Psoriasis clinical presentation

Describe the pathophysiology of psoriasis including types of psoriasis and clinical presentations. 

Psoriasis is a T-lymphocyte-mediated inflammatory disease that results from a complex interplay between multiple genetic factors and environmental influences. Genetic predisposition coupled with some precipitating factor triggers an abnormal immune response, resulting in the initial psoriatic skin lesions. Keratinocyte proliferation is central to the clinical presentation of psoriasis. 

Keratinocyte proliferation is central to the clinical presentation of psoriasis. Keratinocytes are skin cells producing keratin which act as a skin barrier. Increased keratinocyte cell turnover (hyperkeratosis) results in the characteristic thick scaly skin lesions seen in patients with psoriasis.10,11 Hyperkeratosis results from immune derangements. 

In a survey of patients about the sources of advice they use for skin conditions, pharmacists ranked second, just behind physicians. Interestingly, the advice sought seemed to depend on the nature of the condition, in that patients sought more pharmacist advice on conditions such as dermatitis, psoriasis, skin cancer, and acne. To properly assess a patient, pharmacists and other primary care providers must not only understand clinical presentations of common skin disorders, but they must also be able to quickly identify patients that may need referral for further evaluation by a physician. 

Psoriasis is a chronic, inflammatory and hyperprolifera-tive disease of the skin, scalp, nails, and joints, affecting 1 to 2% of the U.S. population. It is found worldwide its frequency varies from 0 to 3% among different ethnic groups. Most of its variable clinical presentations eventuate into erythematous, scaly plaques with or without nail disease and arthritis. Susceptibility to psoriasis is umnistakably heritable, but the phenotype is controlled by multiple genes as well as enviromnental factors. Trauma, stress, and infections are important determinants of disease onset and severity. At the cellular level, psoriasis is characterized by markedly increased epidermal proliferation and incomplete differentiation elongation, dilatation, and leakiness of the superficial plexus of dermal capillaries and a mixed inflammatory and immune cell infiltrate of the epidermis and papillary dermis. A multitude of plausible pathomechanisms... 

Psoriatic patients frequently present with altered ser am urate levels, a disturbance which is commonly attributed to some changes in nucleoprotein metabolism directly linked to the pathological process of the skin lesions in fact, it is well known that an increased turnover rate of the epidermal cells (from the normal value of 27 days to 3-4 days only) is responsible for the psoriatic skin changes (Fitzpatrick and Haynes, 1980). To date, no tracer turnover studies with labelled uric acid have been reported in patients affected by psoriasis. We present here the metabolic results obtained with the aid of C-uric acid in a group of psoriatic patients with various degrees of severity of the disease. The aim of the study was to elucidate some pathophysiologic aspects of uric acid turnover in such clinical conditions. 

Paradoxical inflammation such as psoriasis is a well-known phenomenon of anti-TNFa therapy approved for the treatment of autoimmxme diseases such as rheumatoid arthritis, Crohn s disease, ulcerative colitis and psoriasis. Likewise, infliximab is used to treat refractory sarcoidosis but recently a case of infliximab-induced cutaneous sarcoidosis was reported in a patient with ulcerative colitis [150 ]. The induction of psoriasis and other clinical presentations like psoriasiform exanthema and palmoplantar pustulosis as side effects of infliximab treatment is not xmderstood and the pathogenesis of such reactions has been further obscured by the finding of a patient with Crohn s disease who developed arthritis as well as the skin manifestations cf psoriasis after the administration of infliximab [151 ]. 

Psoriasis is a common inflammatory skin disorder which is estimated to affect 1.5% to 3% of the Caucasian population.1,2 It may present at any age.3,4 Ethnic factors influence disease prevalence. In the United States, prevalence among blacks (0.45% to 0.7%) is lower than in the remainder of the United States population (1.4% to 4.6%).1 Between 10% and 30% of patients with psoriasis will also have psoriatic arthritis.5 In 10% to 15% of psoriatic patients with arthritis, joint symptoms actually appear prior to skin involvement.3 Clinical depression is another frequent comorbid illness in these patients. A recent United States survey showed that 8% to 10% of psoriatic patients aged 18 to 54 years old actively contemplated suicide because of their psoriasis.6... 

There has been a continuing debate over whether or not the clinically uninvolved skin of the psoriatic is actually normal. Is there a way of bringing out latent psoriasis Since the genetic influence in this disease is fairly strong, one would expect all skin cells to have the same abnormality present within them therefore, the uninvolved skin should have an observable abnormality inherent within it. 

At the present time, the efficacy and the clinical benefit of cyclosporin therapy has been conclusively demonstrated for severely affected patients in four diseases autoimmune uveitis, psoriasis, idiopathic nephrotic syndrome and rheumatoid arthritis, as well as in transplant patients. 

Clinically, psoriasis of the hands presents as kerato-tic patches on the palms and often the bony prominences of the hands. The skin lesions on the palms do not display the classical features of psoriatic lesions elsewhere on the body. A high degree of suspicion is necessary to recognise the condition. The presence of psoriatic lesions elsewhere, e.g., on the elbows, knees, trunk and scalp, and the associated nail changes of psoriasis often help the physician to establish the diagnosis. 

An 80-year-old man was referred to dermatology clinic with flexural psoriasis on physical examination painful conjunctival erosions were found [14 ]. The lesions had been present for about 18 months, and the date of start was coincident with a doubling of daily dose of nicorandil. The patient was switched to isosorbide mononitrate, and in about 3 weeks pain disappeared and there was complete healing of the conjuctival erosions. This is the first case report of nicorandil-induced conjuctival erosions, which is completely reversed by drug suspension. 

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