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)

Thirty-six patients with advanced epithelial ovarian cancer received epirubicin as second-line therapy after primary treatment with carboplatin and cyclophosphamide. Thirty-four patients were evaluatable for response, 36 for toxicity. There were 9 responses (response rate 26.4%, 95% CI = 12.9-44.4), 2 complete and 7 partial. Median duration of response was 149 days (range 42-183); 4 patients with partial remission are still on study. Toxicity consisted of fatal cardiac failure and paravenous injection (1 patient), fatal leukopenia and sepsis (1 patient), and severe loss of appetite, nausea and vomiting, fatigue, and general malaise in 3 patients. Platelet nadir grade 4 (WHO) was observed in 2 patients while leukocyte nadir grade 4 was seen in 3 patients. The present study showed a high response rate from standard-dose epirubicin. Toxicity was acceptable in most patients, but 2 patients died from treatment complications which gives a treatment-related mortality rate of 6%. Response was primarily seen in patients with minor tumor load and in good general condition.
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PMID:A phase 2 study with epirubicin as second-line treatment of patients with advanced epithelial ovarian cancer. 891 Jun 29

End-stage renal disease (ESRD) patients, whether they are treated with hemodialysis or continuous ambulatory peritoneal dialysis, frequently suffer from protein-energy malnutrition, which is associated with increased morbidity and mortality. The protein requirements in dialysis patients are increased compared to those of healthy individuals and nondialyzed patients with chronic renal failure. The intake of protein and energy is frequently reduced because of the underlying disease, comorbidity, psychosocial factors, and uremic anorexia (underdialysis). There are several factors in ESRD patients that may enhance protein catabolism and increase protein requirements, such as low energy intake, amino acid abnormalities, metabolic acidosis, endocrine abnormalities (insulin resistance, hyperglucagonemia, hyperparathyroidism, insensitivity to growth hormone and insulin-like growth factor-1, cardiac failure, infection and inflammation, anemia, and physical inactivity. The dialytic procedures per se may enhance protein catabolism due to dialytic losses of protein and amino acids and, in hemodialysis, an inflammatory response to blood-dialyzer interaction. The relative importance of the various factors which cause anorexia and stimulate protein catabolism is still not well understood.
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PMID:Factors contributing to catabolism in end-stage renal disease patients. 939 22

In this case-report we describe the fatal outcome of systemic vasculitis. A 51-year-old man was hospitalised with constant abdominal pain, chest pain, anorexia, fatigue, weight loss, dyspeptic complaints, and a period of high fever at home. Bilateral adrenal enlargement was found without a plausible cause. Endoscopy revealed a reflux oesophagitis grade I, which was treated with famotidine. His complaints disappeared without further treatment. Five days after release from hospital the patient was re-admitted with subfebrile temperature followed by an Addison's crisis due to primary adrenal failure. Laboratory tests for systemic illness were all negative. He was treated with high-dose corticosteroids. Right adrenal biopsy revealed haemorrhage, possibly of older age. After 10 days he returned with severe kidney and heart failure. He was transported to another hospital for haemodialysis. Unfortunately the patient passed away because of cardiac arrhythmias. Postmortem investigation revealed inflammation of middle-sized and small arteries in the adrenal glands, heart, lung and thyroid. In the kidneys, mesangio-proliferative glomerulonephritis was found. A definite classification of the vasculitis could not be made because of the high-dose corticosteroids therapy. Possibly, the haemorrhage of both adrenal glands was caused by venous thrombosis due to the hypercoagulable state, which is often observed in vasculitis.
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PMID:Bilateral adrenal enlargement as a first sign of systemic vasculitis. 944 26

