Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A description is given of an outbreak of equine infectious anaemia (E.I.A.) in Campania [at Naples and Aversa (Caserta)]; it was diagnosed by clinical, pathological and serological examinations (Coggins test). Using the serum of 45 horses with E.I.A. and 11 healthy horses (controls), numerous investigations were carried out on: enzymes, intrinsic coagulation factors, lipids and other substances. The results obtained were very interesting and show that in this disease there are significant increases in many enzymes (LDH, LAP, gamma-GT, CPK, PK and ALD) and copper. Insignificant increases were found in other enzymes (SDH, GLDH, MDH, ICDH, AIP, lysozyme, cholinesterase, GOT and GPT) and also intrinsic coagulation factors, lipid substances (total cholesterol, esterified cholesterol, triglycerides) and glucose. LDH-1-isoenzyme remains unchanged, whilst AcP decreases slightly.
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PMID:Biochemical studies on equine infectious anaemia. 101 May 2

Hematograms, platelet function, and blood-enzyme chemistry were compared in two similar saturation-excursion dives, one conducted in a hyperbaric chamber and the other in the open sea. The chamber dive was more stressful in that it was preceded by a series of bounce decompression dives (one of which produced a 100% incidence of cutaneous pruritus in four subjects) and in that the excursions from saturation depth (60 fsw or 2.818 ATA) were longer and deeper (producing one case of O2 convulsions, one of confirmed decompression sickness, and several of Doppler-detected vascular bubbles). The chamber dive was associated with a marked and significant reduction in circulating platelet count; significant increases in plasma enzyme activities in the victim of O2 toxicity (LDH, CPK) and in one subject with Doppler bubbles and questionable bends symptoms (LDH, GOT, GPT) but not in another; and mild but significant anemia. In the open-water dive, one subject, who developed symptoms of gastroenteritis, showed moderate elevation of LDH, GOT, and GPT activity. No significant change in platelet counts occurred. Both dives were associated with elevated white-cell counts, apparently as a result of numerous minor infections, and reduced sensitivity of platelets of ADP-induced aggregation.
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PMID:Hematology and blood chemistry in saturation diving: II. Open-sea vs. hyperbaric chamber. 122 83

The effect of excessive heat accumulated in the body is life threatening. It could damage not only body fluid electrolyte haemostasis, but kidney, liver, and hematologic function. The example reported herein was a Thai laborer, previously healthy, 32 years of age. He joined the tricycle race from Chiang Mai to Lumpoon, which is about 30 km. The tournament was held on a late morning of high humidity and a temperature of 35 degrees C. After biking 25 km, he began having heavy perspiration and suffered from severe myalgia and high fever. He suddenly lapsed into unconsciousness and fell down. He was admitted to the Lumpoon Hospital because of convulsions, and 2 days afterward, anuria, anemia, thrombocytopenia, coagulopathy, and liver impairment were detected. He was later transferred to the Faculty of Medicine for further intensive treatment. Lab analyses showed marked azotemia (BUN 96 mg%, Cr 10.6 mg%), elevation of muscle enzyme (CPK greater than 1000 U/L, SGOT greater than 650 U/L), liver failure (SGPT greater than 650 U/L, DB/TB = 23.0/30.0 mg%) and disseminated coagulopathy; platelet 17,000/mm3, PT 51.1 sec (control 12.5), and PTT 73.5 sec (control 37.7). He was treated with bicarbonated hemodialysis trice weekly. Blood-exchange transfusion was performed 3 times during the first 2 weeks with 10 units of fresh whole blood in each exchange. His ventilation required support by a ventilator. After a month, his consciousness, the liver function, and hematologic conditions became to recuperate. By 6 weeks postadmission, renal function eventually improved. This report is intended to warn the unprepared athlete entering an extreme, long-lasting exercise in an inappropriate climate.
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PMID:Heat stroke-induced multiple organ failure. 156 92

