Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two of three members (a 29-year-old man [case 1] and a 26-year-old woman [case 2]) of a tourist party to the tropics (Mali) developed a high fever (less than or equal to 40 degrees C), headache, cough, weight loss (less than or equal to 5 kg) and tiredness 3-4 weeks after returning to Germany. In case 1, acute schistosomiasis was tentatively diagnosed as the cause because he reported an attack of dermatitis after exposure to fresh water in an endemic schistosomiasis region and had marked eosinophilia (2118/microliters; 28%) on admission. Serological tests were positive (ELISA with adult antigen, O.D. 0.65 [normal less than 0.15]; with egg antigen O.D. 1.73 [normal less than 0.30], antibody titre in the immunofluorescence test 1:320 [normal less than 1:80]) supported the diagnosis and it was confirmed by demonstrating the parasite, Schistosoma mansoni, in stool but not urine. Findings in case 2 were similar. The third member of the group [case 3], a 58-year-old woman, was symptom-free, but tests revealed schistosomiasis. All three patients were treated with a single dose of Praziquantel (40 mg/kg). A second course of praziquantel (single dose of 40 mg/kg as well as 20 mg/kg three times daily for 3 days) became necessary in case 1, while in case 3 a further single dose of 40 mg/kg was given to ensure a parasite-free state. A follow-up scheme is suggested: clinical examination with white cell and differential counts 1, 3, 6 and 12 months after treatment; three stool and/or urine examinations 3, 6 and 12 months after treatment.
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PMID:[Acute schistosomiasis in travellers to the tropics]. 160 Aug 68

A 29 year old white homosexual man presented with a two and a half week history of severe sore throat, fever, and extreme fatigue. His symptoms did not respond to antibiotics. He had mild bilateral conjunctivitis, a rash over his chest and back, and enlarged lymph nodes, but examination of the nervous system yielded normal results. He had low total white cell and platelet counts. The results of enzyme linked immunosorbent assay for human immunodeficiency virus (HIV) were equivocal when HIV IgM was detected in serum. Despite treatment with ampicillin his temperature remained high and he developed abnormal neurological signs, including a paraparesis and hyperreflexia of the arms. HIV was isolated from lymphocytes from blood and cerebrospinal fluid. Over the next six weeks the patient improved and was discharged. Two months later abnormal neurological signs persisted in his legs. Although various neurological syndromes associated with seroconversion to HIV have been described, this is probably the first report of a patient with myelopathy at the time of seroconversion.
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PMID:Acute myelopathy associated with primary infection with human immunodeficiency virus. 288 58

The retrovirus human T cell lymphotropic virus type III (HTLV-III) can cause no symptoms at all, a syndrome of vague symptoms such as fever and fatigue, or full-blown acquired immune deficiency syndrome (AIDS). Serologic tests for antibodies to HTLV-III are available for identifying the virus; tests for T lymphocyte subset numbers and function and white cell count are also helpful. Management of patients with the virus depends on clinical presentation: Patients who are asymptomatic carriers need only reassurance and follow-up, patients with mild illness need symptomatic treatment and monitoring, and patients with full-blown AIDS need increasing levels of physical and emotional supportive care. Through early diagnosis, treatment when needed, and patient education, primary care physicians can be instrumental in curtailing the spread of HTLV-III infection.
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PMID:HTLV-III infection. A clinical approach to diagnosis and treatment of the 'AIDS virus'. 363 91

Recombinant interferon-gamma was given to patients with tumours by a six-hour intravenous infusion using a portable mini-pump, to assess the side-effects of the drug. At present, 11 patients have been treated; 2 adenocarcinoma of the ovary, 3 squamous carcinoma of the bronchus, 1 adenocarcinoma of the breast, 1 adenocarcinoma of the stomach, 1 Hodgkin's lymphoma, 1 case of two primaries, adenocarcinoma of the breast and ovary, and 1 adenocarcinoma of unknown origin. Two patients received 1 X 10(6) units/m2/infusion, four received 3 X 10(6) U/m2/inf., three received 6 X 10(6) U/m2/inf. and two received 9 X 10(6) U/m2/inf. Two further dose levels will be used in the future; 27 and 51 X 10(6) U/m2/inf. Three 6-hour infusions a week were given for a four week period. The major side-effects of gamma-interferon were dose-related pyrexia with rigors to which there was no tachyphylaxis, acute and chronic tiredness, nausea with or without vomiting, headache, backache and myalgia. There was also a dose-dependent immediate but mild and transient decrease in the total white cell count. All effects have been transient, and none have been severe. We have also noticed that intravenous infusions by mini-pumps are tolerated far better by the patients than conventional drip systems, and we feel mini-pumps are the ideal way to give intravenous infusions.
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PMID:A phase 1 study of recombinant interferon-gamma given intravenously by portable mini-pump: a preliminary report. 624 30

