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)

A 43-year-old man underwent living related-donor renal transplantation because of chronic renal failure in 1991. During the transplant period, both donor and recipient were seronegative for hepatitis B surface antigen (HBsAg). The donor was seropositive for antibody to hepatitis B surface antigen (anti-HBs) due to hepatitis B virus (HBV) vaccination. After transplantation, FK506 and methylprednisolone had been administered to the patient as immunosuppressants. In 1993, HBsAg appeared in his serum. His alanine aminotransferase level elevated gradually during 1995 and then in 1996, general fatigue, ascites and jaundice developed. At this time his serum was positive for hepatitis B e antibody, contained more than 100000 Meq/mL HBV-DNA and 100% precore mutant. Despite subsequent intensive therapy, liver dysfunction progressed and this patient died of hepatic failure 2 months following admission. At autopsy, the liver exhibited cholestasis, fibrosis extending from the portal tracts, mild inflammation and hepatocytes with a ground-glass appearance. In addition, HBsAg and hepatitis B core antigens had accumulated in the hepatocytes. Consequently, the final diagnosis was fibrosing cholestatic hepatitis (FCH) due to precore mutant HBV infection contracted after renal transplantation. It is unclear when and where the recipient liver became HBV infected. Nevertheless, after renal transplantation, while receiving immunosuppressive drugs, HBV appeared to have the potential to cause hepatic failure and FCH may have been a fatal complication for the recipient.
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PMID:Fibrosing cholestatic hepatitis after living related-donor renal transplantation. 987 Aug 1

A 75-year-old woman with complete left bundle branch block underwent electrophysiological study (EPS) to assess the conduction in the His-Purkinje conduction system and to further investigate the electrical instability in the ventricle, which was suggestive by the findings of nonsustained ventricular tachycardia in ambulatory monitoring. Transient complete atrioventricular (AV) block was provoked by ventricular pacing, and the intracardiac recordings proved that the site of AV block was distal to the His bundle. This phenomenon was not related to the rate or the duration of the ventricular pacing. The transient impairment of the conduction appeared to be due to the fatigue phenomenon in the His-Purkinje system.
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PMID:Transient complete atrioventricular block provoked by ventricular pacing in a patient with nonsustained ventricular tachycardia. 1033 38

A 21-year-old male presented with a 1-month history of fever, diarrhea, fatigue, sore throat, mouth lesions, lymphadenopathy, and a 9-kg weight loss. His medical history was remarkable for peptic ulcer disease, urinary tract infections, recent 5-month history of asthma, and pericarditis 4 months earlier. He had two suicide attempts, one of which was prompted by turmoils about his homosexuality, a history of polysubstance abuse, including intravenous drugs, and unsafe sex practices. Initial HIV-1 antibody by ELISA, HIV-1 antigen test, and HIV-1 culture were all negative, as were the urinalysis and serologies for hepatitis B and C. Four months later HIV-1 antigen test was still negative, but ELISA and Western blot test were positive, and his CD4 count was dropping. This case was consistent with severe primary HIV disease, with negative HIV antibody test due to the recent exposure to the virus; seroconversion took approximately 5 months.
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PMID:Fever, Adenopathy, Thrush, and a Negative HIV Antibody Test. 1035 89

A 22-year-old black man developed fever, chills, fatigue, night sweats, tender lymphadenopathy, and a generalized, pruritic, macular eruption 3 weeks after starting minocycline therapy for acne. His illness was also characterized by a palpable spleen tip, marked lower extremity and scrotal edema, and generalized lymphadenopathy. The patient had leukocytosis with a large percentage of atypical lymphocytes on peripheral smear and liver dysfunction. Titers for Epstein-Barr virus, hepatitis B, toxoplasmosis; and cytomegalovirus were all negative. Human immunodeficiency virus-1 viral load and antibodies were also negative. Marked improvement was noted after the discontinuation of minocycline and the use of systemic corticosteroids. With the negative viral serologies, the clinical picture was most consistent with an infectious mononucleosis-like syndrome produced by the minocycline ingestion.
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PMID:An infectious mononucleosis-like syndrome induced by minocycline: a third pattern of adverse drug reaction. 1046 99

