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)

A patient with acute monocytic leukemia and fibrosis presented with severe hypocalcemia producing tetany, myocardial failure, and ventricular tachycardia with torsades de pointes configuration. Hypophosphatemia, hypomagnesemia, an elevated alkaline phosphatase level, and osteosclerosis were also present. Bone marrow biopsy samples showed fibrosis and thickened bony trabeculae lined with large osteoblasts. Tetracycline labeling showed an increased rate of calcification. Complete remission of the leukemia and fibrosis was achieved with a single 3-week course of low-dose cytarabine and hydroxyurea, with resolution of the hypocalcemia and hypophosphatemia. Calcitriol and etidronate disodium were also administered. The calculated left ventricular ejection fraction increased from 15% to 55% with correction of the hypocalcemia. The hypocalcemia and hypophosphatemia in this patient probably resulted from accelerated bone formation stimulated by the leukemic cells. The high dose of calcitriol that this patient received may have contributed to the remission of the leukemia.
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PMID:Accelerated bone formation causing profound hypocalcemia in acute leukemia. 346 37

To characterize the incidence and severity of liver function abnormalities in patients with congestive heart failure, we analyzed systemic hemodynamics and biochemical profiles in 133 patients with stable chronic congestive heart failure, secondary to a dilated cardiomyopathy. The patients were divided into three groups, based on the severity of the reduction in cardiac index (CI). The mean values of all liver function tests in groups 1 (n = 43; CI greater than or equal to 2.0 L/min/m2) and 2 (n = 48; CI greater than 1.5 and less than 2.0 L/min/m2) were essentially normal, except for minimally elevated alkaline phosphatase levels and slightly decreased albumin levels in both groups, and slight increases in levels of gamma-glutamyl transpeptidase and total bilirubin in group 2. In contrast, group 3 patients (n = 42; CI less than or equal to 1.5 L/min/m2) had the most severe heart failure, as assessed by the lowest CI and highest cardiac filling pressures, and significantly higher levels of aspartate aminotransferase (65 +/- 82 U/L), alanine aminotransferase (77 +/- 102 U/L), lactate dehydrogenase (282 +/- 91 U/L), and total bilirubin (29 +/- 14 mumol/L [1.7 +/- 0.8 mg/dL]). The percentage of patients in group 3 with these abnormalities ranged between 27% and 80%. Although linear regression analysis showed that the elevations in right atrial and pulmonary wedge pressures, and the decreases in CI, were significantly correlated with liver function abnormalities, the correlation coefficients were small. Thus, liver function abnormalities remain common in patients with congestive heart failure but are generally small in magnitude and not associated with clinically apparent hepatic disease. It is likely that reduced forward flow and passive backward congestion are both contributing factors in the pathogenesis of these biochemical abnormalities, although nonhemodynamic factors may also be important.
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PMID:Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. 360 80

Cell smears from serous effusions containing large numbers of lymphoid cells were stained by the alkaline phosphatase-anti-alkaline phosphatase technique with a panel of monoclonal antibodies, including anti-B and anti-T cell antibodies and anti-HLA-DR. Samples from 17 patients with lymphoproliferative disorders--such as chronic lymphocytic leukaemia and non-Hodgkin's lymphoma--and from 19 patients who had no evidence of lymphoid neoplasia--for example, cases of carcinoma, cardiac failure--were investigated. The majority of lymphoid cells in reactive effusions were T cells, which lacked HLA-DR and showed a marked excess of helper/inducer cells (mean helper to suppressor ratio of 3 X 5). In contrast, lymphoid cells in samples from nine cases of B cell neoplasia were positive for B cell antigen and HLA-DR. In a further four B cell neoplasms most lymphoid cells were reactive T cells. Two cases of T cell lymphoid leukaemia could also be characterised by immunocytochemical staining, both being classified as T helper cell neoplasms. Labelling was performed on routinely prepared, air dried cell smears, which could be stored in the unfixed state for long periods before staining. The technique may therefore be of use in many clinical cytology laboratories for the diagnosis of effusions containing numerous lymphoid cells.
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PMID:Immunocytochemical staining of T and B lymphocytes in serous effusions. 389 89

