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 medical records of 222 patients with liver abscess at Siriraj Hospital from 1978 to 1985 were analysed. Amoebic abscess was three times more prevalent than pyogenic abscess. In both groups middle aged males were affected more often than others. The main clinical manifestations were fever, right upper quadrant pain and hepatomegaly. History of colitis in the past, marked leukocytosis, elevation of alkaline phosphatase and a single abscess confined to the right lobe were suggestive of amoebic liver abscess. The presence of concurrent abdominal infection, marked anemia and jaundice were associated with pyogenic abscess. Patients with pyogenic abscess developed complications more often and the case fatality rate was greater than patients with amoebic abscess. Most of the patients were successfully treated with a combination of antimicrobials and drainage.
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PMID:Liver abscess: a clinical study of 222 patients. 221 15

A 22-year-old female with active ulcerative colitis developed massive ascites, hypoalbuminemia, and hepatomegaly compatible with thrombosis of the hepatic veins. The diagnosis of Budd-Chiari syndrome was confirmed by ultrasonography, computed tomography, and by liver biopsy. A search of the literature disclosed only three previous reports of Budd-Chiari syndrome occurring in patients with ulcerative colitis. All patients have been young females with active colitis and no other known risk factor for the development of hepatic vein thrombosis. Our patient, unlike the previously reported patients who died, recovered sufficiently to be discharged from the hospital.
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PMID:Recovery from hepatic vein thrombosis (Budd-Chiari syndrome) complicating ulcerative colitis. 319 87

Necropsy materials from 57 cases of generalized amyloidosis in rhesus monkeys were reviewed. Clinically, animals with the disease were characterized by cachexia with muscle wasting, recurrent diarrhea, and arthritis. Gross lesions included hepatomegaly, splenomegaly, chronic/active colitis, fibrous strictures of the cecocolic junction, osteoarthritis, and generalized muscle atrophy. Histologic examination revealed minimal to severe deposits of amyloid in the small intestine (100%), spleen (93%), large intestine (67%), liver (40%), lymph nodes (71%), stomach and/or adrenal gland (32%). More amyloid was deposited in the spleen, liver, and small intestine than in other organs. Shigella sp. were isolated from feces in 23% of the cases and 84% had histologic evidence of colitis. Other findings indicated that 100% of the animals had lung mites, 25% had strictures of the cecocolic junction, and 40% had osteoarthritis. Thirty percent of the cases occurred in animals 10 months to 5 years of age, 10% in ages 6 to 10 years, and 60% in animals greater than 10 years old.
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PMID:Generalized amyloidosis in rhesus monkeys. 375 Jul 36

In 11 patients with childhood amebiasis, only two had dysentery. Additional clinical findings included hematochezia without diarrhea (four patients), dysentery with appendicitis (one patient), exacerbation of ulcerative colitis (two patients), and disseminated infantile amebiasis (two patients). All patients with hematochezia examined by proctosigmoidoscopy had colitis. The diagnosis of amebiasis was confirmed by microscopic examination of fresh stool specimens, pathologic findings, and/or serologic titers. Amebiasis should be considered in the differential diagnosis of infants and children with hematochezia or hepatomegaly, especially in endemic areas.
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PMID:Spectrum of amebiasis in children. 711 1

Amebic liver abscess (ALA) is uncommon in the United States and is potentially lethal when acquired during the first year of life. The clinical course of ALA in a 10-month-old infant is presented and the characteristics of 18 previously described cases of infants with ALA from the United States are reported; this infant population (including our patient) is compared with a population of adults with ALA. In contrast to the initial signs in adults, those in infants are nonspecific and include fever, hepatomegaly, anemia, and elevated levels of transaminases. Colitis may occur in infants, but results of examinations for ova or parasites are usually negative. On presentation the amebic serology for one-third of infants with ALA is negative. The clinical course of ALA in infants is usually fulminant and is associated with a mortality rate of nearly 50%.
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PMID:Amebic liver abscess in infancy: case report and review. 780 46

