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)

New effective therapies have been producing longer survival times for HIV-patients. Thus non-infectious complications of late stage of HIV infection (such as the development of left ventricular dysfunction) have emerged; in fact cardiac involvement has been identified frequently at autopsy and is described in 80% of patients with acquired immunodeficiency syndrome (AIDS) as an evidence of the virus cardiotrophism, while clinical findings of left ventricular dysfunction were only detected in about 15% of the patients. It is possible that the development of heart failure had been underestimated in those years; in fact signs and symptoms of cardiac involvement had been often misinterpreted as the results of non cardiac causes (pulmonary failure or infections) also determining a delay in the beginning of cardiac therapy. The aim of this study was to follow 16 human immunodeficiency-virus positive patients during a 3-year period to evaluate the usefulness of early detection of heart failure in order to start a specific therapy as soon as possible. The follow-up consisted of a clinical and electrocardiographic control every 4 months. Echocardiography was carried out when involvement of the cardiac muscle was suspected. During the follow-up we could reveal an early involvement in 5/16 patients (31.2%) and in 2 of them (40%) early therapy caused clinical and echocardiographic regression of left ventricular dysfunction. The present study demonstrates that periodical clinical and echocardiographic controls are useful in patients with HIV infection.
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PMID:[Early detection of heart involvement using serial cardiologic controls in the follow-up of patients with AIDS]. 961 56

Gelatinous bone marrow transformation (GMT) is a rare disorder of unknown pathogenesis, characterized by fat cell atrophy, focal loss of hematopoietic cells, and deposition of extracellular gelatinous substances, which histochemically are mucopolysaccharides, rich in hyaluronic acid. To elucidate the conditions in which GMT develops, 155 cases of GMT that had been found in our archives among 80,000 marrow biopsies were revised. GMT occurred exclusively in adults, more often in males (n = 101) than in females (n = 54). Incidence and severity of GMT lesions were maximal in young adults. The spectrum of underlying diseases was heterogeneous and age-dependent. Anorexia nervosa, acute febrile states, and AIDS in younger ages (<40 years), alcoholism and lymphomas in middle ages, and carcinomas, lymphomas, and chronic heart failure in older ages (>60 years) were most commonly associated with GMT. Seventy-eight percent of patients with GMT showed weight loss; 81% were anemic. GMT in some cases may be a reversible lesion if the underlying disorder can be eliminated. In conclusion, GMT represents an indicator of severe illness in a patient but is not specific for a particular disease. Because GMT develops in different pathologic conditions, we suggest that basic bioregulatory processes play a role in its pathogenesis.
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PMID:Gelatinous transformation of the bone marrow: the spectrum of underlying diseases. 1063 88

Interest has recently risen regarding thiamine deficiency (beriberi). In industrial countries, not only alcoholics, but also deprived people with malnutrition, elderly patients and patients with AIDS are at risk of thiamine deficiency. Moreover, long-term furosemide use may be associated with thiamine deficiency through urinary loss, contributing to cardiac insufficiency in patients with congestive heart failure. Cardiovascular (wet beriberi) manifestations of thiamine deficiency are characterized by peripheral vasodilatation with increased cardiac output, myocardial lesion, sodium and water retention and biventricular myocardial failure. Treatment consists of thiamine administration with rapid clinical improvement after supplementation.
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PMID:[Cardiac beriberi]. 1081 8

Programmed cell death plays critical roles in a wide variety of physiological processes during fetal development and in adult tissues. In most cases, physiological cell death occurs by apoptosis as opposed to necrosis. Defects in apoptotic cell death regulation contribute to many diseases, including disorders where cell accumulation occurs (cancer, restenosis) or where cell loss ensues (stroke, heart failure, neurodegeneration, AIDS). In recent years, the molecular machinery responsible for apoptosis has been elucidated, revealing a family of intracellular proteases, the caspases, which are responsible directly or indirectly for the morphological and biochemical changes that characterize the phenomenon of apoptosis. Diverse regulators of the caspases have also been discovered, including activators and inhibitors of these cell death proteases. Inputs from signal transduction pathways into the core of the cell death machinery have also been identified, demonstrating ways of linking environmental stimuli to cell death responses or cell survival maintenance. Knowledge of the molecular mechanisms of apoptosis is providing insights into the causes of multiple pathologies where aberrant cell death regulation occurs and is beginning to provide new approaches to the treatment of human diseases.
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PMID:Mechanisms of apoptosis. 1107 1