The moose (Alces alces L.) in an acid rain affected region in south-west Sweden has developed a complex disease with numerous clinical signs, most of which are consistent with those of secondary copper (Cu) deficiency and/or molybdenosis in cattle and sheep. The clinical signs of the moose disease reported to date include diarrhoea, anorexia, emaciation, achromotrichia, alopecia, sudden heart failure and osteoporosis. Findings at necropsy included mucosal oedema, atrophied lymphoid tissues of the mucous membranes of the alimentary tract, neuropathy, neuronal degeneration and uni- or bilateral corneal opacity. In a study of clinically healthy animals from the affected region in Sweden over a 12-year period (1982-1994), the hepatic Cu concentration decreased by 50% and the liver and kidney cadmium (Cd) concentration decreased by 25-35%, while the molybdenum (Mo) concentration increased by 20-40%. These changes are probably related to an increase in the pH of the soil and water in the moose environment and a consequent change in the uptake of these elements by the plants consumed by the moose. It is noteworthy that the occurrence of the disease in the mid 1980s coincided with increased liming undertaken to counteract the noxious effects of acid rain in this region. Clinical signs and lesions of the moose disease resemble those reported for Cu deficiency and/or molybdenosis in cattle and sheep. To elucidate the complex, multi-faceted clinical signs of the moose disease, the clinical signs and necropsy findings are discussed in relation to the biochemical functions of certain well-known Cu-dependent enzymes, e.g. depigmentation of hair due to depressed tyrosinase activity, osteoporosis by depressed lysyl oxidase activity, sudden heart failure due to decreased activity of lysyl oxidase, cytochrome c oxidase and Cu/Zn-superoxide dismutase; in addition, mucosal lesions and ulcerations due to loss of activity of diamine oxidase as well as of lysyl oxidase and cytochrome c oxidase. It is concluded from the present findings that the moose disease is most probably a Cu deficiency and/or a molybdenosis-type syndrome.
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PMID:'Mysterious' moose disease in Sweden. Similarities to copper deficiency and/or molybdenosis in cattle and sheep. Biochemical background of clinical signs and organ lesions. 949 61

The caval syndrome is a serious complication of chronic heartworm (Dirofilaria immitis) disease in dogs and cats. The syndrome is characterized by acute anorexia, respiratory distress, weakness, right-sided cardiac murmur, anemia, hemoglobinuria, hepatic and renal dysfunction, signs of forward and backward heart failure, and, possibly, disseminated intravascular coagulation (DIC). Retrograde migration of adult heartworms from the pulmonary arteries to the right ventricle, right atrium, and venae cavae causes disruption of the tricuspid apparatus. Valvular insufficiency, with concurrent pulmonary hypertension, reduces cardiac output thus resulting in forward and backward heart failure. Additionally, red blood cells are traumatized and hemolyzed as they flow through the mass of worms. Therapy consists of supportive care and the removal of the heartworm mass from the right ventricular inflow tract. Caval syndrome in dogs and cats is associated with high mortality rates and generally has a guarded to poor prognosis.
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PMID:Canine and feline caval syndrome. 975 97

In this study, insomnia in 80-year-olds was related to medical, psychological and social factors. The data were based on examinations every year in people aged between 80 and 89 years. Of 333 people living in the city of Lund and born in 1908, 67% participated. Increased severity of insomnia was significantly associated with use of diuretics, other cardiovascular drugs, hypnotics and laxatives, and with nervousness, difficulty relaxing, anorexia, nausea, constipation, backache, feeling cold, sweating, loss of weight, dizziness, depression, general fatigue, exhaustion, angina pectoris, cardiac insufficiency, worsened objective and subjective health, presence of negative T-waves on ECG, anxiety, total life satisfaction, neuroticism, disbelief in a just world, feeling lonely and lower survival rates. Thus insomnia has widespread associations with different aspects of life in 80-year-olds.
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PMID:Insomnia in an 80-year-old population: relationship to medical, psychological and social factors. 978 73

Malnutrition and hypoalbuminemia, which are prevalent in patients with end-stage renal disease (ESRD), are strong predictors of increased mortality. However, cardiovascular disease predominates among direct causes of death, whereas malnutrition appears to be of minor importance in this respect. Reports in the literature demonstrate that cardiac failure may cause malnutrition and that infection/inflammation may predispose to atherosclerosis as well as to catabolism and hypoalbuminemia. Proinflammatory cytokines, generated in response to cardiac failure, infection, and other inflammatory stimuli, appear to play a pivotal role by causing muscle wasting, hypoalbuminemia, and anorexia as well as reduced cardiac contractility and atherosclerotic vascular disease. We hypothesize that this scenario also applies to ESRD patients, in whom congestion, hypertension, cardiac failure, and ischemic cardiovascular disease are common. Malnutrition rarely may be the direct cause of death, except in elderly dialysis patients, but may contribute to a poor prognosis by aggravating pre-existing heart failure and increasing the susceptibility to infections.
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PMID:Malnutrition, cardiac disease, and mortality: an integrated point of view. 982 Apr 57