The clinical syndrome of "shock liver," also known as ischemic hepatitis, is characterized by sudden elevation (to more than 20 times the upper limit of normal) of SGOT and SGPT in response to cellular anoxia, followed by resolution to near normal levels within seven to ten days. In our experience with ten cases, systemic hypotension was documented in only four, but processes characterized by decreased cellular perfusion were identified in all and included cardiac failure or arrhythmia, sepsis, cerebrovascular accidents, renal failure, and chronic obstructive pulmonary disease. We were also able to document the transient rise in serum bilirubin and alkaline phosphatase levels and prolonged prothrombin time that followed the transaminase elevations by 24 to 48 hours in most cases, followed by rapid resolution. In neither of the two cases in which tissue was available by biopsy after resolution of the biochemical abnormalities did we find the classic histologic picture of necrosis in zone 3 ("centrilobular necrosis"). The clinical picture of shock liver is so characteristic and resolves so rapidly that there should be no confusion with other causes of marked elevations of transaminase levels.
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PMID:Shock liver. 407 Nov 67

Benign liver tumors are relatively uncommon and, even when large enough to be symptomatic, they usually remain undiagnosed prior to exploratory laparotomy. Hemangiomas constitute the majority of benign hepatic neoplasms and are 9 times as frequent in females as in males. Most are asymptomatic but abdominal swelling, a mass, or symptoms due to compression of adjacent organs may occur and abdominal hemorrhage is reported in 4.5% of patients. Hepatic hemangioma may produce a large arteriovenous communication serious enough to cause heart failure. Recently an increased frequency of liver tumors, mostly adenomas, has been noted in women taking oral contraceptives (OCs); the cause has been attributed to estrogens. The exact incidence is unknown but believed to be low. It is most common in women in their late 20s who have been on OCs for 7 years or more. The tumor occasionally completely regresses on withdrawal of the OCs. The tumor may be discovered incidentally at laparotomy or may manifest inself by pain, a palpable mass, or catastrophic hemoperitoneum. Hepatic adenoma is usually a solitary lesion and infrequently degenerates into malignancy. Differential diagnosis includes chronic gall bladder disease and peptic ulcer. Focal nodular hyperplasia (FNH) is apparently much less frequently related to OC use and is less likely to bleed seriously than adenoma. Hepatic chemistry is usually normal in adenoma and FNH, but slight increases in serum bilirubin, serum alkaline phosphatase, and serum transaminase may occur. Primary liver cancer (hepatocellular carcinoma or hepatoma) is mostly a disease of males and in the US and Western Europe seldom develops before age 40. Fibrolamellar carcinoma, which characteristically develops in adolescents and young adults, occurs with equal sex incidence. Doubt has been expressed about its relationship to OCs. In the US about 75% of primary hepatocellular carcinomas are associated with cirrhosis, and about 5% of cirrhosis cases develop primary liver cancer. Clinical manifestations of hepatoma have been divided into 5 groups: frank cancer (62.7%), acute abdominal cancer (8%), febrile cancer (8%), occult cancer (16%), and metastatic cancer (5%). Detection of large amounts of alpha fetoprotein has proven useful in diagnosis of hepatocellular carcinoma, but values may be negative in OC users. It has been estimated that 1/3 to 1/2 of all malignant tumors eventually metastasize to the liver.
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PMID:Hepatic neoplasia: selected clinical aspects. 619 95

