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)

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

Fever is often an indication of a serious illness in children. In areas endemic to malaria, hospital workers should check a febrile child for malaria parasites. Children with a fever associated with meningitis or malaria need immediate attention. To diagnose meningitis: microscopic examination of cerebrospinal fluid obtained by lumbar puncture is the only reliable method. If a febrile child also has a stiff neck, health workers should immediately administer antibiotic treatment without waiting for the results of the lumbar puncture. If available and in epidemic situations, oily chloramphenicol may be administered, since it is effective in a single dose. Treatment with other antibiotics should last for 10 days in children and 14-21 days for young infants. To diagnose malaria in endemic areas: laboratory technicians should examine thick and thin blood films of sick children with fever. Health workers must consider as medical emergencies children who have a slide positive for malaria parasites plus severe anemia, hypoglycemia, deep rapid breathing, any indication of kidney malfunction or failure, or altered consciousness. They should begin antimalarial treatment with quinine, the drug of choice for severe and complicated malaria. In cases of convulsions lasting longer than 5 minutes, health workers should administer anticonvulsants and take actions to prevent aspiration pneumonia. If the fever persists for 14 days or if the child does not emerge from unconsciousness and someone in the family has active tuberculosis, health workers should consider tuberculous meningitis. If a child with malaria has low hemoglobin levels (5 g/dl) and many malaria parasites in the blood and is in heart failure, a blood transfusion (15-20 ml/kg whole blood over 4 hours) and infusion of 1 mg/kg fursemide (to prevent cardiac failure) are needed. If the preceding case has pulmonary edema, a single dose of fursemide at the same dosage is needed to prevent overloading of the circulation. Health workers should closely monitor that intravenous fluids not exacerbate brain swelling.
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PMID:Managing meningitis and severe malaria. 1229 72

On November 15, 2000, a 60-year-old man was admitted to our hospital with progressive dyspnea and right chest pain. He had a 40-year history of occupational asbestos exposure, which began when he was 20 years old. On admission, his chest radiographs showed pleural effusion on the right side, and asbestos bodies were detected in his sputum. Neither a cytological examination of the pleural effusion nor a histological examination of the pleura by percutaneous pleural biopsy revealed malignant cells. In addition, we could not find any other cause for the pleural effusion (such as tuberculosis, collagen disease, or heart failure). In May 2001, the patient also developed pleural thickening and pain in the right hypochondrium, and he was readmitted to our hospital on May 21, 2001. On readmission, an enhanced abdominal CT showed multiple liver tumors, and percutaneous pleural and liver biopsies were performed. The histological findings in the pleura and liver specimens revealed hypocellular collagen tissues without malignant cells. Thus, we could not determine the main cause either of the pleural effusion or of the patient's disease. However, his condition rapidly deteriorated, and he died on August 12, 2001. At the autopsy, bilateral pleural thickening, predominantly on the right side, and invasion of the lungs were observed. The histological findings in the pleural and hepatic tissues revealed hypocellular collagen fibers with a striate pattern and areas of neoplastic spindle cells. He was diagnosed as having malignant desmoplastic mesothelioma with liver metastasis. Cases of malignant desmoplastic mesothelioma have rarely been reported in Japan.
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PMID:[An autopsy case of desmoplastic malignant mesothelioma]. 1242 2

Patients hospitalized with community acquired pneumonia were studied prospectively in two hospitals located in the surroundings of Buenos Aires city. Fifty two patients from General Hospital Manuel Belgrano (HMB) were included from March 1998 to February 1999 and 23 patients from Hospital Dr A. Cetrangolo (HCET) for respiratory disease, were included from June 2000 to May 2001. Patients with lung tuberculosis, lung neoplasia and HIV infection were excluded. Clinical background, signs and symptoms were recorded. Microbiological examinations performed included bacteria, respiratory viruses and mycobacteria. Studies for "atypical" bacteria (Chlamydia spp., Coxiella burnetii, Mycoplasma pneumoniae and Legionella spp.) were carried out by serological methods. No differences in age and gender were observed between both groups. Most frequently observed comorbidities in the HMB group included COPD, diabetes and cardiac failure while in the HCET group these were COPD, asthma and lung fibrosis. Etiology was established in 48% and 65.2% of the patients in the first and second group, respectively. Most frequent agents were Mycoplasma pneumoniae, Streptococcus pneumoniae, influenza A and Legionella spp.; the last one was detected in 12% of the patients. Most of these patients were from HMB and presented a good outcome. Mortality was similar in both groups (13.3%). In the HBM group it was related to the presence of comorbidities in 7 out of 8 cases, and in the HCET group it was a consequence of the worsening of their chronic respiratory failure.
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PMID:[Community-acquired pneumonia in patients in 2 hospital populations]. 1267 53

