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)

Altered cardiovascular and respiratory function is uncommonly encountered in multiple sclerosis, though it may appear late in the course of the disease [4]. Episodes of acute ventilatory failure due to autonomic and/or voluntary respiratory function paralysis have already been described. These episodes are often accompanied by a focal neurological deficit which expresses lesion at the level of the medulla [6]. A demyelinating bulbar lesion leading to altered cardiovascular function is likewise infrequent but when it happens, bradycardia, postural hypotension [2], or acute pulmonary edema without heart failure may occur [1]. We present a case of non cardiogenic acute pulmonary edema which had neither a toxic insult nor an infective agent as etiology, but appeared as the initial manifestation of a multifocal demyelinating syndrome.
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PMID:Neurogenic pulmonary edema: a presenting symptom in multiple sclerosis. 151 69

A case of acute pulmonary edema without cardiac failure, infectious or toxic cause, revealing a Multiple Sclerosis (M.S.), one case of bradycardia during a bout in a known M.S. and one case of orthostatic hypotension without change of cardiac frequency, during a bout of a known M.S. are reported. The common point of these 3 cases is that during their autonomic failure, there were disorders pointing to the medulla oblongata: swallowing difficulties, rotatory nystagmus, vestibulo-cerebellar syndrome, sensory and motor defect of upper limbs. A plaque of M.S. in the medulla oblongata, particularly near the tractus solitarius could explain these cardio-pulmonary abnormalities unusual in M.S.
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PMID:[Cardio-respiratory anomalies in disseminated sclerosis]. 304 35

This study explored the prevalence of comorbid conditions in hospitalized patients with multiple sclerosis (MS) who were 65 years of age or older. Using 1989 data from the Quality of Care Medicare Provider Analysis and Review (MEDPAR) file, hospitalized MS patients were compared with respect to discharge diagnoses to an age- and sex-matched group of hospitalized patients without MS. As expected, the following discharge diagnoses were more common (P < 0.05) for MS patients: urinary tract infection, pneumonia, septicemia and cellulitus. In contrast, MS patients were less likely (P < 0.05) to have discharge diagnoses of acute myocardial infarction, heart failure, hypertension, angina pectoris, cerebrovascular disease, diabetes mellitus and chronic obstructive pulmonary disease. Possible explanations include under-reporting of certain comorbid conditions on discharge records of MS patients, a protective effect of MS or its treatment, reduced prevalence of risk factors, disproportionate mortality in younger MS patients with comorbidity and the benefits of medical surveillance.
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PMID:Patterns of comorbidity in elderly patients with multiple sclerosis. 772 46

A 25-year-old man was hospitalized because of dyspnoea and retrosternal pain. There were clinical and radiological signs of severe left ventricular failure which within a few hours necessitated artificial ventilation. A year before he had been diagnosed as having pseudohyperparathyroidism and disseminated encephalomyelitis. Administration of calcium and vitamin D was only partially efficacious. On admission the calcium concentration was 1.5 mmol/l. The severe left ventricular failure did not respond adequately to the usual therapeutic measures including artificial ventilation and catecholamines. A cumulative dose of about 50 mmol calcium was administered intravenously over 10 days, but marked improvement in myocardial function already became apparent at a calcium concentration of about 1.8 mmol/l. Lasting correction of the hypocalcaemia was achieved with 0.5 g calcium three times daily by mouth and 0.5 mg/d dihydrotachysterol. After transfer to a special neurological department because of an acute attack of multiple sclerosis there was no detectable impairment of cardiac function. This case demonstrates that hypocalcaemic cardiomyopathy should be considered in the differential diagnosis of heart failure in previously well young persons who do not respond adequately to the usual treatment. Myocardial impairment is fully reversible after administration of calcium.
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PMID:[Hypocalcemic cardiomyopathy as the cause of severe left heart failure]. 792 18

Post-traumatic stress-induced disorders are still the focus of interest and most recently discussions are under way whether stress-induced cortisol excess leads to atrophy of the brain. In investigation on carcinogenesis the first reports were published on the use of antisense-oligonucleotides during inhibition of the development of tumours by a humoral mechanism and on the gene-based neuroendocrine differentiation of the lungs, perhaps associated with the basis for the development of small cell carcinoma. The oncogenic action of superoxides has also humoral mediators. Interest in nitrogen oxide is focused on two areas: inflammations and hypertension. Intraluminal NO concentrations increase in asthma 2-10x, in cystitis 30-100x, in Crohn's disease 20-200x. Humoral mechanisms in asthma offer new drugs--inhibitors of the development or action of leucotrienes. The basal NO production is reduced in "essential" hypertension but it is not known whether it is the cause or consequence. IGF-I increases the formation of NO in the vascular wall and thus perhaps reduces vascular contractility. As far as IGF is concerned, it is obvious that if recombinant preparations will be available, they will be tested in amyotrophic lateral sclerosis, myotonic dystrophy, multiple sclerosis, catabolic conditions, osteoporosis, in renal failure and to promote wound healing. STH may also prove useful in cardiac failure, in particular in cardiac cachexia. That TRH has receptors in the gut is not surprising, it acts, however, even there via TSH. Thrombopoietin is being tested in clinical trials. Neocytolysis is a new phenomenon: when erythropoietin secretion declines new erythrocytes disappear and only old ones remain in the blood stream. Alpha-adducin is a renal tubular protein, regulating the sodium balance.
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PMID:[Endocrinology 1996-1997]. 965 Mar 40