Among 2175 patients seen over the last three years in a non-specialized department of internal medicine with no intensive care unit, 100 had supranormal serum lactic dehydrogenase activities. These patients' case-reports have been analyzed. Nearly half the patients (47/100) had a malignant disease (cancer or hemopathy). Among the remaining patients, 19 had a hepatic disorder (alcohol hepatitis in 10, viral hepatitis in 8, and isoniazide hepatitis in 1), 7 had a heart disease (heart failure with hepatomegaly in 5, myocardial infarction in 2), and 27 had various other conditions (including hemolysis in 6 and polymyositis en 3). The value of serum LDH assay is obvious in situations other than acute conditions such as myocardial infarction of pulmonary embolism; these are better known and have not been studied here as their prevalence was low among the patients enlisted in our study. In comparison to other enzymes (alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), transaminases (GOT, GPT) that were also routinely assayed in our patients, abnormal serum LDH activities are much less common and their significance is quite different. An increase in serum and their significance is quite different. An increase in serum LDH activity indicates a serious condition, often with a fatal outcome. The "various other conditions" group includes patients with hemolysis, hepatitis and myositis; the other patients in this group either had severe infectious diseases or died suddenly in the first few days of their hospitalization before diagnosis had been established. Each etiologic group has been analyzed to asses the characteristics of patients with increased LDH activity according to each etiology. Analysis of coincident abnormalities of the other enzymes listed above shows marked differences between etiologic groups; diagnostic accuracy can thus be enhanced in certain conditions. Most patients with malignancies had poorly differentiated tumors, with metastases: 28 had an epithelial tumor, with hepatic and/or bone metastases in 23 cases, 5 had cancer of the liver, 10 had a malignant hemopathy (2 lymphomas, 5 myeloproliferative syndromes, 3 acute leukemias), and 4 had a sarcoma. Cancer of the lung is the most common malignancy (10 cases) and may be responsible for increased serum LDH activity even in patients without metastases. Serum LDH assay is of value for monitoring the course in patients with initially increased activities as it falls under effective therapy and rises during exacerbations.
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PMID:[Value and diagnostic significance of serum lactic dehydrogenase in internal medicine (author's transl)]. 628 24

The authors present the clinical history of a 70-year-old male with arterial hypertension who sought medical advice because of dyspnea on exertion, orthopnea and episodes of paroxysmal nocturnal dyspnea. The electrocardiogram showed left arterial hemiblock and abnormalities of ventricular repolarization compatible with a left lateral endocardiac lesion. Echocardiography revealed a hypertrophied left ventricle with a small ventricular cavity, compatible with an infiltrative-restrictive myopathy. Blood chemistry showed creatinine 4.9 mg/dl, BUN 133 mg/dl and alkaline phosphatase 204 i.v. The patient expired because of intractable heart failure. The histopathological examination of a piece of myocardium (authorized by the family) stained with Congo red confirmed the presence of abundant, diffuse deposits of amyloid, as had been suspected because of the echocardiographic findings.
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PMID:[Cardiac amyloidosis secondary to multiple myeloma detected by echocardiography]. 774 97

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.
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PMID:Clinical, hematologic, and biochemical findings in dogs after induction of shock by injection of heartworm extract. 787 76

A number of simple clinical and laboratory variables were analysed in a group of patients with chronic heart failure to evaluate their prognostic significance. Five hundred and fifty-two patients were followed for a maximum of 13 years with a total exposure time to death or censored survival of 1148 years. Of the clinical variables, diuretic dose and NYHA class were related to mortality (P < 0.01), and ischaemic heart disease was associated with a worse prognosis than other aetiologies (P < 0.05). Of the laboratory variables, abnormalities of liver function tests including bilirubin (P < 0.01), aspartate transaminase (P < 0.005), gamma glutamyl transpeptidase (P < 0.005) and alkaline phosphatase (P < 0.01) were all related to mortality as was plasma urate (P < 0.01). Multivariate survival analysis of all variables showed aspartate transaminase (chi 2 17.36, P < 0.001) accounted for the greatest variance followed by serum bilirubin (chi 2 14.35, P < 0.005). Thus, abnormalities in liver function tests have prognostic importance in chronic heart failure.
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PMID:The importance of abnormalities of liver function tests in predicting mortality in chronic heart failure. 888 55

Calcium deposits account for most of the dry weight of atherosclerotic lesions. Previously considered uncommon, vascular calcification is now known to be present in 80% of significant lesions and in at least 90% of patients with coronary artery disease. Previously considered a passive process, it is increasingly recognized as an active, regulated process. Previously considered benign, it is now becoming recognized as a major risk factor for cardiovascular events, and a major contributor to systolic hypertension, heart failure, plaque rupture and stenosis. To confirm the similarity of vascular calcification with embryonic osteogenesis, we demonstrated the expression of bone morphogenetic protein in calcified human lesions, and we developed an in vitro model of vascular calcification that provides a useful experimental system for elucidating the molecular regulation of this process, which we have shown to include alkaline phosphatase induction and expression of bone matrix proteins and differentiation factors. Understanding the regulatory mechanisms of vascular calcification will allow future therapeutic approaches to prevent and possibly reverse this disease and its clinical consequences.
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PMID:Role of molecular regulation in vascular calcification. 922 60


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