Myeloperoxidase deficiency is a disorder featuring lack in either the quantity or the function of myeloperoxidase–an iron-containing protein expressed primarily in neutrophil granules.

[1] One method of intracellular killing which takes place in the phagolysosomes of neutrophils involves the reaction of myeloperoxidase with hydrogen peroxide (H2O2) acquired in the cells from NADPH oxidase through the respiratory bursts.

[1][2] Although the mechanisms of this process aren’t well understood, there is evidence that this extracellular myeloperoxidase interacts with dendritic cells (cells of the adaptive immune system) in the lymph nodes, leading to a decrease in adaptive immune system activity in response to infection.

Nonetheless, myeloperoxidase-deficient individuals have been found to experience more chronic inflammatory conditions (such as rheumatoid arthritis, pulmonary/skin inflammation, kidney/heart disease, etc.)

[1][2][3] Researchers hypothesize this may be a result of heightened adaptive immune system activity in individuals with myeloperoxidase deficiency.

[4] Primary MPO deficiency is an autosomal recessive genetic disorder, which is caused by mutations in the myeloperoxidase gene on chromosome 17q23.

[5] Secondary MPO deficiency, on the other hand, occurs in various clinical situations as a result of hematological neoplasm, disseminated cancers, some drugs, iron deficiency, lead intoxication, thrombotic disease, renal transplantation, severe infectious disease, diabetes mellitus, neuronal lipofuscinosis, or pregnancy.

[4] Secondary MPO deficiency is typically partial, meaning only a portion of the affected individual’s neutrophils lack functional myeloperoxidase.

[4] Various devices can divide up leukocyte (white blood cell) populations based on their size and peroxidase activity.

[6] Note, myeloperoxidase deficiency can cause false positives in the diagnosis of chronic granulomatous disease, a condition which includes dysfunctional NADPH oxidase.