The current interest in understanding the role of stress-induced cytokines in heart failure relates to the observation that many of the untoward pathophysiologic responses of the failing circulation might be explained by these compounds. These small molecules appear to cause left ventricular dysfunction, precipitate pulmonary edema, cause cardiomyopathy, reduce peripheral organ perfusion, induce ventricular remodeling, activate the fetal gene program in animal models, and cause anorexia and cachexia. Thus, the elaboration of cytokines, similar to the upregulation of neurohormones, may represent a biochemical mechanism that is responsible for producing symptoms and remodeling in heart failure patients. To better understand how cytokines play a role in heart failure, it is important to delineate the concept of cytokine bioactivity in this setting.
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PMID:Cytokines and heart failure. 1042 71

A prospective randomized study was conducted to compare the efficacy and toxicity of two anthracyclines for the treatment of patients with acute myelogenous leukemia (AML). Fifty-eight patients were randomized and received induction therapy consisting of cytosine arabinoside (AraC) 100 mg/m2/day for 7 days combined with either KRN8602 (3'-deamino-3'-morpholino-13-deoxo-10-hydroxycarminomycin hydrochloride [KRN]) 15 mg/m2/day for 5 days (KRN/AraC group) or daunorubicin (DNR) 40 mg/m2/day for 3 days (DNR/AraC group). Complete remission rate was 78.6% (22/28) in the KRN/AraC group and 73.1% (19/26) in the DNR/AraC group. There was a higher incidence of nausea/vomiting and anorexia observed in the KRN/AraC group compared to the DNR/AraC group, while the incidence of other adverse effects (stomatitis, diarrhea, and infectious complications) were similar between both groups. No electrocardiogram (ECG) abnormalities were observed after treatment in the KRN/AraC group, while in the DNR/AraC group, one patient showed ECG abnormality and three patients exhibited either arrhythmia, heart failure, or tachycardia. Mental disorder was reported in two cases in the KRN/AraC group. These findings suggest that KRN/AraC is similar in effectiveness to DNA/AraC but more toxic in central nervous system and gastrointestinal symptoms and less toxic regarding cardiac function in patients with previously untreated AML.
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PMID:A prospective randomized trial of KRN8602 and cytosine arabinoside vs. daunorubicin and cytosine arabinoside in adult patients with newly diagnosed acute myelogenous leukemia. The KRN8602 Leukemia Study Group. 1044 90

Out of 938 parasitologically confirmed patients with visceral leishmaniasis treated with amphotericin B (1 mg/kg bodyweight daily infused in 2 h for 20 days), 935 were cured clinically, 933 parasitologically and 931 ultimately (no relapse within 6 months). Two parasitologically 'not cured' and 4 relapsed patients were cured with 25 infusions, and 1 with double relapse with 30 infusions. The treatment was started only when serum haemoglobin reached 5 g/dL, serum electrolyte imbalance was corrected and sodium stibogluconate-induced myocardial damage stabilized after 10 days' rest. Bronchopneumonia, cardiac failure and acute renal failure caused the death of 1 patient each. Nightblindness, angular stomatitis, neuritis, and petechial haemorrhages improved with appropriate treatment; 2 patients were given blood transfusion for post-treatment anaemia. Nausea and anorexia, and changes in serum creatinine and potassium, became normal in 2 weeks. Immediate withdrawal of the drug and restart after 10 days cured 2 patients who developed acute renal failure. Infusion-related toxicities--shivering, rigor and fever--were minimized but not eliminated by prior administration of hydrocortisone. Tuberculosis and visceral leishmaniasis were treated concurrently. Four pregnant patients were successfully treated without harmful effects on mother and child. It was concluded that the dosage of amphotericin B used was an effective and well-tolerated regimen and achieved 99% cure. Toxicity could be minimized with some precautions. All unresponsive and relapsed patients responded to more amphotericin and no resistance to the drug was seen.
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PMID:Amphotericin B deoxycholate treatment of visceral leishmaniasis with newer modes of administration and precautions: a study of 938 cases. 1049 70


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