Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overt liver disease caused by left-sided heart failure is seldom recognized unless there is obvious hypotension. We now report 4 patients whose initial diagnosis was hepatitis but who were later shown to have central hepatic necrosis associated with left ventricular failure. Signs of right-sided heart failure were absent. Hepatitis was initially suspected in 3 patients because of striking transaminase elevations and in 1 patient because of jaundice and symptoms compatible with hepatitis. Liver biopsies performed on all patients revealed central hepatic necrosis without evidence of acute or chronic hepatitis. Left ventricular failure was documented in all 4 patients. One patient had coronary artery disease, and the other three patients had valvular heart disease. Liver function tests became normal or improved in all cases as the underlying heart disease was treated. We believe that liver dysfunction secondary to left ventricular failure is not uncommon and can be seen in the absence of right-sided heart failure or hypotension.
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PMID:Left-sided heart failure presenting as hepatitis. 63 89

Sera from 40 patients (25 men, and 15 women) with clinical features compatible with the diagnosis of chronic Q fever were received. Total or partial clinical data were available. All of them had serological evidence of chronic Q fever (IgG class anti-phase I titer greater than 800). The final diagnosis was vascular infection in four cases (with two positive cultures for Coxiella burnetii), bone infection in two patients (one positive culture), chronic hepatitis in one patient, and endocarditis in 32. The last patient had an isolated fever with a chronic Q fever serologic profile. Among the 32 with endocarditis, valve replacement was performed in 59%, and valve cultures were positive in 14/18 patients. Twenty-nine of these patients had previously known valvulopathy; 23 were exposed to cattle, sheep or goats; and four had an immunocompromised situation. Ten patients died; two before any treatment, five of cardiac failure during or a few weeks after surgery, and three during the medical treatment. For antibiotic treatment, tetracycline alone was employed in seven cases. For the other patients, combined therapy including tetracycline and another drug (rifampin, fluoroquinolones, cotrimoxazole, or erythromycin) was initiated. Three patients were considered to be completely cured.
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PMID:Chronic Q fever: diagnosis and follow-up. 237 73

Eight hundred Jordanians with liver enlargement were studied: 369 (46%) were males and 431 (54%) females. Ages ranged between 13 and 85 years, with a mean of 47.4%: 766 cases demonstrated a single pathological process while 34 cases showed two or more processes. The most significant findings were: congestion secondary to cardiac failure in 323 cases (38.5%); inflammatory and parasitic processes in 192 cases (22.9%), including acute hepatitis (81 cases), hydatid cyst (63 cases), chronic hepatitis (27 cases), liver abscess (19 cases), brucellosis (one case) and malaria (one case); malignancy in 164 cases (19.6%); liver cirrhosis in 80 cases (9.5%); fatty metamorphosis in 47 cases (5.6%); metabolic and genetic disease in 11 cases (1.3%); miscellaneous conditions in nine cases (1.1%); and 15 apparently normal individuals (1.8%). Cardiac failure was the most frequent cause of hepatomegaly in this sample of Jordanians. Inflammatory processes were the second major cause, followed by malignancy and cirrhosis of the liver.
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PMID:Patterns of hepatomegaly in Jordanians: a prospective study of 800 cases. 407 96

A 64-year-old man developed severe hyperbilirubinemia of predominantly conjugated fraction in 1978, eight years after a myocardial infarction and development of congestive heart failure. In 1975, he was admitted elsewhere for symptoms suggestive of chronic hepatitis, but liver biopsy revealed replacement of hepatocytes by red blood cells which was interpreted as a result of left-sided cardiac failure. In 1978, liver biopsy showed congestive liver disease with cardiac sclerosis. Despite initial improvement, his condition deteriorated, he became encephalopathic, and died in a coma. This case is reported to illustrate that chronic congestive heart failure can present with severe jaundice and terminate in hepatic coma.
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PMID:Severe hyperbilirubinemia and coma in chronic congestive heart failure. 707 14

Interferon (IFN) is effective in treating adults as well as children with chronic hepatitis C. We investigated the efficacy of IFN therapy in 13 children with underlying acute leukemia who had chronic hepatitis C (age range, 5 to 17 years; mean age, 9.9 years). Natural IFN- alpha was administered at a dose of 0.1 mega unit (MU)/kg (maximum dose, 6.0 MU) daily for 2 weeks and then three times per week for an additional 22 weeks (total dose, 8 MU/kg). IFN treatment was initiated at least 2 years after the completion of treatment for acute leukemia. A complete response was obtained in 5 children (38%). The serum level of anti-hepatitis C virus core antibody was closely related to the response to IFN. IFN therapy was well tolerated by all but 1 of the children, who developed mild transient heart failure 4 months after the initiation of therapy. IFN therapy for children with chronic hepatitis C who had underlying acute leukemia was beneficial. However, further trials are required to confirm the safety and improve the dosage schedule of IFN therapy.
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PMID:Efficacy of interferon in treating chronic hepatitis C in children with a history of acute leukemia. 863 63