Carnitine is an ammo acid derivative found in high energy demanding tissues (skeletal muscles, myocardium, the liver and the suprarenal glands). It is essential for the intermediary metabolism of fatty acids. Carnitine is indispensable for beta-oxidation of long-chain fatty acids in the mitochondria but also regulates CoA concentration and removal of the produced acyl groups. AcylCoAs act as restraining factor for several enzymes participating in intermediary metabolism. Transformation of AcylCoA into acylcarnitine is an important system for removing the toxic acyl groups. Although primary deficiency is unusual, depletion due to secondary causes, such as a disease or a medication side effect, can occur. Primary carnitine deficiency is caused by a defect in plasma membrane carnitine transporter in muscle and kidneys. Secondary carnitine deficiency is associated with several inborn errors of metabolism and acquired medical or iatrogenic conditions, for example in patients under valproate and zidovuline treatment. In cirrhosis and chronic renal failure, carnitine biosynthesis is impaired or carnitine is lost during hemodialysis. Other chronic conditions like diabetes mellitus, heart failure, Alzheimer disease may cause carnitine deficiency also observed in conditions with increased catabolism as in critical illness. Preterm neonates develop carnitine deficiency due to impaired proximal renal tubule carnitine re-absorption and immature carnitine biosynthesis. Carnitine stabilizes the cellular membrane and raises red blood cell osmotic resistance but has no metabolic influence on lipids in dialysis patients. L-Carnitine has been administered in senile dementia, metabolic nerve diseases, in HIV infection, tuberculosis, myopathies, cardiomyopathies, renal failure anemia and included in baby foods and milk.
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PMID:Carnitine metabolism and deficit--when supplementation is necessary? 1276 64

Constrictive pericarditis is a rare disease characterized by the encasement of the heart by a rigid, non-pliable pericardium, with impaired diastolic filling of the ventricles. Its etiology is often unclear (42%), but is frequently associated with viral infection and tuberculosis, especially in developing countries. In this article the authors present the case report of a 28 year-old black woman, born and resident in Angola, with a history of tuberculosis, admitted to our hospital with global heart failure. After investigation a diagnosis of constrictive tuberculous pericarditis was established and the patient underwent pericardiectomy. Clinical features and radiologic, electrocardiographic, echocardiographic, computed tomography, nuclear magnetic resonance imaging and hemodynamic findings are discussed. This case illustrates the importance of early pericardiotomy before the appearance of pericardiectomy before end-stage pericardial fibrosis and subsequent increased possibility of an adverse postoperative outcome.
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PMID:Constrictive tuberculous pericarditis: case report and review of the literature. 1284 80

Sputum from 88 patients with different forms of pulmonary tuberculosis complicated by chronic cor pulmonale (CCP) was tested for Mycobacterium tuberculosis (MBT) and nonspecific flora. The high occurrence of multidrug resistance of MBT and nonspecific causative agents are found in patients with signs of heart failure in the presence of decompensatory CCP in 20% of cases, the frequency of concomitant chronic bronchitis was 86%.
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PMID:[Bacterial factors and decompensation of cor pulmonale in patients with pulmonary tuberculosis]. 1291 35

86 patients with chronic obstructive pulmonary diseases (COPD) and tuberculosis in combination with COPD complicated by chronic pulmonary heart (CPH) received a 18-month continuous treatment with enalapril (enap, D. Reddis Laboratories). It was found that the addition of enap, an inhibitor of ACE, to combined therapy of CPH patients is pathogenetic as it results in lowering of blood pressure in pulmonary artery, remodeling of hypertrophic right ventricle of the heart and decline of left ventricular dysfunction, in improvement of functional state of the lungs, in arrest of progression of cardiac failure. Long-term administration of the drug induced no serious side effects and is well tolerated.
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PMID:[Efficacy of long-term enalapril use in combined therapy of chronic pulmonary heart]. 1293 8

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

Tumour necrosis factor-alpha (TNFalpha) is a proinflammatory cytokine that is synthesised by a variety of cell types in response to infectious or inflammatory stimuli. Although TNFalpha plays an adaptive role in immune protection and wound healing at 'physiological' levels, excess TNFalpha production can lead to adverse consequences. TNFalpha is a pivotal cytokine involved in the pathogenesis and progression of rheumatoid arthritis (RA). TNFalpha antagonists have been shown to be effective in the treatment of signs and symptoms of RA and the US FDA has approved three TNFalpha antagonists, etanercept, infliximab, and most recently, adalimumab, for the treatment of RA. However, differences have emerged, with respect to their demonstrated efficacy in other diseases (e.g. Crohn's disease). Worldwide, over half a million patients have been treated with TNFalpha antagonists and concerns regarding their safety have been raised. There is a risk of reactivation of granulomatous diseases, especially tuberculosis, with all three agents and appropriate measures should be taken for detection and treatment of latent infections. An association between non-Hodgkin's lymphoma and treatment with TNFalpha antagonists has been reported, although patients with active, long-standing RA are already known to have an increased incidence of non-Hodgkin's lymphoma. No associations with solid tumours have been found to date. The biological plausibility of lymphomas associated with immunomodulatory agents raises concern and vigilance is appropriate until the relationship is fully characterised. Large phase II and III trials have shown a detrimental effect of TNFalpha antagonists in advanced heart failure and these agents should be avoided in this population. Rare case reports of drug-induced lupus, seizure disorder, pancytopenia and demyelinating diseases have been noted after TNFalpha antagonists and continued vigilance is warranted in patients on TNFalpha antagonists for the development of these diseases. At present there is no evidence implicating TNFalpha antagonists with embryotoxicity, teratogenicity or increased pregnancy loss.
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PMID:Safety of tumour necrosis factor-alpha antagonists. 1506 85


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