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Biomedical subjects

David A Fairhurst

Publications and source records attributed to David A Fairhurst.

3 recordsLinked to original sources
PubMed2006

Interaction between genetic control of vascular endothelial growth factor production and retinoid responsiveness in psoriasis.

Vascular endothelial growth factor (VEGF) promotes angiogenesis, and elevated levels are found in plaques of psoriasis. Two VEGF polymorphisms, +405 and -460, are associated with early-onset psoriasis and are close to the functional activator protein-1 site (+419) through which retinoids, an established systemic therapy for psoriasis, can block production of VEGF. We report that peripheral blood mononuclear cells (PBMCs) and epidermal keratinocytes (KC) from patients with psoriasis demonstrate differential, genotype-dependent, regulation of VEGF. For PBMCs, VEGF genotype distinguishes two groups of patients with psoriasis - "high and low VEGF producers" (P < 0.001). In contrast, KC production of VEGF is not genotype dependent. However, the effects of all-trans retinoic acid (RA) on cellular expression of VEGF are determined by both cell type and genotype. RA inhibits KC production of VEGF in a genotype-dependent manner (P < 0.005) whereas RA stimulates PBMCs production irrespective of VEGF genotype (P < 0.001). We also report that the -460 VEGF polymorphism appears to have a clinical pharmacogenetic role in predicting response or non-response of psoriasis to acitretin (P = 0.01). In future, determination of VEGF gene polymorphisms and thus individual patient VEGF "signatures" may be used as a prognostic factor for psoriasis susceptibility/severity and as a means for optimizing treatment response.

Acitretin↗
PubMed2005

Optimal management of severe plaque form of psoriasis.

Psoriasis is a chronic, inflammatory, hyperproliferative skin disease that affects 1-2% of the general population in the UK and US. Plaque psoriasis is the most common form, accounting for approximately 90% of cases. The disease is usually chronic and persistent, although up to 50% of patients may enter spontaneous remission for varying periods of time. There is no cure for psoriasis; therefore, the aim of treatment is to minimize the extent and severity of the disease to the point at which it no longer substantially disrupts the patient's quality of life. First-line therapy of psoriasis usually consists of topical agents, such as emollients, tar, dithranol, and vitamin D3 analogs. In cases of severe, extensive psoriasis, where topical therapy is either impractical or not sufficiently effective, systemic treatment may be warranted at the outset. In these circumstances, the therapeutic options include: (i) intensive inpatient or day center topical therapy; (ii) phototherapy; and/or (iii) systemic agents. There are now a number of systemic agents available for the treatment of severe psoriasis, but all have potential adverse effects. We review the current treatment options, which include the use of phototherapy and systemic agents, and provide recommendations on their use in clinical practice. Importantly, treatment should be tailored to each individual patient depending on concurrent medical problems (which might preclude certain agents), patient choice and acceptance of the risk of adverse effects.

Administration, Oral↗