Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-four cases of Legionnaires' disease were diagnosed at the Wadsworth Veterans Administration Hospital during a 5-month period. All cases occurred in persons exposed to the hospital environment during the usual incubation period of Legionnaires' disease. The clinical illness was quite characteristic. All patients complained of weakness, malaise, anorexia, and cough. Rigors, diarrhea, and pleuritic pain were frequent symptoms. All patients had a maximum temperature of greater than or equal to 39.4 degrees C. Thirteen of 22 patients had relative bradycardia. Chest roentgenograms documented pneumonia in all patients. Leukocytosis, hyponatremia, hypophosphatemia, and abnormal liver-function test results were typical. Diagnosis was made by serologic criteria in 20 patients, postmortem examination of tissue in two, and both serology and tissue examination in two. Four patients in whom the disease was not suspected died of Legionnaires' disease. One patient died of unrelated causes. Fifteen of 19 survivors received erythromycin therapy. The presentation of Legionnaires' disease was characteristic enough to allow early, specific therapy.
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PMID:Legionnaires' disease: clinical features of 24 cases. 68 39

Eighteen patients with solid tumours were treated with human recombinant interferon-gamma at escalating dose levels starting at 1 X 10(6) units/m2 per infusion and rising through 3 X 10(6), 6 X 10(6), 9 X 10(6) and 22 X 10(6) to a maximum of 110 X 10(6) units/m2 per infusion. The IV infusions were given three times a week over a 4-week period. Side effects were seen in all patients, but were mild except at the highest dose. Acute dose-related effects included pyrexia, tiredness, thirst, chills and rigors. Chronic dose-related effects included anorexia, lethargy, weakness, disorientation, a trace of proteinuria and minimal rises in liver enzymes. In addition, effects were observed which were not related to dose. These included headache, nausea and vomiting, backache, myalgia, flatulence and a mild, transient reduction in neutrophils and erythrocytes. At the highest dose level dose-limiting toxicity was observed, consisting in severe tiredness and anorexia, hypotension, disorientation and changes on the electrocardiograph. Overall, toxicity was similar to that seen with preparations of interferon-alpha, except that no tolerance to the effects of interferon-gamma was noted. We observed less hepatic and haematological toxicity, but also recorded flatulence, handcramps and electrocardiograph changes, which have not been reported with interferon-alpha. When given according to this regimen, doses of 22 X 10(6) units/m2 per infusion of recombinant interferon-gamma were generally well tolerated by the patients.
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PMID:A toxicity study of recombinant interferon-gamma given by intravenous infusion to patients with advanced cancer. 309 8

A case of cryptococcal meningitis in a patient with the acquired immunodeficiency syndrome (AIDS) is described, as well as the epidemiology, pathogenesis, clinical manifestations, diagnosis, and therapeutic management of the disease. In July 1987 a 38-year-old white man was admitted to the hospital because of confusion, disorientation, and headache. His medical history was notable for a positive human immunodeficiency virus test. Culture of the cerebrospinal fluid was positive for Cryptococcus neoformans. The patient was started on amphotericin B 16 mg/day (0.3 mg/kg/day) intravenously and flucytosine 2 g every six hours (150 mg/kg/day) orally. Despite premedication with diphenhydramine and acetaminophen, he experienced rigors that were treated with hydrocortisone and meperidine. Three weeks later he was discharged on flucytosine 2 g orally every six hours and amphotericin B 50 mg intravenously every other day. One week later the patient developed fever and chills; blood cultures were positive for methicillin-sensitive Staphylococcus aureus, and his peripheral leucocyte count was 1.8 X 10(3)/cu mm. Flucytosine was discontinued, and he was treated with intravenous nafcillin while remaining on amphotericin B. In October the patient complained of nausea, vomiting, weakness, and agitation. A CSF latex agglutination titer for cryptococcal antigen was 1:32. He was treated with amphotericin B 50 mg daily until symptoms resolved and then continued on amphotericin B 50 mg twice weekly. Cryptococcosis is the most common life-threatening fungal infection among AIDS patients. In contrast to immunocompetent hosts, this population invariably develops disseminated disease, with 85% having meningeal involvement. The most effective therapy for cryptococcal meningitis in patients with AIDS has not been established.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Management of cryptococcal meningitis in patients with AIDS. 341 73

