Cases reported "Methemoglobinemia"

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1/20. Hb chile [beta28(B10)Leu-->Met]: an unstable hemoglobin associated with chronic methemoglobinemia and sulfonamide or methylene blue-induced hemolytic anemia.

    Among the causes of life-long cyanosis are congenital methemoglobinemia due to M hemoglobins, congenital methemoglobinemia due to methemoglobin reductase deficiency, a small number of low oxygen affinity hemoglobins, and a small number of unstable hemoglobins that spontaneously form methemoglobin in vivo at an accelerated rate. We report an unstable hemoglobin with these characteristics that was observed in a family of indigenous (native American) origin living near Santiago, chile. This variant has the substitution beta28(B10)Leu-->Met, unambiguously corresponding to the dna mutation of CTG-->ATG in beta-globin gene codon 28.
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2/20. Haemolytic anaemia after oral self-giving of naphthalene-containing oil.

    A clinical case of suicide attempt by means of oral self-giving of naphthalene-containing oil in an old man was reported. Clinical features showed haemolytic anaemia supported by a decrease of haemoglobin concentration and red blood cell count, an increase of bilirubin (prevalently indirect) and lactate dehydrogenase and very low levels of haptoglobin. Methaemoglobin (metHb) measured at admission to the Emergency Room and 19 days after poisoning was still above normal limits. No deficiency of glucose-6-phosphate dehydrogenase was detected. The clinical manifestations ameliorated after treatment with concentrated red blood cells and ascorbic acid, with fast normalization of metHb. The clinical picture appeared almost normal 1 month after poisoning. The clinical diagnosis was 'haemolytic anaemia caused by naphthalene'. Absence of glucose-6-phosphate dehydrogenase deficiency probably reduced the severity of poisoning.
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3/20. Hemolytic anemia after methylene blue therapy for aniline-induced methemoglobinemia.

    methylene blue is utilized as the main treatment of methemoglobinemia conventionally, but it may be ineffective in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency. We report a G6PD-deficient patient who suffered from aniline-induced methemoglobinemia with initial good response Heinz body but hemolytic anemia appeared later 3 d after methylene blue therapy. G6PD deficiency was identified. He recovered uneventfully with hydration, packed blood transfusion and adjuvant luvela-N(dl-alpha-tocopheryl nicotinate) medication. Caution should be taken in using methylene blue as antidote of acute methemoglobinemia, especially when a history of G6PD deficiency is obscure.
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4/20. 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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5/20. Perinatal toxicity of domestic naphthalene exposure.

    Naphthalene-containing mothballs can cause methemoglobinemia on inhalation. We describe a mother with hemolytic anemia and methemoglobinemia associated with elevated levels of naphthalene following exposure to mothballs. Her newborn infant had identical symptoms requiring mechanical ventilation and an exchange transfusion for resolution.
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6/20. hemolysis and methemoglobinemia secondary to rasburicase administration.

    OBJECTIVE: To report a case of hemolytic anemia and methemoglobinemia developing after rasburicase administration to a patient with glucose-6-phosphate dehydrogenase (G6PD) deficiency. CASE SUMMARY: A 50-year-old African American man was hospitalized with new onset seizure, diabetic ketoacidosis, respiratory failure, and acute renal failure. serum uric acid concentrations were elevated, and the patient was treated with one dose of intravenous rasburicase 22.5 mg for acute renal failure secondary to hyperuricemia. Routine arterial blood gas analyses performed after rasburicase was administered revealed elevated methemoglobin concentrations, which peaked at 14.7%. Hemolytic anemia developed as evidenced by a fall in blood hemoglobin from 14.8 to 5.3 g/dL. The patient made a full recovery following aggressive fluid therapy, blood transfusions, and respiratory support. G6PD deficiency was subsequently confirmed. The Naranjo probability scale indicated that rasburicase was a probable cause of hemolytic anemia and methemoglobinemia. DISCUSSION: Rasburicase is contraindicated in patients with G6PD deficiency as it may cause hemolytic anemia and methemoglobinemia. As of September 26, 2005, simultaneous occurrence of hemolytic anemia and methemoglobinemia has not been reported in patients receiving rasburicase. CONCLUSIONS: As of September 26, 2005, screening for G6PD deficiency should be performed whenever possible prior to chemotherapy administration in patients at risk of developing tumor lysis syndrome.
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7/20. methemoglobinemia and hemolytic anemia after phenazopyridine hydrochloride (Pyridium) administration in end-stage renal disease.

    phenazopyridine is a commonly used urinary tract analgesic. As illustrated by the case we have reported, its use may be complicated by the development of methemoglobinemia and hemolytic anemia, especially in patients with renal insufficiency.
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8/20. methemoglobinemia and hemolytic anemia associated with campylobacter jejuni enteritis.

    A 7-week-old infant with methemoglobinemia, hemolytic anemia, and inadequate weight gain was found to have a campylobacter jejuni gastrointestinal tract infection. Known etiologies of methemoglobinemia such as oxidative drug exposure, deficiency of NADH-methemoglobin reductase, and hemoglobin m disorder were excluded. The patient had a twin brother (probably identical) who had neither methemoglobinemia nor stool cultures positive for C. jejuni. The twin essentially served as an experimental control, making other environmental or genetic causes of methemoglobinemia unlikely in the patient. Both the methemoglobinemia and the C. jejuni infection responded to adequate treatment with erythromycin. The association of a C. jejuni infection with methemoglobinemia is discussed in light of previous associations of enteritis and methemoglobinemia in infants.
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9/20. methemoglobinemia: nitrobenzene ingestion.

    In an unusually severe case of multiple toxin ingestion, a 48-year-old man ingested approximately 300 cc of Hoppe's Gunpower Solvent #9, which contains kerosene, denatured ethyl alcohol, oil and nitrobenzene. The major manifestation was nitrobenzene-induced methemoglobinemia of rapid onset. Treatment involves the judicious use of 1% methylene blue plus, in severe cases, hemodynamic and ventilatory support. The patient recovered after 48 hours and was transferred to the psychiatric service with continued follow-up for a mild poison-induced hemolytic anemia.
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10/20. Unfavorable neonatal outcome after intraamniotic injection of methylene blue.

    A case is presented in which methylene blue dye was injected intraamniotically to confirm rupture of the membranes. Significant neonatal morbidity occurred as a direct result of the methylene blue dye injection. A syndrome of toxic side effects is described including hemolytic anemia, hyperbilirubinemia, and methemoglobinemia. The metabolic process is discussed. The authors suggest discontinuing the intraamniotic injection of methylene blue dye as a diagnostic aid.
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