A case of retroperitoneal liposarcoma that was removed after transarterial embolization is reported. A 62-year-old man was admitted with body weight loss and general fatigue. Computed tomography revealed an extrarenal tumor, 27 x 17 x 11 cm in size, in the left retroperitoneal space. Arteriography revealed that the hypervascular tumor was fed from the left renal artery, the left adrenal artery and the left lumber arteries (L1-L4). At first the patient underwent transarterial embolization of the left renal artery and the left lumbar arteries (L1, L3, L4). Twenty-two days later he underwent surgical excision of the tumor with combined resection of the left kidney and the descending colon. The resected tissue weighed 2,500 g. Histological examination revealed liposarcoma, pleomorphic type. His postoperative course was uneventful, and he has remained free of disease for 15 months.
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PMID:[Surgical removal of retroperitoneal liposarcoma after transarterial embolization: a case report]. 1050 Sep 57

In this article, we report the case of a 16-month-old German boy who was admitted to the Children's Hospital of Stuttgart with a 4-week history of intermittent fever, decreased appetite, weakness, fatigue, and difficulty sleeping. He was healthy at birth and remained so for the first 15 months of his life. On admission, physical examination showed enlarged cervical, axillary, and inguinal lymph nodes, as well as hepatosplenomegaly. Laboratory data revealed pancytopenia, elevated liver function tests, and hypergammaglobulinemia. Blood, stool, and urine culture results were negative. Viral infections and rheumatologic and autoimmune disorders were ruled out, but a positive titer for Leishmania antibodies was noted. In a liver and bone marrow biopsy, the amastigote form of the parasite could not be seen in cells. The promastigote form of Leishmania was found and the diagnosis of visceral leishmaniasis was made by combining the cultures of both the liver and the bone marrow biopsy material in 5 mL 0.9% saline on brain heart infusion agar, supplemented with defibrinated rabbit blood and incubated at 25 to 26 degrees C for 5 days. The parasite was identified by Southern blot analysis as Leishmania infantum. Specific therapy with the antimonial compound sodium stibogluconate with a dose of 20 mg/kg body weight was begun immediately. Within 4 days, the patient became afebrile. The side effects of treatment, including erosive gastritis, cholelithiasis, worsening hepatosplenomegaly, elevation of liver enzymes, pancreatitis, and electrocardiogram abnormalities, necessitated the discontinuation of treatment after 17 days. On discharge 4 weeks later, the patient was stabilized and afebrile with a normal spleen, normal complete blood count, normal gammaglobulins, and decreasing antibody titers to Leishmania. During the next 24 months, the patient experienced intermittent episodes of abdominal pain, decreased appetite, recurrent arthralgia, and myalgia. But at his last examination in January 1998, he was well; all symptoms mentioned above had disappeared. Because the child had never left Germany, nonvector transmission was suspected and household contacts were examined. His mother was the only one who had a positive antibody titer against Leishmania donovani complex. She had traveled several times to endemic Mediterranean areas (Portugal, Malta, and Corse) before giving birth to the boy. But she had never been symptomatic for visceral leishmaniasis. Her bone marrow, spleen, and liver biopsy results were within normal limits. Culture results and polymerase chain reaction of this material were negative. A Montenegro skin test result was positive, indicating a previous infection with Leishmania. Western blot analysis showed specific recognition by maternal antibodies of antigens of Leishmania cultured from the boy's tissue. Visceral leishmaniasis is endemic to several tropical and subtropical countries, but also to the Mediterranean region. It is transmitted by the sand fly (Phlebotomus, Lutzomyia). Occasional nonvector transmissions also have been reported through blood transfusions, sexual intercourse, organ transplants, excrements of dogs, and sporadically outside endemic areas. Only 8 cases of congenital acquired disease have been described before 1995, when our case occurred. In our patient, additional evaluation showed that the asymptomatic mother must have had a subclinical infection with Leishmania that was reactivated by pregnancy, and then congenitally transmitted to the child. Visceral leishmaniasis has to be considered in children with fever, pancytopenia, and splenomegaly, even if the child has not been to an endemic area and even if there is no evidence of the disease in his environment, because leishmaniasis can be transmitted congenitally from an asymptomatic mother to her child.
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PMID:Congenital transmission of visceral leishmaniasis (Kala Azar) from an asymptomatic mother to her child. 1054 91

