Cases reported "Anemia, Hemolytic"

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1/11. Hemolytic anemia as a sequela of arsenic intoxication following long-term ingestion of traditional Chinese medicine.

    We report on a 51-yr-old woman who developed intravascular hemolytic anemia caused by arsenic after long-term ingestion of a traditional Chinese medicine (TCM). Twelve years before the admission, she was diagnosed as neurocysticercosis. She has ingested a TCM for about 12 yr instead of undergoing medical therapy for the disease. She was presented with a severe Coombs'-negative hemolytic anemia with hemosiderinuria. The urine arsenic level was elevated suggesting the arsenic intoxication as a cause of the anemia. She was treated successfully with therapeutic red cell exchange without any sequelae.
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2/11. dapsone-induced methemoglobinemia and hemolytic anemia.

    The treatment of two common adverse effects of dapsone (methemoglobinemia and hemolytic anemia) is discussed, and a case of acute dapsone intoxication is described. A pregnant 29-year-old woman was admitted to an emergency room three hours after ingesting 50 tablets of dapsone (100 mg each) and six alcoholic drinks. One hour after admission 50 g of activated charcoal was given p.o., and 65 mg of methylene blue was given i.v. The patient was found to have a methemoglobin concentration of 25.1%. Arterial blood gases while the patient was breathing 4 L/min of oxygen by nasal cannula were PO2, 136 mm Hg (72.1% saturation); PCO2, 28.9 mm Hg; bicarbonate content, 18.9 mmol/L; and pH, 7.42. oxygen therapy was changed to 100% oxygen by face mask, 50 g of activated charcoal in sorbitol was administered p.o., and another 65 mg of methylene blue was given i.v. Two more 50-g doses of activated charcoal in sorbitol were given (18.5 and 22 hours after dapsone ingestion). methylene blue 130 mg was given 14 hours after dapsone ingestion, and 65 mg was given 21, 36, and 55.5 hours after ingestion. Methemoglobin concentrations never rose above 20% after the sixth dose of methylene blue. On hospital days 2 and 3, laboratory values were consistent with a diagnosis of hemolytic anemia; the patient received two units of packed red blood cells. The hematocrit decreased over the next three days to 23.9%, and the patient received four units of packed red blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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3/11. A series of patients in the emergency department diagnosed with copper poisoning: recognition equals treatment.

    Only scarce data are available on chronic copper poisoning in general toxicology literature. This paper reports four patients with chronic copper poisoning and one patient with acute poisoning. The cases with chronic poisoning in our study consisted of four members of a farmer family presenting to the emergency department (ED) with malaise, weakness, abdominal pain, headache, dizziness, tightness in the chest, leg and back pain, accompanied by significant anemia (hemoglobin [Hb]: 8.7 - 9.5 g/dl). They were hospitalized and investigated thoroughly, although there were no other findings or clues enlightening the etiology of anemia. The anemia was attributed to chronic copper exposure acquired from vegetables containing copper. The diagnosis was established by ruling out other possible etiologies and history coupled with laboratory findings. The patients were discharged with the recommendation on diet to avoid consumption of pesticide-treated vegetables. Their Hb values were between 10 and 11.4 g/dl on the 15th day, and between 12 and 14 g/dl after two months. Their symptoms had also resolved completely in two months. The patient with acute intoxication (5th case) had ingested copper oxychloride with suicidal intent. He was admitted with anuria and hemolytic anemia. After being hospitalized for fifteen days, he was diagnosed with chronic renal failure and was scheduled for a dialysis program. Acute poisoning is more deliberate, while chronic exposure may result in atypical findings. In conclusion, physicians working in primary care and EDs should consider copper poisoning in patients presenting with anemia, abdominal pain, headache, tightness in the chest, and leg and back pain.
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4/11. lead poisoning from a gunshot wound. Report of a case and review of the literature.

    A man was hospitalized on three occasions for symptoms of lead intoxication 20 to 25 years after a gunshot wound that resulted in retention of a lead bullet in his hip joint. The potential for lead toxicity as a complication of a lead missile injury appears to be related to (1) the surface area of lead exposed for dissolution, (2) the location of the lead projectile, and (3) the length of time during which body tissues are exposed to absorbable lead. Cases of lead poisoning of immediate onset resulting from lead shot have been reported in europe, but all documented cases of ammunition-related plumbism reported in the united states have involved synovial fluid dissolution of a single lead bullet over many years. The solvent characteristics of synovial fluid and associated local arthritis are apparently important factors in the dissolution and absorption of lead from projectiles located in joints. awareness that lead intoxication can be a complication of retained lead projectiles should allow rapid institution of appropriate diagnostic and therapeutic modalities when such a clinical situation arises.
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5/11. A case of lead intoxication: clinical and biochemical studies.