The appearance of moderate jaundice with mildly raised levels of plasma bilirubin is an uncommon complication of thyrotoxicosis and is usually accompanied by signs of right heart failure. Some described cases were actually related, at least in part, to autoimmune chronic hepatitis. In this paper we describe a case of thyrotoxicosis accompanied by deep jaundice with very high levels of bilirubin occuring in the absence of cardiac failure and with no signs of hepatitis. Jaundice disappeared shortly after the start of thyrostatic drug treatment, supporting a possible detrimental effect of hyperthyroidism on the hepatic bilirubin metabolism.
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PMID:Appearance of severe jaundice after radiometabolical treatment of thyrotoxicosis. 1021 89

Intrahepatic cholestasis has rarely been observed in patients with thyrotoxicosis and generally occurs in association with coexistent congestive heart failure. We report the case of a 63-year-old man who was referred to our Institution because of jaundice and hyperthyroidism. During his hospital stay, his plasma bilirubin level reached 27.41 mg/dL. Clinical, biohumoral, and instrumental examinations excluded heart failure and autoimmune or viral hepatitis. After the start of therapy with methimazole, thyroid hormone and plasma bilirubin levels decreased progressively and simultaneously, eventually returning to normal. Plasma bilirubin values as high as the ones we recorded, in the absence of congestive heart failure or autoimmune chronic hepatitis, have not, to our knowledge, been previously reported.
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PMID:[Hyperthyroidism and cholestasis: a case report]. 1034 8

Standard treatment for chronic hepatitis C is with interferon (IFN)-alpha and ribavirin for 6-12 months. In dialysis patients only interferon therapy is currently used due to the lack of knowledge concerning ribavirin dosage and side-effects. The aim of this study was to investigate if ribavirin can be added to interferon when treating dialysis patients with hepatitis C. Five patients on haemodialysis and one patient on peritoneal dialysis with chronic hepatitis C, five with genotype 1 and one with genotype 4, were given interferon-alpha2b 3 MU thrice weekly for 4 weeks, whereafter ribavirin 200-400 mg was added, for an intended total treatment period of 28 weeks. Ribavirin plasma concentrations were monitored, using HPLC. Four patients completed the treatment. One patient suffered marked side-effects from interferon and therapy was terminated. One patient developed heart failure and died after 14 weeks of treatment but the death was not considered treatment related. Based on plasma concentrations, ribavirin doses were frequently adjusted initially. The target concentration (10-15 micromol/L) was reached with average daily doses of 170-300 mg ribavirin. Ribavirin induced anaemia was managed with high doses of erytropoietin (20 000-30 000 IU/week). Five of six patients became hepatitis C virus (HCV)-RNA negative during treatment, but four relapsed post-treatment; one is HCV-RNA negative. Hence ribavirin, in combination with IFN-alpha, can be used to treat dialysis patients with HCV. However, this requires reduced ribavirin doses and close monitoring of ribavirin plasma concentrations and haemoglobin. Ribavirin-induced anaemia can be managed with high doses of erythropoeitin.
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PMID:Ribavirin treatment in dialysis patients with chronic hepatitis C virus infection--a pilot study. 1145 81

Pulmonary hypertension (PH) appears to be more frequent and more rapidly progressive in HIV+ patients than in the general population. We describe 2 cases of PH in HIV+ patients disclosed by right-side heart failure. The patients were ex-intravenous drug users. On had AIDS and the other was asymptomatic. Both patients had cured hepatitis B and chronic hepatitis C and both died 10 and 11 months after PH diagnosis. Pulmonary hypertension is a likely diagnosis in HIV+ patients with unexplained dyspnea. For primary PH patients, HIV+ serology should be performed. There is probably an indirect mechanism linking PH and HIV. The role of associated chronic hepatitis C is unknown. Treatment of PH is symptomatic using diuretics, calcium-channel inhibitors, and anticoagulation, but with no real efficacy in terms of prognosis. Antiretroviral therapy is recommended. In the future treatment with epoprostenol may perhaps provide improvement in the prognosis of PH in HIV+ patients.
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PMID:[Pulmonary hypertension in HIV-infected patients]. 1154 53

A 30-year-old Japanese woman weighing 35 kg with severe hemochromatosis due to multiple transfusions was referred to our clinic for treatment of severe aplastic anemia (SAA). The patient had heart failure with an ejection fraction of 36% requiring diuretics and a severe liver dysfunction with an indocyanine green clearance rate of 18%, as well as other transfusion-related complications such as chronic hepatitis due to hepatitis C virus and diabetes mellitus. She was treated with a non-myeloablative preparative regimen that included fludarabine monophosphate (Flu, 120 mg/m(2)), cyclophosphamide (CY, 1200 mg/m(2)) and antithymocyte globulin (ATG, 15 mg/kg) followed by allogeneic peripheral blood stem cell transplantation (PBSCT) from her HLA-matched sister. The regimen was well tolerated, and engraftment rapidly occurred without any therapy-related complications. Chimerism analysis on day 14 after transplant showed reconstitution with 100% donor cells. She no longer needed transfusion after day 23 and has been well in 90% Karnofsky status at 4 months post transplant. The clinical course of this patient indicates that this preparative regimen enables SAA patients with severe organ failure to safely undergo allogeneic stem cell transplantation.
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PMID:Successful non-myeloablative stem cell transplantation for a heavily transfused woman with severe aplastic anemia complicated by heart failure. 1178 31


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