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INTRODUCTION

Inflammatory dermatoses may be categorized based on the pattern of inflammation1 and epidermal changes.2 With psoriasis as the prototype, the psoriasiform dermatitides are characterized by regular elongation of rete ridges.3 This may result from increased keratinocyte proliferation due to more rapid turnover of stem cells or an increased pool of proliferating cells. Epidermal thickening may affect any or all of the layers of the epidermis. The stratum corneum may be thickened (hyperkeratosis) and may retain nuclear remnants (parakeratosis). Thickening of the granular layer or spinous layer is termed “hypergranulosis” or “acanthosis,” respectively.

In psoriasis, there is prominent parakeratosis associated with a thin to absent granular layer. Rete ridges show clubbing, are uniformly elongated, expanded at the tips, and fused. The epidermis shows thinning of the suprapapillary plates. Neutrophils migrate from dilated capillaries in the papillary dermis and extend into the stratum corneum to form Munro microabscesses. A number of inflammatory dermatoses share these features, including psoriasis, reactive arthritis, pityriasis rubra pilaris, and lichen simplex chronicus (LSC).4 However, just as there are differences in the clinical appearance and pathogenesis, there are often discrete histologic differences in epidermal changes and distribution or composition of inflammation that allow these dermatoses to be distinguished from each other. Nevertheless, in many cases clinicopathologic correlation is essential to render a final diagnosis.

MAJOR PSORIASIFORM DERMATOSES

Psoriasis

Psoriasis is a chronic papulosquamous disease affecting about 2% to 3% of the worldwide population. There is considerable geographic and ethnic variation in incidence. For example, psoriasis is more prevalent in American, Canadian, and European populations but infrequent in Native Americans and Asians.5 The onset is typically in the third decade, with a second peak in the sixth.6 Psoriasis is characterized by an increased epidermal turnover rate,7 leading to thickening of the epidermis and accumulation of scale. Certain areas of the skin are preferentially involved, including the scalp, groin, elbows, knees, umbilicus, and lumbar spine.8 The disease follows a chronic relapsing course characterized by remission and exacerbation. About 20% to 30% of patients develop psoriatic arthritis. Additionally, there is an increased risk for cardiometabolic diseases and possibly an association with other comorbidities such as chronic renal disease, inflammatory bowel disease, hepatic disease, certain malignancies, infections, and mood disorders.9

The etiology of psoriasis is multifactorial. Environmental factors such as drugs, smoking, drinking, diet, infections, and mental stress play a role.10 Additionally, there is a genetic/epigenetic component, as is shown by the high concordance for disease in monozygotic twins.11 Initially, linkage analysis of multiple affected psoriasis families have identified at least 12 chromosomal loci, so-called psoriasis-susceptibility regions (PSORS), that were considered likely to harbor psoriasis genes. Later, genome-wide association studies, which analyzed single nucleotide polymorphisms (SNPs) in psoriasis and control patients, have identified over 50 regions associated with risk for psoriasis. Genes that have ...

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