Cell suicide is a normal process that participates in a wide variety of physiological processes, including tissue homeostasis, immune regulation, and fertility. Physiological cell death typically occurs by apoptosis, as opposed to necrosis. Defects in apoptotic cell-death regulation contribute to many diseases, including disorders associated with cell accumulation (e.g. cancer, autoimmunity, inflammation and restenosis) or where cell loss occurs (e.g. stroke, heart failure, neurodegeneration, AIDS and osteoporosis). At the center of the apoptosis machinery is a family of intracellular proteases, known as 'caspases', that are responsible directly or indirectly for the morphological and biochemical events that characterize apoptosis. Multiple positive and negative regulators of these cell-death proteases have been discovered in the genomes of mammals, amphibians, insects, nematodes, and other animal species, as well as a variety of animal viruses. Inputs from signal-transduction pathways into the core of the cell-death machinery have also been identified, demonstrating ways of linking environmental stimuli to cell-death responses or cell-survival maintenance. Knowledge of the molecular mechanisms of apoptosis has provided important insights into the causes of multiple diseases where aberrant cell-death regulation occurs and has revealed new approaches for identifying small-molecule drugs for more effectively treating these illnesses.
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PMID:Drug discovery opportunities from apoptosis research. 1110 94

A drug overdose (OD) is the body's response to being overwhelmed by too much of a substance. Overdoses are not always life-threatening, but can lead to unconsciousness, failed breathing, heart failure, and seizures. Many overdoses are the result of taking drugs of inconsistent strength or drugs that are mixed with other substances. Guidelines are given to recognize and prevent drug overdoses.
Newsline People AIDS Coalit N Y 1998 Jun
PMID:Overdose prevention & survival. Harm Reduction Coalition. 1136 71

A growing body of literature indicates that cytokines regulate skeletal muscle function, including gene expression and adaptive responses. Tumour necrosis factor-alpha (TNF-alpha) is the cytokine most prominently linked to muscle pathophysiology and, therefore, has been studied most extensively in muscle-based systems. TNF-alpha is associated with muscle catabolism and loss of muscle function in human diseases that range from cancer to heart failure, from arthritis to AIDS. Recent advances have established that TNF-alpha causes muscle weakness via at least two mechanisms, accelerated protein loss and contractile dysfunction. Protein loss is a chronic response that occurs over days to weeks. Changes in gene expression required for TNF-alpha induced catabolism are regulated by the transcription factor nuclear factor-kappaB which is essential for the net loss of muscle protein caused by chronic TNF-alpha exposure. Contractile dysfunction is an acute response to TNF-alpha stimulation, developing over hours and resulting in decreased force production. Both actions of TNF-alpha involve a rapid rise in endogenous oxidants as an essential step in post-receptor signal transduction. These oxidants appear to include reactive oxygen species derived from mitochondrial electron transport. Such information provides insight into the cellular and molecular mechanisms of TNF-alpha action in skeletal muscle and establishes a scientific basis for continued research into cytokine signalling.
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PMID:Cytokines and oxidative signalling in skeletal muscle. 1141 34

Defects in the regulation of apoptosis (programmed cell death) contribute to many diseases, including pathologies associated with cell loss (e.g. stroke, heart failure, neurodegeneration and AIDS), and disorders characterized by a failure to eliminate harmful cells (e.g. cancer, autoimmunity). Apoptosis is caused by activation of intracellular proteases, known as caspases, which are responsible directly or indirectly for the morphological and biochemical events that characterize the apoptotic cell. Numerous caspase regulators have been discovered, which respond to environmental stimuli and influence the decision of cell death and survival. Knowledge of the molecular details of apoptosis regulation, and the three-dimensional structures of proteins constituting the apoptosis core machinery has revealed new strategies for identifying small-molecule drugs that could one day yield more effective treatments for a wide variety of illnesses.
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PMID:Apoptosis-regulating proteins as targets for drug discovery. 1142 40

Dementia in the elderly used to be rare, but why has it become a major social threat today? There can be many potential answers, but an ultimate one is clear: the longer life expectancy today. This knowledge indicates that "advanced aging" is a primary suspect in the origin of senile dementia. If so, then why can many elderly remain healthy at the same old age? We know, for example, that elderly people commonly have a certain degree of atherosclerosis and osteoporosis, but only some of them develop severe clinical symptoms at the same age. These different outcomes generally can be explained by "risk factors" in life (exercise, diet, individual background, etc). It thus appears to be a general pattern that advanced aging (after age 80) will set the stage for various senile disorders, but risk factors largely determine the onset age as well as individual specificity of their clinical manifestations. In this context, senile disorders including senile dementia would differ fundamentally from the pathogen-caused conventional diseases (AIDS, polio, cancer, Down's, etc.) by origin, incidence, and intervention strategy. This view would call into question the current definition of senile dementia as a conventional "disease" (Alzheimer's). The term "Alzheimer's disease" originally referred to "midlife" dementia, but it is defined today to be the same medical entity as senile dementia on the basis that they both display the same hallmarks and symptoms despite their onset age difference. Now, after in-depth scrutiny, we finally come to realize that they are not the same disease, but as different as heart failure at midlife versus the "same" failure at advanced age (i.e., a conventional disease versus a senile condition). Thus, by eliminating the age difference, the new definition has converted a senile condition into a conventional "disease", thereby changing the course of its scientific inquiry to miss the main targets. This may be why after extensive studies for 25 years, the origin of senile dementia has remained an enigma.
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PMID:Alzheimer movement re-examined 25 years later: is it a "disease" or a senile condition in medical nature? 1150 85

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


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