Sulfhemoglobinemia | |
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Specialty | Hematology |
Symptoms | Cyanosis, urinary tract infection and chronic constipation |
Complications | Hypoxemia, methemoglobinemia, and hypoxia |
Duration | 100-120 days (lifespan of red blood cells) |
Causes | Sulfur medications such as phenacetin, metoclopramide, dapsone, phenzopyridine, and trimethoprim-sulfamethoxazole; hydrogen-sulfide-producing intestinal bacteria, such as Morganella morganii |
Risk factors | Pulmonary arteriovenous malformation |
Prevention | Avoidance of sulfur-containing compounds including drugs |
Treatment | Blood transfusions |
Sulfhemoglobinemia is a rare condition in which there is excess sulfhemoglobin (SulfHb) in the blood. The pigment is a greenish derivative of hemoglobin which cannot be converted back to normal, functional hemoglobin. It causes cyanosis even at low blood levels.
It is a rare blood condition in which the β-pyrrole ring of the hemoglobin molecule has the ability to bind irreversibly to any substance containing a sulfur atom. [1] [2] When hydrogen sulfide (H2S) (or sulfide ions) and ferrous ions combine in the heme of hemoglobin, the blood is thus incapable of transporting oxygen to the tissues.
Symptoms include a blueish or greenish coloration of the blood (cyanosis), skin, and mucous membranes, even though a blood count test may not show any abnormalities in the blood. This discoloration is caused by greater than 5 grams per cent of deoxyhemoglobin, or 1.5 grams per cent of methemoglobin, or 0.5 grams per cent of sulfhemoglobin, all serious medical abnormalities.[ citation needed ]
Sulfhemoglobinemia is usually drug induced, with drugs associated with it including sulphonamides, such as sulfasalazine or sumatriptan. Another possible cause is occupational exposure to sulfur compounds.[ citation needed ]
It can also be caused by phenazopyridine. [3]
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The condition generally resolves itself with erythrocyte (red blood cell) turnover, although blood transfusions can be necessary in extreme cases.[ citation needed ]
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