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 60-year-old male was admitted to our hospital complaining abdominal pain and fatigue. Complete blood count showed as follows; WBC 3,900/microliters (48% of monocytes), Hb 11.5 g/dl, Plt 0.9 x 10(4)/microliters. Marrow smears showed the presence of phagocytic histiocytes that consist 22.4% of total nuclear cells. Laboratory findings showed as follows; BUN 109.5 mg/dl, Creatinine 7.4 mg/dl, CPK 1,259 IU/l, Aldolase 195 IU/l, Myoglobin 4,200 mg/dl. Serological studies showed a 16-fold increase in herpes-simplex virus (HSV) antibody titers 4 weeks after admission. So we diagnosed his illness as virus-associated hemophagocytic syndrome (VAHS) and rhabdomyolysis that were associated with HSV. We performed three times of hemodialysis for acute renal failure and used prednisolone for VAHS. These treatments were successful, and he made a complete recovery from illness. VAHS complicated by rhabdomyolysis is very rare, and we think this case is full of suggestions.
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PMID:[A case of virus-associated hemophagocytic syndrome (VAHS) complicated by rhabdomyolysis which were associated with herpes-simplex virus infection]. 868 66

We refer in the present article, the first case found in our laboratory of Monoclonal gammapathy of the IgD type. A 47-year-old man presented at the emergency department with a history of malaise, lethargy, tiredness, thirstiness and obscure depositions. Clinical examination revealed a normocytic anaemia. The plasma urea was 423 mg/dl and the plasma creatinine was 15, 3 mg/dl. He was admitted to hospital with a diagnosis of acute renal failure. The later electrophoresis in serum revealed a little monoclonal band that was identified as IgD-lambda type by immunofixation electrophoresis. In urine electrophoresis was observed a beta-band. Bone marrow biopsy revealed a 20% of plasmocytic cells. Renal biopsy was compatible with myelomatose lesions. Osteolytic lesions were observed.
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PMID:[A case of monoclonal gammapathy type IgD]. 901 14

HELLP syndrome in the parturient (hemolysis, elevated liver enzymes, and low platelet count) is associated with poor maternal and fetal outcomes. Maternal mortality has been estimated to be as high as 24%. Patients with HELLP syndrome are also at greater risk of pulmonary edema, adult respiratory distress syndrome, abruptio placentae, disseminated intravascular coagulation, ruptured liver hematomas, and acute renal failure. Perinatal mortality is equally high, ranging from 79 to 367 per 1,000 live births, and neonatal complications correlate with the severity of maternal disease. Many clinicians view HELLP syndrome as an entity of preeclampsia, and because of varied symptomatology, the initial diagnosis may be obscured. Prodromal signs include: (1) weakness and fatigue, (2) nausea and vomiting, (3) right upper quadrant and/or epigastric pain, (4) headache, (5) changes in vision, (6) increased tendency to bleed from minor trauma, (7) jaundice, (8) diarrhea, and (9) shoulder or neck pain. Before delivery, aggressive obstetric management is directed toward stabilization of the affected organ systems, if possible, and timely interruption of the pregnancy in the early phase of the accelerated disease progression. Definitive therapy is delivery. Parturients with HELLP syndrome are often critically ill; their infants are frequently premature and their conditions are compromised. Management criteria should include a multidisciplinary approach in a tertiary care center. Obstetric anesthesia personnel should perform a thorough preanesthetic evaluation and be familiar with the pathophysiologic changes of this syndrome. Determining the anesthetic of choice depends on the patient's condition, fetal well-being, and the urgency of the situation. In the presence of severe coagulopathy, regional anesthesia is contraindicated.
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PMID:HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) pathophysiology and anesthetic considerations. 922 38

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

Acute tumor lysis syndrome (ATLS), a condition which results from a rapid destruction of tumor cells with massive release of cellular breakdown products, has been well described following the treatment of various malignancies. However, only a handful of cases of spontaneous ATLS have been reported in the literature. We describe the first reported case of spontaneous ATLS in acute myeloid leukemia (AML). A previously healthy 63 year old woman presented with a two month history of fatigue and a one week history of easy bruising. On admission she had oliguric acute renal failure, with marked elevation in serum uric acid and phosphate. A bone marrow biopsy showed AML M7 with fibrosis. The renal failure resolved with supportive care and institution of allopurinol therapy. Following this, AML induction chemotherapy resulted in complete remission. Her biochemical and clinical course were very similar to the classical ATLS seen in patients after chemotherapy. Therefore, this case represents a rare instance of acute renal failure from spontaneous ATLS, and in our opinion the first reported occurrence of spontaneous ATLS associated with AML.
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PMID:Spontaneous acute tumor lysis syndrome in acute myeloid leukemia? A single case report with discussion of the literature. 964 77

A 47-year-old woman was admitted to our hospital for evaluation of general fatigue and dyspnea. She had been diagnosed with progressive systemic sclerosis (PSS) when she was 39 years of age, on the basis of Raynaud's phenomenon, proximal sclerosis, and pigmentation of the skin. On admission, her blood pressure was 206/128 mmHg. Funduscopy revealed grade III (Keith & Wagener) hypertensive retinopathy. Laboratory data showed positivity for anti-nuclear antibody and anticardiolipin beta 2 glycoprotein I antibody, and the plasma level of renin activity (PRA) was abnormally high. Chest X-ray and UCG revealed massive pericardial effusion. On the second hospital day, she was operated on for pericardiodiaphragmatic fenestration. The volume of pericardial effusion amounted to more than 2000 ml. Post operative malignant hypertension persisted. Laboratory data showed thrombocytopenia, hemolytic anemia, and acute renal failure. We diagnosed scleroderma renal crisis (SRC) associated with antiphospholipid syndrome. Following the initiation of angiotensin converting enzyme inhibitor (ACE-I) combined with calcium antagonist and alpha-one blocker, her blood pressure and PRA decreased. She also had been treated with aspirin 81 mg daily. These therapies were effective in recovering the platelet count and stopped the progression of anemia and renal failure. Although either the finding of large pericardial effusion or SRC is associated with poor prognosis in PSS, this case has had a good clinical course. In this case, the findings suggested that anti-phospholipid antibody may have contributed to the pericarditis and SRC.
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PMID:[A case of scleroderma renal crisis with massive pericardial effusion and positivity on antiphospholipid antibody test]. 965 14

