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)

Occurrence of fever in a patient with liver cirrhosis should suggest the following: 1. Endotoxemia. Endotoxins are normally present in portal blood; in hepatic cirrhosis they are insufficiently cleared by the liver and their presence can be demonstrated in the systemic circulation by the "limulus test". Fever is one of the many consequences ascribed to the presence of endotoxins in the blood. 2. Infections. Cirrhosis and alcoholism (which often accompanies it) impair host defenses against bacteria and other organisms. Thus, infections are actually more frequent in hepatic cirrhosis as is shown by the example of bacterial endocarditis. Spontaneous bacterial peritonitis must be searched for carefully when ascites is present. 3. Alcoholic hepatitis. This diagnosis is established histologically. The usual symptoms, occurring with variable incidence, include anorexia, nausea and vomiting, abdominal pain, fever and jaundice in the presence of hepatomegaly, leukocytosis and an elevated SGOT. Differential diagnosis from obstructive jaundice and a severe prognosis without alcohol abstinence make early diagnosis mandatory. Its evolution in cirrhosis can be astonishingly rapid. In the absence of hepatic encephalopathy, corticosteroids do not appear to be recommended. 4. Hepatoma.
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PMID:[Fever and liver cirrhosis]. 22 38

Sixteen cases of chronic Q fever are described. In eight there was a history of exposure to infection from farms or farm products. All had valvular heart disease, involving the mitral valve in nine and the aortic valve in seven. Infection occurred on a prosthetic valve in two patients. Arterial embolism was common. Venous thrombosis occured in three patients, and pulmonary embolism occurred in three other patients. Complement fixing antibodies to phase 1 antigen were found in a titre of 1:200 or greater in all except two patients. In one of these post-mortem examination revealed rickettsial bodies in mitral valve vegetations, and in the other Coxiella burneti was isolated from heart valve tissue. The majority presented with infective endocarditis but two presented primarily with liver disease. All patients had evidence of liver involvement and in one this led to death from cirrhosis. Abnormal tests of liver function, particularly hyperglobulinaemia, raised alkaline phsophatase and abnormal bromsulphthalein retention were found in all patients. Hepatic histology was abnormal in all eight patients in whom it was studied. The commonest features were mononuclear cell infiltration of the portal tracts and prominence of the sinusoidal Kupffer cells. Patchy focal necrosis of parenchymal cells, granulomata, fatty change, and eosinophilia of the sinusoidal walls were also noted in several patients and cirrhosis developed in one. Six patients had a purpuric rash, and in 12 there was thrombocytopenia. It is suggested that the presence of hepatomegaly and liver involvement and thrombocytopenia may help to differentiate Q fever endocarditis from bacterial endocarditis. Raised serum IgM and IgA levels occured frequently, but with only a moderate dominance of IgM. Sheep cell agglutination and latex fixation tests for rheumatoid factor were occasionally positive. Several features of the disease suggest the possibility that immune-complex mechanisms may play a role in chronic Q fever. Treatment was with prolonged courses of tetracycline usually combined with lincomycin. Seven patients underwent valve replacement surgery for haemodynamic reasons. Five patients died; two from heart failure, one from cirrhosis, one seven days after valve replacement and one from intraperitoneal haemorrhage following percutaneous liver biopsy. Three patients have survived for more than five years, and another six for more than three and a half years after diagnosis. Of these nine patients, three received medical therapy alone and six required valve replacement as well. Antibiotics have been discontinued in four patients who have had valve surgery and three others. Six patients had received antibiotics for continuous periods varying from 29-62 months. In the period after stopping therapy varying from 15-21 months, no relapse has occured. A seventh patient, who had received antibiotics for four months prior to valve replacement, has survived 43 months after the withdrawal of antibiotics...
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PMID:Chronic Q fever. 94 Sep 18

A 25-year-old man was admitted to Juntendo University Hospital with chief complaints of nocturnal dyspnea and shortness of breath on Sept. 22, 1983. He had no history of rheumatic fever or bacterial endocarditis. He was violently kicked in the chest while practicing Shorinji-Kempo (Karate) in July 1977. His heart murmur was first noticed in April 1978, but he was asymptomatic for six years after the accident until transient nocturnal dyspnea developed January 1983. Physical examination on admission revealed a grade 4/6 apical holosystolic murmur, a markedly accentuated third sound, and hepatomegaly of two finger breadth in the right midclavicular line. An electrocardiogram revealed sinus tachycardia (100/min), left atrial overload and left ventricular hypertrophy. Chest radiography showed slight cardiac enlargement with a cardiothoracic ratio of 55%, and slightly increased pulmonary vascular markings. Two-dimensional echocardiography showed a markedly prolapsed posterior mitral leaflet and fluttering in diastole. Cardiac catheterization showed elevated pressure of pulmonary capillaries (a: 16, v: 30, mean: 19 mmHg), the pulmonary artery and the right ventricle. Left ventriculography revealed grade four (Sellers) mitral regurgitation. Mitral valve replacement was performed on October 13, 1983. A chorda tendinae supporting the posterior leaflet of the mitral valve was found to be ruptured just above its origin from the posterior papillary muscle. Histological examination of the resected valve showed increased spongiosa tissue which mimicked so-called myxomatous changes, but it seemed preferable to interpret this as a "secondary change due to increased hemodynamic stress" rather than the "primary change".
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PMID:[Traumatic mitral insufficiency: a case report]. 406 43

Hepato-splenic scintigraphy with 99mTc-S-colloid was performed in twelve patients with bacterial endocarditis. These images showed that the size of the liver varied from normal to a severe hepatomegaly, depending on the presence of congestive heart failure. Intrahepatic distribution of the radiocolloid was slighty irregular in all cases. The spleen was conspicuously enlarged, and showed irregular distribution of the radiopharmaceutical. In some cases intrasplenic concentration defects caused by infarcts, abscesses or cysts, were observed. The relative uptake of radiocolloid by the spleen, varied from hypo- to hyperconcentration according to the degree of lymphoid hyperplasia caused by the infection. In two cases, both with congestive heart failure, concentration of the radiocolloid was evident in the bone marrow. The scintigraphic pattern observed in these patients with bacterial endocarditis can be easily differentiated from that caused by only congestive heart failure, which is similar to the observed in patients with cirrhosis of the liver and/or portal hypertension.
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PMID:[Hepato-splenic scintigraphy in finding indications of bacterial endocarditis. Preliminary report]. 719 44

Aorto-atrial fistula is a rare anomaly of the heart that may be the result of congenital or acquired conditions, such as bacterial endocarditis, paravalvular abscess, aortic dissection, or a complication of cardiac surgery. A 50-year-old female patient presented at the clinic with the complaint of dyspnea and abdominal distention due to ascites. On admission, her functional capacity was New York Heart Association (NYHA) class III. A physical examination revealed a systolic murmur, which was best audible in the right parasternal side, ascites, and hepatomegaly. An aorto-right atrial fistula was detected using transthoracic echocardiography and confirmed with transesophageal echocardiography and aortography. The patient had a history of previous cardiac surgery, anticoagulant use, and heart failure; therefore, percutaneous intervention was preferred to surgery as a result of the high surgical risk. A successful closure of the fistula was performed with an Amplatzer Duct Occluder II device. The patient demonstrated a dramatic response to the treatment, resulting in a decrease in the ascites and halving of her diuretic dose within 1 week. Her functional capacity improved to NYHA class II, and right atrial pressure decreased to 8 mmHg after a month.
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PMID:Heart failure due to aorto-right atrial fistula and successful treatment with percutaneous closure. 3062 3