One thousand six hundred and ninety-five inhabitants of 3 rural villages on Ukerewe Island, Lake Victoria, Tanzania, were examined by clinical, parasitological, ultrasonographic and--in part--serological means to evaluate Schistosoma (S.) mansoni-related morbidity on a community level. Villagers frequently complained of typical colitis symptoms (abdominal pain 80.1%, bloody stools 43.1%, diarrhoea 35.1%); haematemesis, on the other hand, was rare (and reports doubtful in most cases). 16.9% of the population had been given praziquantel previously. Overall S. mansoni prevalence was 86.3%, with a median egg output of 176 eggs per gram (e.p.g.) and maximum output of 17,984 e.p.g. Children and adolescents were infected more severely than adults, men more severely than women. Pretreated individuals excreted significantly fewer ova (median 124 vs 192e.p.g., P < 0.001). Hepatomegaly (determined by ultrasonography) was present in 35%, splenomegaly in 80%. Organomegaly was significantly related to egg output. Pretreated persons had lower rates of splenomegaly and left lobe hepatomegaly. Low-degree periportal fibrosis was common, while severe grades of fibrosis (MANAGIL score II and III) were present in about 6%. About 10% had other abnormalities on liver sonography (irregular parenchymal texture and/or shape); these person passed significantly more S. mansoni ova than others. Clear sonographic signs of portal hypertension were seen in 2.1%. Serum procollagen-IV-peptide and gamma-glutamyl-transferase levels were increased in persons with severe periportal fibrosis, irregular liver texture of portofugal collateral vessels. Thus, S. mansoni infection in the western part of Ukerewe Island is frequent and often severe, leading to a high prevalence of gastrointestinal symptoms. Hepatosplenic involvement does occur, although symptomatic cases of portal hypertension were not identified beyond doubt. The overall level of schistosomal morbidity is thus considered intermediate. Serum procollagen-IV-peptide may be a promising marker of schistosomal liver disease. Our data suggest that S. mansoni infection may also be related to diffuse liver parenchyma alterations in this area.
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PMID:Schistosoma mansoni-related morbidity on Ukerewe Island, Tanzania: clinical, ultrasonographical and biochemical parameters. 949 Nov 1

We report a retrospective study of 115 hospitalized non-immunocompromised adults with proved or presumed diagnosis of cytomegalovirus infection. Clinical symptoms were fever (95%), constitutive symptoms (80%), joint and muscle pain (41%), shivering (32%), abdominal pain (26%), non-productive cough (20%), cutaneous eruption (20%), and diarrhea (10%). Examination found hepatomegaly (25%), splenomegaly (23%), cutaneous rash (20%), adenopathy (19%), pharyngitis (9%), jaundice (3%) or signs of meningeal irritation (1%). Seventeen patients had a gastrointestinal form (hepatitis, jaundice, colitis, antral gastritis or cholecystitis), eight had a pattern of hemopathy, two interstitial pneumonitis, two pericarditis, two immune thrombocytopenic purpura, two a polymyalgia rheumatica-like pattern, one thrombotic thrombocytopenic purpura, one cutaneous vasculitis and one meningoencephalitis. Sixty-four percent of the patients had atypical lymphocytosis. Hepatocellular injury occurred in 90% of the patients. Nineteen of the patients had biological immune abnormalities. Cytomegalovirus infection should be mainly suspected in any patient with persistent fever, isolated or associated with signs of poor specificity, or in some patients with visceral manifestations of initially unknown origin.
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PMID:Clinical and laboratory findings of cytomegalovirus infection in 115 hospitalized non-immunocompromised adults. 1147 69