The effect of the converting enzyme inhibitor captopril as long term treatment was investigated in 14 patients with severe congestive heart failure in a double blind trial. Captopril reduced plasma concentrations of angiotensin II and noradrenaline, with a converse increase in active renin concentration. Effective renal plasma flow increased and renal vascular resistance fell; glomerular filtration rate did not change. Serum urea and creatinine concentrations rose. Both serum and total body potassium contents increased; there were no long term changes in serum concentration or total body content of sodium. Exercise tolerance was appreciably improved, and dyspnoea and fatigue lessened. Left ventricular end systolic and end diastolic dimensions were reduced. There was an appreciable reduction in complex ventricular ectopic rhythms. Adverse effects were few: weight gain and fluid retention were evident in five patients when captopril was introduced and two patients initially experienced mild postural dizziness; rashes in two patients did not recur when the drug was reintroduced at a lower dose; there was a significant reduction in white cell count overall, but the lowest individual white cell count was 4000 X 10(6)/l. Captopril thus seemed to be of considerable value in the long term treatment of severe cardiac failure.
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PMID:Captopril in heart failure. A double blind controlled trial. 638 12

In order to determine the effects of repetitive compression-decompression cycles on hematologic and hemostatic factors in humans, 14 subjects were exposed to 150 ft sea water gauge (fswg) for 30 min with standard U.S. Navy decompression on each of 12 consecutive days. Red blood cell number, volume, and size distribution; hemoglobin concentration; hematocrit; white blood cell number and differential counts; platelet number and volume; prothrombin and partial thromboplastin times; and fibrinogen and fibrin/fibrinogen degradation products were measured in venous blood samples collected before the first and after alternate dives. Subjects in the study had no symptoms other than pruritus and occasional fatigue following the exposures. More than 60% had venous gas emboli detectable by precordial doppler monitoring which generally persisted for 3-5 h after surfacing. Results show a small decrease in red cell mass, with an increase in size distribution and no change in mean corpuscular volume. No change in total white cell number was noted, but the basophilic granulocytes and atypical lymphocytes were elevated at the end of the series. A biphasic change was noted in monocyte number, and immature neutrophilic granulocytes were reduced. No change in platelet number or volume, or in the prothrombin/partial thromboplastine time, was apparent. Although fibrinogen concentration significantly decreased during the exposures, fibrin/fibrinogen degradation products remained undetectable. All changes remained in a clinically acceptable range.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hematologic and hemostatic changes with repetitive air diving. 646 54

A case of erythroleukemia coexistent with pulmonary emphysema is reported. A 67-year-old male was admitted to our hospital in May 1981, with a few year history of cough, sputum and fatigue. He had already been diagnosed as having pulmonary emphysema and moderate anemia. On physical examination, except for pallor, no other findings were remarkable. The initial hematological examination showed hemoglobin, 9.6 g/dl, red cell count, 251 x 10(4)/microliters, platelet count, 7.3 x 10(4)/microliters, white cell count, 2600/microliters with neither myeloblasts nor erythroblasts. A sternal marrow aspiration revealed 21% myeloblasts and 40% erythroblasts including 7.5% megaloblastoids. Periodic Acid Schiff staining was strongly positive for a part of erythroblasts. A chest X-P finding was typical for pulmonary emphysema. Pulmonary function was moderately damaged. He was started on chemotherapy with AAAP (ACNU 50 mg/d i.v. drip over 4 hr x 4d, adriamycin 20 mg/d i.v. push x 4d, Methotrexate 20 mg i.v. push x 4d). The first course of AAAP brought him a complete remission with both disappearance of myeloblasts and erythroid precursors with megaloblastoid nuclei in the marrow and the normalization of white cell count and platelet count in the blood. He was discharged in September 1981 after completion of a consolidation chemotherapy with AAAP. Since then, he received two courses of AAAP as an intensification chemotherapy and has been in complete remission for more than 13 months. His pulmonary function has not been affected and no myocardial damage has been seen throughout AAAP therapy. Thus, AAAP therapy seems to be an excellent chemotherapy even for an aged patient with erythroleukemia.
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PMID:[A case report of an aged patient with erythroleukemia coexistent with pulmonary emphysema, responding well to AAAP therapy]. 696 34

