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Query: UMLS:C0023890 (cirrhosis)
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The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Among a total of 634,440 autopsy cases in "The Annuals of Pathological Autopsy Cases in Japan" from 1958 to 1984, 929 cases with nonspecific myocarditis were registered. The average incidence was 0.15%, fluctuating around 3- to 5-year intervals with a remarkable rise observed after 1974. The major complications in cases of myocarditis were pneumonitis, hepatitis or hepatic cirrhosis, pancreatitis, malignancies, lymphatic or thymic involvements. A clinicopathological study of 36 cases of myocarditis and 27 cases of postmyocarditic cardiomegaly indicated a classification of acute, subacute, healing and chronic or recurrent stages as well as dilatation-hypertrophy- and right ventricle-dominant types. Acute myocarditis was characterized by diffuse inflammatory cell infiltration and showed various types of arrhythmias and shock. Subacute myocarditis showed ventricular dilatation, edematous interstitium and severe congestive heart failure. Chronic myocarditis with dilatation and/or hypertrophy and irregular fibrosis included right ventricular involvement, endomyocardial disease, sick sinus syndrome in selected cases, congestive heart failure in most cases, and showed a male predominancy. Postmyocarditic cardiomegaly was similar to chronic myocarditis but showed more hypertrophy, preexcitation waves and prominent negative T waves in electrocardiography and sudden death.
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PMID:Nonspecific myocarditis: a statistical and clinicopathological study of autopsy cases. 252 82

Myocarditis attended chronic active hepatitis in 22 patients (in 13 of them the outcome of hepatitis was liver cirrhosis). Twelve patients recovered, postmyocarditis cardiosclerosis developed in 6 and 4 patients died. Chronic myocarditis in the stage of aggravation was revealed in 3 cases at autopsy and severe postmyocarditis cardiosclerosis with manifested dilatation of the heart cavities in 1 case.
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PMID:[Myocarditis in chronic active hepatitis]. 272 95

A rare chronic course of Budd-Chiari syndrome associated with thrombosis of the portal vein was observed in a 30-year-old male patient suffering from postmyocarditic cardiosclerosis. At the age of 24 the patient had infectious allergic myocarditis, was hospitalized and rehospitalized for circulatory insufficiency. Upon 3 years since the disease onset the patient was admitted to a hematological department for progressive enlargement of the spleen. The diagnosis on discharge was idiopathic myelofibrosis with portal hypertension. The treatment included prednisolone, blood transfusions, myelosan. In 1987 the patient presented with enlarged liver and spleen, ascites, gastric and esophageal varicosis, augmenting hepatic insufficiency clinically evaluated as hepatic cirrhosis. Postmortem examination revealed macrofocal cardiosclerosis, splenomegaly, ascites, portal varicosis, enlarged nutmeg liver with smooth surface. Microscopically there was phlebosclerosis and phlebothrombosis varying in duration and involving predominantly medial branches of the hepatic and portal veins, liver fibrosis. The findings provided evidence for the final diagnosis of Budd-Chiari syndrome running an uncommon chronic course.
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PMID:[The chronic form of the Budd-Chiari syndrome]. 297 4

From 1969 to 1973, 68 patients were admitted to the 4th Division of Medicine of the Brescia Civil Hospital with the diagnosis of viral myocarditis. The patients were divided into two groups according to the results of the Coxsackie virus complement fixing antibodies test: Group 1 (42 patients) with a fourfold or greater rising antibody titre; Group 2 (26 patients) with a negative serum test. Both groups were examined after a follow-up period of 15 years. Ten patients from Group 1 died. The diagnoses were chronic myocarditis (three cases); chronic cardiomyopathy-pulmonary embolism (one case); chronic cardiomyopathy-liver cirrhosis (one case); dilated cardiomyopathy-sudden death (two cases); congestive cardiomyopathy (three cases). No Group 2 patients died. The 15-year mortality rate of Group 1 was significantly higher than that of Group 2 (Fisher Test: p less than 0.005). In conclusion, the natural history of Coxsackie virus heart disease is characterized by two possibilities: a complete recovery from a clinical point of view, in some cases with only minor T wave abnormalities, or evolution into a chronic disease (dilated cardiomyopathy) having a high mortality rate within 10 years of the onset of the acute disease.
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PMID:Coxsackie virus heart disease: 15 years after. 322 24