History and presenting signs and symptoms in 26 Hungarian Gaucher patients are described in order to promote recognition of non-diagnosed patients. Macrophages accumulating glucocerebrosidase due to deficient glucocerebrosidase activity may be present in many organs leading to a wide variety of clinical manifestations. The most common presenting signs and symptoms are splenomegaly, hepatomegaly, hypersplenism with anemia and thrombocytopenia, and bone deterioration. Rare manifestations of Gaucher disease including glomerulonephritis, pericarditis, pericardial calcification, haemorrhagic colitis and amyloidosis are also discussed.
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PMID:[Presenting signs and symptoms in Gaucher disease]. 1243 34

Amebiasis can be considered the most aggressive disease of the human intestine, responsible in its invasive form for clinical syndromes, ranging from the classic dysentery of acute colitis to extra-intestinal disease, with emphasis on hepatic amebiasis, unsuitably named amebic liver abscess. Found worldwide, with a high incidence in India, tropical regions of Africa, Mexico and other areas of Central America, it has been frequently reported in Amazonia. The trophozoite reaches the liver through the portal system, provoking enzymatic focal necrosis of hepatocytes and multiple micro-abscesses that coalesce to develop a single lesion whose central cavity contains a homogeneous thick liquid, with typically reddish brown and yellow color similar to "anchovy paste". Right upper quadrant pain, fever and hepatomegaly are the predominant symptoms of hepatic amebiasis. Jaundice is reported in cases with multiple lesions or a very large abscess, and it affects the prognosis adversely. Besides chest radiography, ultrasonography and computerized tomography have brought remarkable contributions to the diagnosis of hepatic abscesses. The conclusive diagnosis is made however by the finding of Entamoeba histolytica trophozoites in the pus and by the detection of serum antibodies to the amoeba. During the evolution of hepatic amebiasis, in spite of the availability of highly effective drugs, some important complications may occur with regularity and are a result of local perforation with extension into the pleural and pericardium cavities, causing pulmonary abscesses and purulent pericarditis, respectively The ruptures into the abdominal cavity may lead to subphrenic abscesses and peritonitis. The treatment of hepatic amebiasis is made by medical therapy, with metronidazole as the initial drug, followed by a luminal amebicide. In patients with large abscesses, showing signs of imminent rupture, and especially those who do not respond to medical treatment, a percutaneous drainage must be performed with either ultrasound or computerized tomography guidance. Surgical drainage by laparotomy is reserved to patients with secondary infections.
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PMID:Hepatic amebiasis. 1295 80

Extracts from Boswellia serrata have been reported to have anti-inflammatory activity, primarily via boswellic acid-mediated inhibition of leukotriene synthesis. In three small clinical trials, boswellia was shown to improve symptoms of ulcerative colitis and Crohn's disease, and because of its alleged safety, boswellia was considered superior over mesalazine in terms of a benefit-risk evaluation. The goal of this study was to evaluate the effectiveness of boswellia extracts in controlled settings of dextran sulfate- or trinitrobenzene sulfonic acid-induced colitis in mice. Our results suggest that boswellia is ineffective in ameliorating colitis in these models. Moreover, individual boswellic acids were demonstrated to increase the basal and IL-1beta-stimulated NF-kappaB activity in intestinal epithelial cells in vitro as well as reverse proliferative effects of IL-1beta. We also observed hepatotoxic effect of boswellia with pronounced hepatomegaly and steatosis. Hepatotoxity and increased lipid accumulation in response to boswellia were further confirmed in vitro in HepG2 cells with fluorescent Nile red binding/resazurin reduction assay and by confocal microscopy. Microarray analyses of hepatic gene expression demonstrated dysregulation of a number of genes, including a large group of lipid metabolism-related genes, and detoxifying enzymes, a response consistent with that to hepatotoxic xenobiotics. In summary, boswellia does not ameliorate symptoms of colitis in chemically induced murine models and, in higher doses, may become hepatotoxic. Potential implications of prolonged and uncontrolled intake of boswellia as an herbal supplement in inflammatory bowel disease and other inflammatory conditions should be considered in future clinical trials with this botanical.
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PMID:Effects of Boswellia serrata in mouse models of chemically induced colitis. 1553 33


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