.
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PMID:Hereditary hemochromatosis: diagnosis and treatment in primary care. 1054 25

Hepatic IVC disease (HVD), a disease caused by complete obstruction or stenosis of inferior vena cava (IVC) near cava-atrial junction is endemic in Nepal. It is a chronic disease characterized by upper abdominal pain, hepatomegaly, splenomegaly and dilated superficial veins in the body trunk. Ascites commonly, with high protein content is a feature of acute and subacute stages and during acute exacerbation of the chronic disease. We assessed the occurrence of bacterial peritonitis among patients of HVD with ascites. One hundred and sixty seven consecutive patients with ascites, which included 91 patients with HVD were examined for the presence of bacterial peritonitis. The ascitic fluids were examined for total and differential WBC count. The fluid and the blood were cultured for aerobic microorganisms by bedside inoculation in blood culture bottles. HVD is a common cause of non-cirrhotic high protein content ascites in Nepal. It was uniquely associated with high incidence of bacteremia (61%) and high incidence of mono-bacterial peritonitis (67%) from Gram-negative enteric bacteria (58.5%) and Staphylococcus aureus (42.5%). Ascites and bacterial peritonitis generally occurred almost simultaneously in these patients. It is postulated that when bacteremia occurred the defective portion of IVC near the cava-atrial junction become infected resulting in hepatic venous outflow obstruction and formation of ascites with high protein content. And spread of infection from the infected IVC to the peritoneum resulted in bacterial peritonitis.
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PMID:Bacterial peritonitis in hepatic inferior vena cava disease: a hypothesis to explain the cause of infection in high protein ascites. 1224 91

Visceral leishmaniasis, or kala-azar, is a chronic disease caused by Leishmania donovani, Leishmania chagasi or Leishmania infantum. The disease is transmitted through the bite of a species of sandfly of the genus Phlebotomus, releasing amastigote parasites that invade various organs of the body and eventually result in such conditions as anemia, splenomegaly and hepatomegaly. Although no vaccine exists for the disease, diagnostic techniques based not only on pathological tests, but more sophisticated detectors such as polymerase chain reaction, enzyme-linked immunosorbent assay, latex agglutination and immunochromatographic strip testing have been developed. Traditional treatment for the disease consists of two pentavalent antimonial drugs, sodium stibogluconate and meglumine antimoniate, but the growing resistance to these drugs has compelled scientists to search for new efficient compounds. (c) 2002 Prous Science. All rights reserved.
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PMID:Visceral Leishmaniasis: Clinical Features, Pathology, Diagnosis and Chemotherapeutic Developments. 1267 77

Schistosomiasis, a chronic disease with considerable social impact, is an important health problem in many countries. To investigate the possible use of immunomodulators as coadjuvants in the treatment of chronic Schistosoma mansoni infection, we evaluated the effect of dexamethasone on histological, hematological, and biochemical parameters that reflect disease severity and morbidity. Animals treated from the first day or after 35 days of infection, were analyzed. In both groups, dexamethasone: (1) induced a decrease in the number of granulomas in hepatic tissue without affecting the alanine aminotransferase profile, (2) reduced splenomegaly and hepatomegaly associated with disease, and (3) improved hemoglobin concentration, hematocrit values and reduced the percentage of reticulocytes, preventing the development of anemia that occurs in the chronic phase of infection. These data suggest that treatment with dexamethasone results in a mild course of murine schistosomiasis and point to this drug as a promising agent to complement S. mansoni specific treatment.
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PMID:Dexamethasone treatment improves morphological and hematological parameters in chronic experimental schistosomiasis. 1499 68


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