    A 23-year-old Japanese male with severe lead intoxication accompanied by hemolytic anemia was studied. The patient had taken 12 g to lead in about a month. He had moderate hemolytic anemia (Hb 8.9 g/100 ml) with reticulocytosis ranging from 2.5 to 11.7%. Peripheral blood smear showed nucleated red cells (42/200 white blood cells) and marked basophilic stippling in the red cells. Activities of erythrocyte enzymes were either normal or increased except for pyrimidine 5'-nucleotidase (P5N) and delta-aminolevulinic acid dehydratase (ALA-D) both of which were found to be decreased, being 48.8% and 4.1% of the normal controls respectively. Erythrocyte reduced glutathione (GSH) was high (145.6 mg/100 ml RBC). Erythrocyte pyrimidine nucleotides were accumulated up to 10.2% of total nucleotides. The level of lead in peripheral blood was 112 microgram per 100 ml blood. Ca2 -Na2-EDTA was given to the patient as treatment. The level of lead in the blood decreased gradually and hemolytic anemia improved. Basophilic stippling in the red cells disappeared. These results confirmed the findings of Valentine et al [1] that lead-induced deficiency of P5N resulted in basophilic stippling and hemolytic anemia just like hereditary hemolytic anemia due to P5N deficiency.
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6/11. Acute intravascular hemolysis due to accidental formalin intoxication during hemodialysis.

    A patient accidentally exposed to formalin during hemodialysis developed acute intravascular hemolysis. in vitro study showed that formalin has direct oxidant action on red blood cells. Formalin intoxication should be recognized as a cause of acute hemolysis during hemodialysis and is not invariably fatal, provided further exposure is stopped in time and the complications prevented.
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7/11. Formic acid burn--local and systemic effects. Report of a case.

    Formic acid is an organic acid which has mainly been used in industry, but in recent years its use in agriculture has greatly increased in the Scandinavian countries. Formic acid is more caustic to the skin than acetic acid. However, reports on formic acid burns are scarce in the medical literature, and no serious burn has previously been described. A few reports on formic acid ingestion have been published. It is of great interest that formic acid has been shown to play the major role in the methanol poisoning syndrome. A case of severe burn with undiluted formic acid is reported. In the beginning, the dermal injury seemed to be of minor degree, but then the patient, a 15-year-old girl, developed signs of systemic formic acid intoxication, including metabolic acidosis, intravascular hemolysis and hemoglobinuria. These signs were similar to those described as a result of formic acid ingestion. The systemic effects were successfully treated without late sequelae, but the burn turned out mainly to be full-thickness, resulting in major scarring, as commonly seen after various chemical burns.
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8/11. Hemolytic anemia following succimer administration in a glucose-6-phosphate dehydrogenase deficient patient.

    Because of its favorable side effects profile, the oral chelating agent dimercaptosuccinic acid is often used for treatment of lead intoxication. We report a case of a 45-year-old black male with glucose-6-phosphate dehydrogenase deficiency and a 17 year history of occupational lead exposure who developed hemolysis during treatment with dimercaptosuccinic acid for symptomatic lead intoxication.
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9/11. Acute sodium chlorite poisoning associated with renal failure.

    A 25-year-old Chinese male presented with generalized cyanosis and respiratory distress. The patient was known to have ingested 10 g of sodium chlorite in a suicide attempt. methemoglobinemia was found and intravenous methylene blue was given repeatedly. However, the therapy could not prevent an acute hemolytic crisis. methemoglobinemia remained profound (43.1%) and disseminated intravascular coagulation ensued. He was put on CAVHD to correct the fluid overload and probably to remove the active metabolites of the chlorite. After 24 h, the methemoglobin was reduced to 16.9%. However, the development of acute renal failure further complicated the clinical course. Percutaneous renal biopsy suggested a picture of acute tubulointerstitial nephropathy. In addition, hemodialysis was continued for 4 weeks. After 3 months, renal function normalized. To our knowledge, there has been no clinical report of human intoxication with sodium chlorite.
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10/11. lead poisoning: association with hemolytic anemia, basophilic stippling, erythrocyte pyrimidine 5'-nucleotidase deficiency, and intraerythrocytic accumulation of pyrimidines.

    Lead intoxication is accompanied by an acquired deficiency of erythrocyte pryimidine-specific, 5'-nucleotidase. Genetically determined deficiency of this enzyme is associated with chronic hemolysis, marked basophilic stippling of erythrocytes on stained blood films, and unique intraerythrocytic accumulations of pyrimidine-containing nucleotides. The present report documents that lead-induced deficiency when sufficiently severe gives rise to findings similar to the hereditary disorder. Whereas pyrimidine-containing nucleotides are virutally absent in the erythrocytes of normal and reticulocyte-rich blood, 12% of erythrocyte nucloetides in the blood of a patient with lead intoxication contained cytidine. Nucleotidase activity was about 25% that in normal erythrocytes and 15% or less of that expected in comparable reticulocyte-rich blood. The distribution of nucleotidase activity in patient erythrocytes is unknown, and much more severe deficiency could have been present in subsets of the cell populations analyzed. The findings indicate that the hemolytic anemia and increased basophilic stippling characteristic of certain cases of lead intoxication may share a common etiology with essentially identical features of the genetically determined disorder.
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