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MTX<br />

8721<br />

FMETX<br />

91822<br />

phenazopyridine, sulfonamides, local anesthetics, dapsone, or following ingestion of nitrites or nitrates.<br />

Congenital methemoglobinemias are rare. They are due either to: -A deficiency of methemoglobin<br />

reductase (also called cytochrome B5 reductase or diaphorase) in erythrocytes, an autosomal recessive<br />

disorder -One of several intrinsic structural disorders of hemoglobin, called methemoglobin-M, all of<br />

which are inherited in the autosomal dominant mode Sulfhemoglobin: Sulfhemoglobinemia often<br />

accompanies methemoglobinemia. Sulfhemoglobinemia can be due to exposure to trinitrotoluene and/or<br />

zinc ethylene bisdithiocarbamate (a fungicide). The formation of sulfhemoglobin cannot be reversed and<br />

there is no therapy for sulfhemoglobinemia. Because patients with sulfhemoglobinemia also often have<br />

methemoglobinemia, therapy is directed at reversing the methemoglobinemia present. Symptoms of both<br />

methemoglobinemia and sulfhemoglobinemia are caused by anoxia and are characterized by cyanosis.<br />

Useful For: Diagnosis of methemoglobinemia and sulfhemoglobinemia Differentiation of<br />

methemoglobinemia and sulfhemoglobinemia from other causes of cyanosis (eg, congenital heart disease)<br />

Interpretation: In congenital methemoglobinemia, the methemoglobin concentration in blood is about<br />

15% to 20% of total hemoglobin. Such patients are mildly cyanotic and asymptomatic. In acquired (toxic)<br />

methemoglobinemia, the concentration may be much higher. Symptoms may be severe when<br />

methemoglobin is >40% of hemoglobin. Very high concentrations may be fatal. This is a consultative<br />

evaluation in which the history and previous laboratory values are reviewed by a hematologist who is an<br />

expert on these disorders. Appropriate tests are performed and an interpretive report is issued.<br />

Reference Values:<br />

Definitive results and an interpretive report will be provided.<br />

Clinical References: Beutler E: Methemoglobinemia and sulfhemoglobinemia. In Hematology. 5th<br />

edition. Edited by E Beutler, MA Lichtman, BS Caller, TJ Kipps. New York, McGraw-Hill Book<br />

Company, 1995, pp 654-663<br />

Methotrexate, Serum<br />

Clinical Information: Methotrexate is an antineoplastic agent that inhibits the enzyme, dihydrofolate<br />

reductase. Such inhibition causes a stoppage of synthesis of tetrahydrofolate that, in turn, results in an<br />

inhibition of nucleotide and ultimately of DNA synthesis. Methotrexate is effective against malignancies<br />

with rapid cell proliferation such as acute lymphoblastic leukemia, choriocarcinoma, trophoblastic tumors<br />

in women, and carcinomas of the breast, tongue, pharynx, and testis. When used as an antineoplastic agent<br />

against these tumors, it is administered at high dose (2.5 mg/kg or 3.3 mg/kg), and usually is followed by<br />

leucovorin (folinic acid) rescue to salvage nontumor cells.<br />

Useful For: Following therapy, serum concentration is used to judge whether the drug is being cleared<br />

appropriately and verify that a nontoxic level has been attained.<br />

Interpretation: Following a 4 to 6 hour intravenous infusion of methotrexate, postinfusion<br />

concentrations greater than the following indicate an increased risk of toxicity if conventional low dose<br />

leucovorin rescue is given: -24-hour postinfusion concentration: 5.0 mcmol/L to 10.0 mcmol/L -48-hour<br />

postinfusion concentration: 0.5 mcmol/L to 1.0 mcmol/L -72-hour postinfusion concentration: 0.1<br />

mcmol/L<br />

Reference Values:<br />

Nontoxic drug concentration after 72 hours:

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