Erythropoietic hypoplasia occurring in the absence of abnormalities in the leukopoietic and thrombocytopoietic series is often defined as "pure red cell aplasia" (PRCA). This condition may appear as an acquired defect of either acute or chronic type, and a congenital form as well. The chronic form of acquired PRCA occurred mostly in adults. It has been reported that a demonstrable thymoma occurred in more than 50% of patients with PRCA. Recent studies suggested that it may contribute to several immune mechanisms. Here we report a case of thymoma with PRCA whose clinical presentations include severe anemia, shock with severe metabolic acidosis, high levels of several organ enzymes (SGOT, SGPT, LDH, CPK, Amylase) and acute renal shutdown with similar manifestations to septic shock. Our explanation to his condition is multi-organ tissue hypoxia caused by severe anemia. Hemophagocytic syndrome was found by the repeated bone marrow smear before death. The clinical course of this patient was so impressive as to be presented here for discussion.
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PMID:[Thymoma with pure red cell aplasia and hemophagocytic syndrome--one case report]. 184 51

A case of severe acute rhabdomyolysis (RML) is reported which was caused by marked hypokalemia associated with long-lasting diarrhea. Since the patient not only had severe muscular symptoms but also intense hemorrhagic diathesis and anemia, the first diagnosis on admission was acute leukemia. Due to the increasing occurrence of acute RML associated with different clinical conditions, including hematologic disorders, the hematologist should keep in mind the possibility of RML, both as a primitive disorder or complication, and require CPK and myoglobin assay routinely.
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PMID:[Generalized hemorrhagic diathesis and anemia of sudden onset caused by rhabdomyolysis diagnosed as acute leukosis]. 219 28

A patient with Graves' disease associated with severe muscle weakness who was finally diagnosed as polymyositis by pathological examination of the muscle is reported. A 28-year-old women was incidentally found to have hyperthyroidism when she consulted a hospital for the evaluation and treatment of anemia in 1979. She was treated with methimazole for approximately a month when she stopped the medication by herself. Approximately two yr later (Nov. 4, 1981) she consulted another hospital with complaints of palpitation and muscle weakness. Diagnosis of hyperthyroidism due to Graves' disease and thyrotoxic myopathy were made, followed by the treatment with radioiodine (4 mCi of 131I). She was further treated with propylthiouracil (PTU). Four yr after the treatment, serum thyroid hormone concentration declined to the lower level than normal and serum TSH concentration increased. She was subsequently treated with synthetic I-T4. Despite the fact she became euthyroid with the treatment, muscle weakness as well as elevated concentrations of muscle enzymes were not improved. Muscle biopsy was made in July 1983, and she was diagnosed as immune polymyositis and treatment with prednisolone and cyclophosphamide in addition to PTU or I-T4, was started. With the treatment, serum LDH decreased to the normal range. However she still has muscle weakness and serum concentrations of CPK and aldolase are still in higher levels than normal range.
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PMID:A case of Graves' disease associated with polymyositis. 209 Jun 76

A 22-month-old female infant with an accidental methanol poisoning is presented. Her serum methanol level was 25 mg/dl. The clinical and biochemical features were as follows: coma, hyperventilation, metabolic acidosis, paralytic mydriasis, hypoglycemia, increased anion and osmolal gap, DIC, elevated CPK and LDH, anemia and abnormal EEG. She was treated with bicarbonated solutions and continuous infusion of ethanol. The pathophysiology, diagnosis and treatment of this poisoning is herein revised. DIC and enzymatic alterations are specially remarked.
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PMID:[Accidental methanol poisoning in an infant girl. Physiopathology, diagnosis and treatment]. 380 Jan 75

