No abstract available.
Methemoglobinemia*

The high level of Methemoglobinemia influences the combination of blood with oxygen and oxygen transfer to cells which can lead to the life in the normal condition. Methemoglobine is a component of erythrocyte in a very small amount(less than 1% of total Hemoglobine). An increased Methemoglobine leads to the disorder of oxygen delivery. The clinical symptoms are direct proportional with the methemoglobinemia level. The hypermethmoglobinemia includes the congenital- methemoglobinemia and the acquired methemoglobinemia. The congenital hypermethemoglobinemia attibuted to a partly or completed deficiency of Methemoglobine reductase in patients with the deficiency of genetic heterozygous - enzyme or abnormal methemoglobine: the acquired methemoglobinemia occurred after exposure with the chromatic compound, food, water with much nitrate or use of some drugs. The quantitative analysis of methemoglobinemia has a values in the diagnosis, treatment and prognosis
Methemoglobinemia ; Prognosis

This report a case of a ten-year-old female with progressive cyanosis and dyspnea on exertion. Clinical and laboratory work up ruled out a cardiac and pulmonary pathology warranting further investigation for possible hemoglobinopathies. Enzyme assay showed deficiency in cytochrome b5 reductase seen in patients with congenital methemoglobinemia. Ascorbic acid at 200mg daily afforded gradual improvement in cyanosis.
Methemoglobinemia ; Cyanosis

No abstract available.
Child* ; Humans ; Methemoglobinemia*

No abstract available.
Ascorbic Acid ; Dapsone ; Methemoglobinemia

The hyper-methemoglobinemia causes the oxygen transfer disorder. The clinical symptoms depends on the level of methemoylobinemia. Hypermethemoglobinemia can be congenital or acquired hypermethemoglobinemia. The congenital hypermethemoglobinemia caused by partial or total methemoglobine reeducates deficiency in patients with rare genetic heterozygous enzyme deficiency due to the abnormal hemoglobin. The acquired hypermethemoglobinemia occurred after exposure to colour compound, food and drinking water with nitrate or drugs. The determination of causative agent of hypermethemoglobin help treating more effectively
Methemoglobin ; Hemoglobins, Abnormal ; Therapeutics ; Methemoglobinemia

Pulse oximeters measure the arterial oxygenation by determining the color of the blood between a light source and a photodetector. The light source consists of two light-emitting diodes (LEDs) that emit light at known wave lengths, 660 nm red light and 940 nm infrared light. The ratio of pulse-added red absorbance at 660 nm to pulse-added infrared absorbance at 940 nm is used to generate the oximeter's estimate of arterial saturation (SpO2). Pulse oximeters can determine the concentration of only two hemoglobins, reduced (HHb) and oxyhemoglobin (HbO2), so they can't distinguish the dyshemoglobins (methemoglobin, carboxyhemoglobin) which have light absorbances similar to that of HHb or HbO2. If the concentration of dyshemoglobin is above the normal range, pulse oximeters would give erroneous SpO2 readings. We experienced a case which showed a low SpO2 reading but had normal ABGA findings due to unsuspected methemoglobinemia.
Methemoglobinemia* ; Oxygen ; Oxyhemoglobins ; Reading ; Reference Values

BACKGROUND: To determine whether N-acetylcysteine(NAC) reduces methemoglobin. METHOD: We carried out an in vivo experiment in rats, weighed about 300g. Each rat was ingested 200mg of dapsone(4,4'diaminodiphenyl sulphone) to induce methemo- globinemia. After 1 hour, 30 rats were received NAC 160mg(2ml) and another 30 rats, served as control, were received 2ml of normal saline orally,4 times hourly. Serum methemoglobin concentrations were checked 1,6, and 24 hours after dapsone ingestion. RESULT: The methemoglobin concentrations on each time were 27.1+/-5.8%,23.5+/-8.8%, 17.1+/-6.4%(mean+/-SD) in control group and 25.5+/-6.3%, 25.5+/-8.8%, 65.5+/-31.2%(mean+/-SD) in NAC group. There were no differences on methemoglobin concentrations at 1 and 6 hours between two groups(P>.05). At 24 hours, the methemoglobin concentrations of NAC group was significantly higher than those of control group(P<.01). CONCLUSION: NAC had no therapeutic effects on dapsone induced methemoglobinemia in this experimental setting.
Acetylcysteine* ; Animals ; Dapsone ; Eating ; Methemoglobin ; Methemoglobinemia* ; Rats

Congenital methemoglobinemia is caused by NADH-methemoglobin reductase deficiency in more than half of the total reported cases. NADH-methemoglobin reductase deficiency is an uncommon hereditary disorder producing methemoglobinemia and cyanosis in the homozygous subject. A majority of the patients born with these abnormalities have only a cosmetic defect-asymptomatic cyanosis. Congenital methemoglobinemia due to NADH-methemoglobin reductase deficiency is an autosomal recessive disorder and classified into 4 types according to the pathophysiology of the disorder. In type I, the deficiency of NADH-methemoglobin reductase is restricted to erythrocytes of patients with mild cyanosis, and 7 missence mutations have been reported in the case of type I. We report the first Korean pediatric case of type I congenital methemoglobinemia due to NADH- methemoglobin reductase deficiency with a review of the literature.
Cyanosis ; Cytochrome-B(5) Reductase ; Erythrocytes ; Humans ; Methemoglobinemia* ; Oxidoreductases*

Primaquine is often administered for the hypnozoite stage of Plasmodium vivax and Plasmodium ovale. Primaquine (with clindamycin) is also an alternative drug for treatment of pneumocystis pneumonia when trimethoprim/sulfamethoxazole cannot be used. Primaquine may cause methemoglobinemia, an altered state of hemoglobin in which the ferrous state of heme is oxidized to the ferric state. We report a case of methemoglobinemia caused by a standard dose of primaquine plus clindamycin in a 27-year-old female recipient of a kidney transplant who was diagnosed with pneumocystis pneumonia.
Adult ; Clindamycin ; Female ; Heme ; Humans ; Kidney ; Methemoglobin ; Methemoglobinemia* ; Plasmodium ovale ; Plasmodium vivax ; Pneumonia, Pneumocystis ; Primaquine*