Recently, several class-related adverse events have been recognized with antiretroviral drugs. For nucleoside analogue reverse transcriptase inhibitors. (NRTI), lactic acidosis with hepatomegaly and hepatic steatosis have been reported. These appear to occur at a low frequency, but with a high fatality rate. We report a case of fatal lactic acidosis in a patient with acquired immunodeficiency syndrome (AIDS) treated with stavudine (d4T), lamivudine (3TC) and indinavir (IDV). A 48-year-old male AIDS patient was admitted with complaints of general fatigue and dyspnea. His medications at presentation included d4T, 3TC and IDV. Physical examination demonstrated icteric sclerae and abdominal tenderness with hepatomegaly. Laboratory data demonstrated a severe metabolic acidosis with an anion gap due to lactate accumulation. Despite intensive treatment, cardiorespiratory arrest occurred and this could not be resuscitated.
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PMID:[Fatal lactic acidosis in a patient with acquired immunodeficiency syndrome treated with stavudine, lamivudine and indinavir]. 1065 86

A toxoplasmic uveitis case was reported on the focus of impairment of pathological findings and serological antibody titers after chemotherapy. A chief complaint of a 60-year-old male was a decreased and blurred vision in his right eye for 2 weeks after experiencing tremendous stress and fatigue. A steroid therapy for 3 weeks was not effective and the retinal lesion became necrotic. Anti-Toxoplasma gondii antibody titer was checked to be a strong positive by both ELISA and indirect latex agglutination assay (ILA). He was treated with Fansidar F for 8 weeks. His vision improved as the necrotic lesion healed by scarring, but the antibody titers still remained very high without any signs of negative conversion. It is suggested to be a recurrent case of the past asymptomatic infection by presumed immune suppression caused by excessive stress.
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PMID:A toxoplasmic uveitis case of a 60-year-old male in Korea. 1074 56

Aviation medicine came into existence as a recognized entity when certain standards were established during and shortly after World War I. During this time, accident rates were high. In fact, a larger number of pilots were dying in accidents than in combat. Figures from Great Britain's casualty list at the close of the first year of World War I indicated that for every 100 aviators killed, 60 died as a result of some individual physical defect, 30 from some form of recklessness or careless behavior, 8 as a result of some mechanical defect in the airplane, and only 2 at the hands of the enemy. Aviators were found to be in poor physical condition. Because there were no established regulations with regard to workloads, aviators were frequently found to have been flying to a point beyond exhaustion. Because of workload, chronic fatigue, and emotional stress, aviators were constantly called upon to perform superhuman feats when not in peak physical condition. Errors in judgement were common. The majority of pilots lost weight as a somatic sign of stress. This was recognized by Theodore Lyster [corrected] who had recently been appointed as the Chief Surgeon, Aviation Section of the U.S. Army. Such problems were not diagnosed by medical officers because they were not trained to recognize them. Theodore Charles Lyster [corrected] was the son of Captain William J. and Martha Doughty Lyster [corrected]. He was an Army "brat" who entered the world on July 10, 1875. His childhood was spent in various posts around the country. At the age of 7, Lyster [corrected] contracted yellow fever while living in Fort Brown, TX. The boy was treated by William Gorgas, a young post surgeon. Gorgas was credited with the young boy's recovery. Later, Gorgas was to marry Lyster's [corrected] aunt making Lyster [corrected] his nephew by marriage. Having survived the yellow fever infection, young Lyster [corrected] had a lifelong immunity to the disease.
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PMID:Brigadier General Theodore C Lyster [correction of Lister], MD: father of American aviation medicine. 1091 89

This report describes a case of diabetes insipidus associated with acute myelogenous leukemia. An 11-year-old boy presented with fatigue, polydipsia and polyuria. His evaluation revealed a diagnosis of acute myelogenous leukemia FAB-M2, and a water deprivation test confirmed the diagnosis of central diabetes insipidus. His brain magnetic resonance imaging (MRI) showed a thickened, enhancing pituitary stalk with absence of the normal hyperintense signal in the posterior pituitary. He was treated with systemic chemotherapy, intensive intrathecal therapy, and 1,000 cGy to the pituitary. The patient achieved a remission but continued to need desmopressin therapy to control his diabetes insipidus. Diabetes insipidus is a rare complication of acute myelogenous leukemia that can be caused by leukemic infiltration of the pituitary. The diabetes insipidus is irreversible despite intensive systemic and central nervous system chemotherapy and radiation.
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PMID:Diabetes insipidus as a presenting symptom of acute myelogenous leukemia. 1103 61


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