One-hundred-forty postmortem liver specimens from patients with cardiac disease or pre-terminal hypotensive shock were examined in order to characterize the histopathologic features of ischemic and congestive hepatic disease. The study group included patients with arteriosclerotic, valvular or hypertensive heart disease, primary pulmonary disease with cor pulmonale, myocarditis, cardiomyopathy, and shock. The hepatic lesions included centrilobular congestion alone (10%), congestion with necrosis (77%), centrilobular necrosis with inflammatory reaction (neutrophil or mononuclear cell) (27%), cardiac sclerosis (48%) and regenerative hyperplasia (23%). Cardiac sclerosis, the most common form of hepatic fibrosis seen, consisted of eccentric thickening or occlusion of the walls of central veins and perivenular scars extending into the lobular parenchyma. Regeneration of liver cells was manifested by either liver-cell plate thickening within a retained cord-like framework or by nodular masses of hepatocytes (nodular regenerative hyperplasia). Only one case of developing cirrhosis was identified in this series. The morphologic features outlined in this study should provide a useful basis for the classification of liver injury in cardiac disease and shock.
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PMID:Morphologic features of hepatic injury in cardiac disease and shock. 372 87

In the annuals of autopsy records in Japan, edited by the Japanese Society of Pathology and covering 20 years, from 1958 to 1977, 377841 autopsy cases are registered with a short summary of the pathology findings. Of these, 434 cases with idiopathic, interstitial, viral, non-specific (NSM) and giant cell (GCM) myocarditis were found. The incidences of NSM and GCM were 0.11 and 0.007%, respectively. The annual incidence of NSM showed periodic fluctuations with in 5-year intervals and increased remarkably after 1974. Incidence of GCM showed a similar fluctuation but with a one to two year delay of peaks. The male to female ratio was 1.2: 1 and the age distribution had two peaked patterns for both sexes, though these peaks were scattered widely from neonate to elderly patients. The regional distribution of NSM showed a concentration in the middle portion of Honshu and its regional annual incidence had propagation waves from the central area to peripheral areas. The same tendency was observed in GCM cases. Hokkaido was characterized by a low incidence of NSM and no GCM. Complications of myocarditis included pancreatitis, pneumonitis, interstitial nephritis, meningoencephalitis, hepatitis, hepatic cirrhosis and a considerable incidence of malignancies. Antibiotics, antineoplastic agents, steroids and irradiation therapy were the main forms of treatment applied before or after the start of myocarditis.
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PMID:Twenty year autopsy statistics of myocarditis incidence in Japan. 382 May 37

An autopsy case of hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis is reported in a 43-year-old male. His mother died suddenly at 55. At the age of 39 the patient felt fatigue and feverish sensation followed by dyspnea and palpitation on exertion. He responded to beta-blocker and was discharged on the 51st hospital day. He died suddenly during his work three years and one month after discharge. The heart weighs 700 g. The thickness of the ventricular septum measures up to 3.2 cm, and that of the left ventricular posterior wall 2.2 cm. Subaortic endocardium is moderately thickened. Many patchy fibroses of various sizes and broad linear fibroses are mainly observed in the ventricular septum and in the left ventricular free wall. Microscopic examination shows severe fascicular disarray of hypertrophied myocardial fibers in the ventricular septum and in a part of the left ventricular anterior wall. Pericardial fibrosis, granulation tissue with many capillaries, and slight lymphocytic infiltrate are also noted. These findings suggest that the patient have both congenital hypertrophic cardiomyopathy and myocarditis. There are following possibilities as regards the relation between the two: first, haphazard association of cardiomyopathy with myocarditis; secondly, myocarditis triggered the onset or progression, or both, of cardiomyopathy. He also had liver cirrhosis, probably alcoholic, which appears to accelerate the progression of myocardial disarray and fibrosis.
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PMID:[Hypertrophic obstructive cardiomyopathy with extensive myocardial fibrosis: case report with autopsy]. 403

Legionnaires' disease, although primarily seen as a pulmonary affection, may also manifest systemic involvement. Evidence is given to demonstrate bacteremia and focal myocarditis in a patient with cirrhosis and pneumonia.
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PMID:Extrapulmonary histopathologic manifestations of Legionnaires' disease: evidence for myocarditis and bacteremia. 699 Aug 89

In a young male chronic generalized HBV infection (acute viral hepatitis in childhood, HBsAg, HBeAb, HBcAb in the blood serum) ran with a long-term fever and involvement of many organs and systems (the liver, lungs, CNS) complicating the diagnosis. The patient died in the presence of CNS affection and hepatorenal insufficiency. At biopsy and autopsy it was established that the patient had active hepatic cirrhosis, fibrosing alveolitis, pulmonary vasculitides, chronic pneumonia, cerebral vasculitis, myocarditis and postmyocarditis cardiosclerosis, necrotizing myositis, Sjogren's syndrome, mesangioproliferative glomerulonephritis.
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PMID:[The unique course of a chronic generalized infection with the hepatitis B virus (a clinico-morphological observation)]. 904 68


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