Copper sulphate was administered by the oral or intravenous route to five dromedary camels. Two camels (1 and 2) receiving copper sulphate at 200 mg per kg per day by drench died within 8 days and camel 3, receiving 100 mg per kg per day by the same route, was slaughtered on day 172. Intravenous injection of 2 mg per kg per day caused the death of camel 4 on day 95 and camel 5, treated similarly, was slaughtered on day 138. Anorexia, dullness, diarrhoea, dehydration and recumbency in camels 1 and 2 were probably clinical signs of copper toxicity. Camels 3, 4 and 5 lost weight. Jaundice was not a prominent clinical sign. The main lesions in camels 1 and 2 were fatty change and necrosis of the liver cells, dilatation and necrosis of kidney tubules, catarrhal abomasitis, enteritis and congestion of the blood vessels of the heart. In camels 3, 4 and 5 the hepatic lesions were mild, with leucocytic infiltration and gastrointestinal and heart lesions were either mild (camel 3) or absent (camels 4 and 5). Cytoplasmic copper granules in hepatic cells were generalized in distribution but more concentrated in the centrilobular zone. In the kidney these granules were confined to the cells of the proximal convoluted tubules. Copper accumulated in the liver and kidneys of all the camels and zinc accumulated in the liver and kidneys of those receiving copper sulphate intravenously. Macrocytic hypochromic anaemia developed in camels 3, 4 and 5 and haemoconcentration in camels 1 and 2. The concentration of serum copper, zinc and iron increased in animals 1, 2 and 4, and unbound iron binding capacity decreased in four camels. There was a rise in the activity of gamma GT, GOT, LDH and CPK in the serum of all the animals. Serum ALP activity, however, increased in camels 1 and 2 and decreased in camels 3, 4 and 5.
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PMID:Experimental copper poisoning in the camel (Camelus dromedarius). 809 11

This 50-year-old male was admitted to the hospital on April 1983 with complaints of severe chest pain attacks 2 weeks previously. Laboratory data: On admission the blood findings were Hb 14.3 Gm/dl of blood, RBC 4.70 million/mm3, WBC 11,600/mm3 and a platelet count of 1.1 million/mm3. ECG showed elevation of ST-T in V1 to V4. Serum LDH and CPK levels were high. He was diagnosed as acute myocardial infarction with thrombocythemia. Three days after admission he abruptly fell into a semicomatose state and left hemiplesia. Head computed tomography showed a large, low-density lesion in the right mid-cerebral artery area, and we also diagnosed cerebral infarction. He was given nimustine (ACNU) 100 mg/week three times as remission induction therapy. For maintenance chemotherapy, at first we administered mitobronitol (DBM) 150 mg/day then changed to intermittent administration of ACNU 100 mg. On September 1991, the patient was admitted to the hospital with progressive anemia and uncontrollable thrombocythemia. Bone marrow chromosome analysis revealed aneuploidy. The patient received interferon alpha 3 million unit/day. The thrombocythemia could be controlled but his general condition deteriorated. On April 1992, he died of interstitial pneumonia.
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PMID:[A case of essential thrombocythemia with clonal evolution in the terminal phase]. 812 97

High prevalence of anemia and iron deficiency state are found among athletes. To determine the influence of sports activities on the hematological state, we have performed hematological tests and examined the iron metabolism, in addition to some serum enzyme activities and some characters of red blood cells before and after exercise in high school boy athletes. The red blood cell count, hemoglobin level, and hematocrit value were significantly lower than those in the non-athletes boy students. The serum ferritin level in the athletes was significantly lower than that in the control group and healthy adults. Iron deficiency anemia was found in 12% of the athletes. The serum haptoglobin level in the athletes was significantly lower than that in the control group and the level before exercise, suggesting intravascular hemolysis, but the serum hemopexin level showed no difference before and after exercise, suggesting that the hemolysis was not so severe. The serum CPK and myoglobin levels showed a significant increase after exercise, but those levels were quite lower than that of muscle diseases. These findings suggest that daily exercise is closely associated with the increased risk of iron deficiency state, particularly in the high school boy athletes. The mechanism of hemolysis in athletes may partly depend on the increased fragility of iron deficiency red blood cells on mechanical strength.
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PMID:[Sport-anemia: studies on hematological status in high school boy athletes]. 874 90


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