We describe a 19-year-old woman developing acute left ventricular heart failure during her first exacerbation of multiple sclerosis. Histopathologic examination of myocardial tissue showed extensive myocytolysis. A left ventricular assist device was implanted. Three months later the cardiac function was restored and the left ventricular assist device was explanted. After 1 year the patient still remains well and her cardiac function is normal.
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PMID:Weaning from mechanical support in a patient with acute heart failure and multiple sclerosis. 1073 18

Dexanabinol is a non-psychotropic cannabinoid NMDA receptor antagonist under development by Pharmos Corp for the potential treatment of cerebral ischemia, glaucoma, Alzheimer's disease, cardiac failure, head injury and multiple sclerosis (MS) [311522]; it is in phase III trials for traumatic brain injury (TBI) [388709]. Dexanabinol was licensed to Pharmos for development from its originator, the Hebrew University of Jerusalem [180441]. Pharmos is seeking to enter into a strategic agreement with another company to develop and commercialize dexanabinol [317369]. Unlike its enantiomer, HU-210 (Yissum Research Development Co), dexanabinol does not interact with cannabinoid receptors [223330]. It has also exhibited more effective antioxidant and anti-inflammatory properties than MK-801 (dizocilpine; Merck & Co Inc) [167980], [168212]. In addition, dexanabinol is generally well tolerated and appears toxicologically safe [170116]. Pharmos has been awarded a Small Business Innovation Research grant from the National Institutes of Health (NIH) National Institute of Neurological Disorders and Stroke, Division of Stroke and Trauma. The grant covers the development of new prodrugs and novel formulations of dexanabinol and will support additional study of dexanabinol compounds for various indications. The prodrugs being studied are part of the group of compounds that include dexanabinol [247958]. A Notice of Allowance was received in March 1999 on a patent covering the use of the drug in the treatment of MS [324163]. The use of dexanabinol and its derivatives to treat MS is described in US-05932610 [358503]. An oral formulation of dexanabinol is claimed in US-05891468. Dexanabinol analogs with special utility in acute and chronic pain are claimed in US-04876276, while dexanabinol analogs for neuroprotection are claimed in US-06096740. Pharmos estimates that the worldwide market for dexanabinol in the treatment of severe head trauma may reach $1 billion per year [319244].
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PMID:Dexanabinol Pharmos. 1124 4

Monoclonal antibodies are increasingly used to modulate immunologically mediated diseases such as rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, Crohn's disease, multiple sclerosis and systemic vasculitis. Constructs of monoclonal antibodies to tumour necrosis factor (TNF) alpha differ with respect to their structure, effects and immunogenic side effects. Clinical experience with TNF alpha-neutralizing therapy has revealed several other side effects over the past few years. The most important is increased infection rates, especially the activation of (latent) tuberculosis, although other opportunistic infections such as listeriosis, Pneumocystis carinii pneumonia, histoplasmosis, candidiasis and aspergillosis have also been reported. Furthermore, results from clinical studies indicate that TNF alpha-neutralizing therapy should not be given to patients with cardiac failure (NYHA class III or IV) or a history of demyelinating disease. An increased incidence of malignancies has not been observed up to now, but data from the long-term follow-up are not yet available.
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PMID:[The treatment of chronic inflammatory diseases with monoclonal antibodies against tumor necrosis factor: side effects, contraindications and precautions]. 1235 84

Until recently, national coding and analysis of routine mortality statistics in most countries included only underlying cause of death. There were changes in the rules for selection and coding of underlying cause in England in 1984 and 1993. We report on trends in mortality rates in an English region from 1979 to 1998, comparing multiple-cause and underlying-cause coded rates, for individual diseases that were affected by coding changes. Among many others, these include pneumonia, venous thromboembolism, heart failure, respiratory distress syndrome, tuberculosis, diabetes, dementia, alcohol and drug abuse, epilepsy, multiple sclerosis, stroke, asthma, peptic ulcer, appendicitis, and cancers of the breast, colon and prostate. Comparisons over time of mortality rates based on underlying cause alone will be misleading when the time-period crosses years in which rules changed for selecting underlying cause.
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PMID:Trends in mortality rates comparing underlying-cause and multiple-cause coding in an English population 1979-1998. 1457 3

Mitoxantrone is an immunosuppressive drug usually delivered in severe relapsing remitting multiple sclerosis. It can also be used in secondary progressive and progressive relapsing remitting multiple sclerosis. Left ventricular ejection fraction has to be monitored because of the cardiotoxicity risk of mitoxantrone. Acute cardiac side effects in multiple sclerosis have not yet been described. We report the single case of an acute heart failure occurring in a cohort of more than 800 patients treated with mitoxantrone. We discuss about interruption criteria as maximal cumulative dose allowed and left ventricular ejection fraction cut off value.
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PMID:[Acute heart failure in a patient treated by mitoxantrone for multiple sclerosis]. 1497 18


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