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Psoriasis and Myeloperoxidase Deficiency

Activation of neutrophils has been described in the physiopathology of psoriasis. To our knowledge, only 2 observations of pustular psoriasis associated with myeloperoxidase (MPO) deficiency have been mentioned in the literature [1, 2]. We report here the first case of psoriasis vulgaris associated with MPO deficiency suggesting that this granule enzyme pathway may not be necessary in the mechanisms leading to psoriasis. A 61-year-old man was admitted for a mild thrombopenia which had first been noted 4 years previously. He had suffered from a diffuse psoriasis since the age of 32 and had presented many gout crises. Psoriasis was treated with calcipotriol, and gout was treated with allopurinol and colchicine. The patient was a nonsmoker, was in good health and was not suffering from any hemorrhagic disorder or infectious diseases. His mother and his son also suffered from psoriasis. Clinical examination was normal except for the diffuse psoriasis (trunk, buttocks, head and limbs). Biological evaluation revealed a low platelet count (107 ! 109/l, normal: 150–400) associated with multiple aggregates on an EDTA tube. On a citrate tube, the platelet count was normal (172 ! 109/l) without aggregates. The neutrophil count was normal (4.29 ! 109/l), but a complete MPO deficiency was observed. No anemia was noted and there was no inflammation. Electrolytes, urea nitrogen, creatininemia and liver function tests were normal. Search for autoantibodies (antinuclear, anti-doublestranded-DNA, anti-extractable-nuclear-antigens, antiphospholipid, anti-neutrophil cytoplasmic and antiplatelet autoantibodies) as well as monoclonal gammopathy was negative. Thyroid function tests were normal. No infectious disease was evidenced with serological screening including search for intracellular organisms, HIV, hepatitis B and C viruses. We concluded there was a false thrombocytopenia due to EDTA-induced aggregation associated with a total granulocytes MPO deficiency and psoriasis vulgaris. A microabscess of psoriasis is generally considered to be composed of neutrophils [3], and neutrophil stimulation has been reported in this disorder [4]. Interleukin-8, which is a strongly chemotactic and an activator factor for neutrophils, as well as C5a (also a neutrophil chemotactic fragment) are observed in psoriasis pustules [5]. Moreover, increased phagocytosis of neutrophils in patients with psoriasis has also been described [6]. MPO belongs to a family of related proteins which includes eosinophil peroxidase, thyroid peroxidase and lactoperoxidase. The MPO gene is a14-kb gene located on the long arm of chromosome 17. This enzyme catalyzes hydrogen peroxide production which is involved in the response against bacterial and fungal organisms. MPO deficiency is either an autosomally inherited defect or a disorder acquired during the course of a blood dyscrasia. In the literature, patients lacking MPO rarely show increased susceptibility to infections, as was the case for our patient. This is probably due to the presence of a substitute MPO-independent microbicidal system. To our knowledge, there are only 2 observations in the literature regarding an association of MPO deficiency and psoriasis [1, 2]. They concern 2 cases of pustular psoriasis. Besides psoriasis, other types of neutrophilic dermatoses such as pyoderma gangrenosum of Sweet’s syndrome [7] have been reported in the presence of MPO deficiency. As the role of MPO and more generally the activation of neutrophils are sometimes mentioned in the pathogenesis of psoriasis, we feel that this kind of association can shed light on the latter.