Muscle involvement in hypothyroidism commonly manifests as fatigue, myalgias, stiffness and slowed reflexes. We report a case of transient acute renal failure related to rhabdomyolysis and myoglobinuria in a 40 year old man that revealed the diagnosis of hypothyroidism with myopathy. The patient had proximal muscle weakness and tenderness, markedly raised muscle enzymes and deranged renal functions that normalised with thyroid replacement therapy. Hypothyroidism, though rare, should be considered a definite and authentic cause of rhabdomyolysis.
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PMID:Myoglobinuria and transient acute renal failure in a patient revealing hypothyroidism. 1077 35

Numerous cases of drug-induced hemolytic anemia have been described in patients treated with penicillin or cephalosporin. Second and third generation cephalosporins are more commonly implicated in hemolytic reactions than first generation cephalosporins. We report a case of severe cefotetan-induced hemolytic anemia in a previously healthy 46-year-old woman undergoing an elective hysterectomy. The patient received 2 g of intravenous cefotetan intraoperatively and subsequently at 12 and 24 h post-operatively. She complained of diarrhea and fever on the third post-operative day and was seen in her gynecologist's office on the fifth post-operative day (hemoglobin = 10.5 g/dL). On the seventh post-operative day, she complained of fever and soreness around the suprapubic catheter site and was given a prescription for 500 mg oral cephalexin four times a day. The next day she was seen in the gynecologist's office and reported feeling better. Ten days after the operation her fatigue worsened and her hemoglobin was 4.8 g/dL. She was transfused with 3 units of packed red blood cells (PRBC) and was given 1 g of cefotetan intravenously. During the transfusion of the second unit of PRBC nursing staff observed gross hemoglobinuria and she subsequently developed acute renal failure. Laboratory chemistry parameters were consistent with severe acute hemolysis. The patient's direct antiglobulin test was reactive and her serum reacted with cefotetan-coated red blood cells (RBCs) and serum plus soluble cefotetan reacted with untreated RBCs. The titration endpoint of the serum against cefotetan-coated RBCs was 40,960, while the serum plus soluble cefotetan against uncoated RBCs was 2,560. This case of severe cefotetan-induced hemolysis was complicated by an acute hemolytic event that occurred during the transfusion of PRBC. Clinical and transfusion service staff must consider drug-induced hemolysis in the differential diagnosis of acute anemia.
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PMID:Drug-induced hemolysis: cefotetan-dependent hemolytic anemia mimicking an acute intravascular immune transfusion reaction. 1081 91

A 53-year-old woman developed fever and fatigue after eating raw oysters, and consulted a local clinic. She exhibited liver dysfunction and jaundice, and was therefore referred and admitted to our hospital. Hepatitis A was diagnosed based on virus markers, and palliative therapy was administered. After admission, the increased levels of transaminases and lactic acid dehydrogenase (LDH) normalized rapidly. However, marked thrombocytopenia was observed, and steroid pulse therapy was administered. Thereafter, idiopathic anemia developed, and a bone marrow puncture was performed. Bone marrow smears showed marked depletion of cells of the erythroblastic and megakaryocytic series. Parvovirus B19 infection was ruled out, and an additional steroid was administered. However, the patient's anemia and thrombocytopenia persisted. She suffered a prolonged period of cholestasis and died of acute renal failure. At autopsy, the bone marrow revealed severe erythroblastopenia. A diagnosis of thrombocytopenia due to an autoimmune mechanism was made on the basis of elevated levels of platelet-associated immunoglobulin G (PAIgG) and immune complex. Furthermore, the advanced anemia was complicated by concurrent hemolysis. This case may provide information useful for clarifying the pathogenesis of hematopoietic disorders complicated by hepatitis.
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PMID:[Autoimmune thrombocytopenia and erythroid hypoplasia associated with hepatitis A]. 1107 Sep 36

Two cases of alcoholics associated with rhabdomyolysis and acute renal failure were reported. Case 1 was a 67-year-old male who had complained of general fatigue and generalized muscle pain. He had drunken and slept outdoor in winter until he was found. Laboratory data on admission showed remarkable elevation of muscle enzymes (AST, LDH, CPK) and serum levels of myoglobin, BUN, and Cr. He was treated with hemodialysis because of acute renal failure caused by rhabdomyolysis and recovered from renal failure. Case 2 was a 50-year-old male who had been unconscious and suffered from muscle weakness. He had drunken and slept in the bed for several days without eating any food until he was found by his sister. Laboratory data on admission showed remarkable elevation of muscle enzymes and serum levels of myoglobin, BUN, and Cr. It also showed hypoglycemia and hyponatremia. He developed into acute renal failure caused by rhabdomyolysis, but had a good clinical course without hemodialysis. The rhabdomyolysis of case 1 might have been caused by alcohol and sleeping outdoor in winter. That of case 2 might have been caused by alcohol and pressure necrosis due to immobility for several days in his bed.
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PMID:[Two cases of alcoholics associated with rhabdomyolysis and acute renal failure]. 1246 66


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