Cases reported "Sulfhemoglobinemia"

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1/11. An adolescent case of sulfhemoglobinemia associated with high-dose metoclopramide and N-acetylcysteine.

    We describe the case of an adolescent girl who received high-dose metoclopramide in combination with oral N-acetylcysteine therapy for acute acetaminophen toxicity. Whole blood-sample analysis for abnormal hemoglobin pigments established the diagnosis of sulfhemoglobinemia. metoclopramide has been shown to cause sulfhemoglobinemia, particularly when used in repeated high doses. Although N-acetylcysteine alone has not been associated as the cause, we suggest that sulfhemoglobine-mia is a potential complication in patients treated with metoclopramide for the nausea that often accompanies oral N-acetylcysteine therapy for acetaminophen toxicity. cyanosis without respiratory distress should suggest this diagnosis. ( info)

2/11. phenazopyridine-induced sulfhemoglobinemia.

    OBJECTIVE: To report a case of sulfhemoglobinemia in a patient receiving phenazopyridine for a urinary tract infection. CASE SUMMARY: A 63-year-old white woman presented to the emergency department with complaints of fatigue and bluish discoloration of her body that had gradually progressed over the previous 6-8 weeks. About 4 months prior to presenting to the emergency department, she had started taking phenazopyridine, an over-the-counter medication for symptoms of dysuria. Because the cyanosis did not improve after the patient received oxygen and methylene blue, sulfhemoglobinemia was suspected and confirmed by spectrophotometer analysis. DISCUSSION: Sulfhemoglobin is a green-pigmented molecule containing a sulfur atom in one or more of the porphyrin rings. It is a rare cause of cyanosis, which is usually drug induced. sulfhemoglobinemia is suspected when a cyanotic patient has normal to near-normal oxygen tension, laboratory reports of elevated methemoglobin, and does not respond to methylene blue therapy. sulfhemoglobinemia is relatively rare, despite the widespread use of drugs that have been reported to cause it. Predisposing factors, such as chronic constipation, present in our patient, have been suggested as a source of hydrogen sulfide. CONCLUSIONS: This case of sulfhemoglobinemia, which occurred after the patient took phenazopyridine, is considered a probable adverse event according to the Naranjo probability scale. ( info)

3/11. Delayed sulfhemoglobinemia after acute dapsone intoxication.

    A case of acute dapsone intoxication due to voluntary ingestion of 3 g of this drug as a suicide attempt is described. A severe methemoglobinemia developed, accompanied by intense cyanosis, dyspnea, headache, and nausea. Subsequently, significant sulfhemoglobinemia responsible for prolonged cyanosis was observed, as well as mild hemolytic anemia. Relapses of methemoglobinemia after methylene blue treatment required repeated administration of the reducing agent. The need of a careful follow-up for several days in this type of intoxication is emphasized. ( info)

4/11. Hemolytic anemia and sulfhemoglobinemia due to phenacetin abuse: a case with multivisceral adverse effects.

    The authors report a case of recurrent sulfhemoglobinemia resulting from a chronic abuse of phenacetin. cyanosis was accompanied by hemolytic anemia and numerous features of tissue aging. While phenacetin was found to be the oxidizing drug, no source of sulfur was identified. The origin of sulfhemoglobinemia in man is discussed and the possible role of intraerythrocytic glutathione is emphasized. ( info)

5/11. metoclopramide-induced sulfhemoglobinemia.

    metoclopramide, a drug with oxidant activity, has infrequently been reported to cause methemoglobinemia in infants. We present a unique case in which a patient on chronic metoclopramide therapy developed sulfhemoglobinemia that resolved with subsequent discontinuation of the drug. Mechanisms that may be important in the formation of sulfhemoglobin also are discussed. ( info)

6/11. flutamide-induced cyanosis refractory to methylene blue therapy.

    flutamide, an anti-androgen used in prostate cancer therapy, is also a derivative of aniline. Mild, usually asymptomatic, methaemoglobinaemia has been reported. We report a patient receiving flutamide therapy who developed cyanosis, dyspnoea and anaemia, initially attributed to marked methaemoglobinaemia by the CO-Oximeter method. An unsuccessful trial of methylene blue therapy led to the finding of marked sulphaemoglobinaemia. Sulphaemoglobinaemia has not previously been reported with flutamide use. Recognition of this association is important, given the refractoriness of sulphaemoglobinaemia to methylene blue therapy. ( info)

7/11. Congenital sulfhemoglobin and transient methemoglobinemia secondary to diarrhoea.

    sulfhemoglobinemia and methemoglobinemia are common causes of cyanosis arising due to accumulation of abnormal heme pigment. We present an unusual case of congenital sulfhemoglobinemia along with diarrhoea induced methemo-globinemia in a neonate. A high index of suspicion and a proper diagnostic approach is needed to determine the true frequency of their occurrence together. ( info)

8/11. A case of sulfhemoglobinemia and emergency measurement of sulfhemoglobin with an OSM3 CO-oximeter.

    We describe a case of sulfhemoglobinemia associated with toxic paint ingestion. blood gases, oxygen content, and fractional hemoglobin derivatives were assayed with Radiometer 520 and OSM3 instruments. Although the CO-oximeters indicated the presence of sulfhemoglobin (SulfHb), the results were not quantitative. An OSM3 service software program was activated to obtain the actual concentrations of the hemoglobin fractions. Subsequently, we evaluated the performance of the OSM3 service program for the analysis of SulfHb by performing precision studies and comparing OSM3 results with those of an AVL 912 CO-oximeter. Retrospectively, we determined that the patient's specimens contained 6% SulfHb. There was an obvious deviation between standard OSM3 oxyhemoglobin fraction measurements and those obtained by using its service program-the effect of a high SulfHb content. ( info)

9/11. sulfhemoglobinemia after dermal application of DMSO.

    A 43-y-old Caucasian female applied 4 ounces of dimethyl sulfoxide (DMSO) to her lower abdomen for treatment of interstitial cystitis. Within 24 h she developed fatigue, cyanosis and dyspnea with mild exertion. She sought medical attention 10 d later, at which time initial laboratory tests revealed a methemoglobin level of 47%. Two doses of 1 mg methylene blue/kg i.v. were given without significant improvement in either her cyanosis or methemoglobin level. Repeat analysis the day following admission using an outside lab demonstrated a sulfhemoglobin level of 6.2% and a methemoglobin level of < 0.1%. No prior reports have associated sulfhemoglobin formation with DMSO application. carbon monoxide-oximetry may falsely identify sulfhemoglobin as methemoglobin; sulfhemoglobinemia should be considered in cases of methemoglobinemia refractory to methylene blue therapy. ( info)

10/11. Pseudomethemoglobinemia: a case report and review of sulfhemoglobinemia.

    OBJECTIVES: To see if methemoglobin could potentially be misdiagnosed and the limitation of present cooximeters. PATIENT: A 17-year-old girl who overingested a combination of cimetidine, acetaminophen, ibuprofen, and naproxen in a suicide attempt. METHOD: Use of pulse co-oximeters to aid in the diagnosis of suspected sulfhemoglobinemia. RESULTS: diagnosis of sulfhemoglobinemia achieved with final confirmation made with gas chromatography. Patient steadily improved with supportive care. CONCLUSIONS: There is a potential for the diagnosis of methemoglobin with some of the limitations of present co-oximeters. The laboratory diagnosis of sulfhemoglobinemia can be difficult to make. ( info)
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