Prolactin: does it have a role in the pathogenesis of psoriasis?

BACKGROUND: The aetiopathogenesis of psoriasis is still not fully understood. Recently, it has been reported that prolactin (PRL) exerts a proliferative effect on human keratinocytes in vitro. PRL may, therefore, play an important role in the pathogenesis of psoriasis. OBJECTIVE: To assess the serum PRL level in patients with psoriasis vulgaris (PV). METHODS: Serum levels of PRL were estimated in 12 patients with PV (age: 11-45 years with mean +/- SD 30.4 +/- 10.2 years; sex: 7 males, 5 females) and the results were compared with those in 9 patients with atopic dermatitis (age: 15-47 years with mean +/- SD 28.1 +/- 11.9 years; sex: 4 males, 5 females) and 20 normal control subjects (age: 16-45 years with mean +/- SD 36.1 +/- 11.9 years; sex: 15 males, 5 females). RESULTS: Serum PRL in PV (mean +/- SD 25.8 +/- 16.1 ng/ml) was significantly higher compared to those in atopic dermatitis (mean +/- SD 9.1 +/- 4.7 ng/ml) and normal control subjects (mean +/- SD 10.3 +/- 5.3 ng/ml; ANOVA --> p = 0.0008). Three patients with PV (2 males and 1 female with ages of 35, 40 and 11 years, respectively) had the highest serum levels well above the normal range but they were <100 ng/ml, the minimum limit for the diagnosis of prolactinoma (chi2 test --> p <0.025). CONCLUSION: Since PRL belongs to the growth hormone family, its raised serum level may have a role in the hyperproliferation of kerationocytes in vivo, the hallmark of the psoriasis disease process.

Leukocyte-extracellular matrix interactions in psoriasis.

BACKGROUND: The basic phenomenon in psoriasis appears to be a directed leukocyte migration that in a great part, depends on the cell-extracellular matrix (ECM) interactions. METHODS: To evaluate the leukocyte-ECM interactions in psoriasis, we investigated the adherence of peripheral blood mononuclear cells (PBMC) and polymorphonuclear leukocytes (PMNL) to ECM components (collagen type I, IV, laminin, and fibronectin), using crystal violet staining and measuring absorbance at 570 nm. RESULTS: In the most active cases of psoriasis (pin-point and guttate type) of short duration, we found a decreased adherence of PBMC to collagen type IV. In a majority of cases of actively spreading plaque psoriasis of large extent and longer duration, there was decreased adherence to all ECM components, especially to collagen type IV and laminin. The adhesion of PMNL to collagen type IV (but not to other ECM components) was increased only in cases of short duration. Preliminary data suggest that etretinate treatment may modulate leukocyte adherence to the ECM components in patients with psoriasis. CONCLUSIONS: The decreased in vitro adherence of PBMC to ECM components, especially those of the basement membrane, may reflect their in vivo activation and migration to the epidermis, which is a basic phenomenon in psoriasis that could be affected by etretinate therapy.