From 1973 to 1983 nine cases of Brucella melitensis infection were hospitalised at the Centre hospitalier universitaire vaudois (CHUV), Lausanne. In each case, the infection was acquired in a Mediterranean country (4 cases in Italy, 2 in Spain, 2 in Portugal and 1 in Greece). In 6 of the cases the disease was acquired by ingestion of dairy products and in 2 cases by direct animal contact. Despite classical initial symptomatology (fever, rigors, weakness), the time from first symptoms to diagnosis varied between 10 days and 5 months. This delay probably explains why 6 of 9 patients were admitted because of septic complications: orchi-epididymitis, arthritis, meningitis and endocarditis. With prolonged antibiotherapy, the evolution was favourable in all cases. The patient who presented with endocarditis required emergency aortic valve replacement. Culture of the valve showed the presence of 10(9) B. melitensis/g of tissue. Cure was achieved by the administration of streptomycin and tetracycline for 6 weeks, followed by cotrimoxazole for one year. These cases show that the diagnosis of Brucella infection is becoming rare in Switzerland. It is often not suspected, and prompt diagnosis is delayed until further complications occur. Serology and blood cultures should be done in every patient presenting with fever after a stay in endemic countries.
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PMID:[Brucellosis: a varied clinical presentation in 9 patients]. 633 95

Episodic muscular weakness, commonly associated with alterations of serum potassium, is the cardinal feature of periodic paralysis. The combination of transient hyperkalaemia and rigors occurring during febrile episodes of malaria is suggested as the underlying cause which precipitated the muscular paralysis. Three patients with malaria who developed a similar paralysis during the paroxysms of fever are described to illustrate this.
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PMID:Periodic paralysis complicating malaria. 702

The Waterhouse-Friderichsen (WFS) syndrome, also known as purpura fulminans, is described as acute hemorrhagic necrosis of the adrenal glands and is most often caused by meningococcal infection. This clinical entity is more frequently seen in the pediatric than the adult population and is associated with a high morbidity and mortality. The initial presenting complaints for patients with the WFS usually include a diversity of nonspecific, vague symptoms such as cough, dizziness, headache, sore throat, chills, rigors, weakness, malaise, restlessness, apprehension, myalgias, arthralgias, and fever. These symptoms are usually abrupt in their onset. Petechiae are present in approximately 50-60% of patients. The clinical diagnosis of WFS may be relatively straightforward or extremely challenging. Patients who appear in the initial and nontoxic-appearing stage without any skin lesions may be difficult to distinguish from a benign viral illness. When a patient presents with fever and petechiae, WFS must be considered, even when the patient has a non-toxic appearance. Due to the rapid progression and often devastating consequences, therapy should be instituted as soon as the diagnosis is suspected.
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PMID:Rupert Waterhouse and Carl Friderichsen: adrenal apoplexy. 969 86

The refreshing Bayes perspective has much to offer biostatistics. Yet, from its 225-year-old roots sprung difficulties that blocked its growth at the beginning of the 20th century. Computational obstacles in concert with an inability to identify the best indifferent prior revealed a weakness on which frequentists capitalized. It took Bayesians 40 years to recover, allowing the infant field of biostatistics to fall firmly in the hands of the frequentists. Recent disillusionment with the frequentist perspective, and its hegemony of p-values, has produced a second opportunity for the Bayesian philosophy to make solid contributions to clinical trials.However, difficulty with the applicability of the likelihood principle, problems with prevalent prior 'disinformation' in clinical medicine, in concert with the complexity of truly representative loss functions threaten again to thwart the Bayesian march into biostatistics. Seven suggestions are offered to the Bayesians to help them adapt to the rigors of clinical research.
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PMID:Bayesians in clinical trials: asleep at the switch. 1757 87