A 54 year-old woman who had a 6 month history of polyarthralgias, oral ulcers, weight loss and fatigue was admitted to the Urawa Municipal Hospital. She developed high fever, dyspnea and thrombocytopenia. Chest radiograph revealed massive right pleural effusion. At this time, laboratory investigations gave the following results: hemoglobin 12.7 g/dl, WBC 7700/microliters and platelet count 9.2 x 10(4)/microliters. Antibody to DNA was negative. Antinuclear antibody was positive at a titer of 320x in a centromere pattern; Anti-RNP and anti-Sm antibodies were negative. CH50 was 18.6 u/ml. C3 was 42.9 mg/dl. C4 was 11.5 mg/dl. Circulating immune complex (Clq) was 30.5 micrograms/ml. Circulating lupus anti-coagulant and anticardiolipine antibodies were positive. Thoracocentesis was performed; the material was a straw-colored exudate with over two thousands white cell per ul and showed marked reduction of complement titiers and elevated immune complex levels. She was then diagnosis as having SLE. Two weeks after admission, progressive leukopenia and anemia succeedingly occurred and resulted in severe pancytopenia. Bone marrow biopsy demonstrated marked marrow fibrosis and increased reticulin content with no evidence of malignancy. Steroid pulse therapy for 3 days started, and subsequently she was treated with 60 mg/day of prednisolone. Three weeks after starting on steroids, the massive pleural effusion was completely disappeared and complement titiers were normalized. Circulating immune complex has not been detected any more. After 8 weeks, the peripheral blood count was normalized. The dose of prednisolone was reduced progressively. On this occasion, the biopsy showed normocullular marrow with a marked reduction in the amount of reticulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of systemic lupus erythematosus presenting with myelofibrosis as a cause of pancytopenia]. 797 29

A 31-year-old Japanese male who complained of low-grade fever, fatigue and generalized lymphadenopathy had shown an increase in peripheral white cell count, and 84% of peripheral blood cell and 76% of nuclear bone marrow cells consisted of small cleaved lymphoblastic abnormal cells with or without barely visible nucleoli. Cytogenic study of cervical lymph node biopsy specimens showed a t(14;18)(q32;q21) chromosome translocation. Histologically the lymph node cells were classified according to the International Working Formulation as follicular small cleaved-cell lymphoma. Molecular analysis of DNA fragments of peripheral lymphocytes revealed both J-H gene and bcl-2 oncogene rearrangements. Immunophenotypes of peripheral lymphocytes, bone marrow cells and lymph node cells expressed a clonally distinct B-cell population bearing surface immunoglobulin-G, kappa-chain, CD-10, CD-19, CD-20, CD-21 and OKIa-1 antigens. We diagnosed this case as follicular lymphoma in the leukemic phase,
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PMID:[Follicular lymphoma associated with t(14;18)(q32;q21) chromosome translocation and bcl-2 gene rearrangement: report of a case]. 849 10

Cisplatin is a known cause of hemolytic uremic syndrome (HUS). The acute, fulminant form of cisplatin-induced HUS is almost always fatal. We present a 67-year-old Hispanic woman who was treated with cisplatin for squamous cell carcinoma of the tongue. Three days after receiving the treatment, she presented with increasing fatigue, decreased urine output, and confusion. Physical examination was remarkable for tachycardia of 130 beats/min, peripheral edema, and mental obtundation. Laboratory investigations showed a white cell count of 5,500/microL, hemoglobin level of 9.6 g/dL, hematocrit of 29.6%, and platelet count of 13,000/microL. Schistocytes were present on peripheral smear. Screening for disseminated intravascular coagulation was negative. Serum chemistry values included blood urea nitrogen 111 mg/dL, creatinine 3.8 mg/dL, and lactate dehydrogenase (LDH) 927 IU. The patient underwent hemodialysis and therapeutic plasma exchange (TPE), using fresh frozen plasma (FFP). Dialysis was no longer required after the fifth day. TPE was performed daily until the platelet count normalized on the 13th day, after which intertreatment intervals were extended until normalization of LDH levels on the 50th day. We conclude that the normally fatal, fulminant form of cisplatin-induced HUS can be successfully treated with standard TPE, using FFP replacement.
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PMID:Successful treatment of cisplatin-induced hemolytic uremic syndrome with therapeutic plasma exchange. 970 19


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