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Posted on:06-Jan-2014
Psoriasis is a fascinating disease for a serious student of dermatology. It gives an insight into the scientific progress through ages as well as the human behaviour. It is a disease frought with myths and unfounded fears . Understanding of psoriasis is a feat by itself. Recognizing this difficulty the famous dermatologist Bechet years ago remarked as “psoriasis is an antidote to dermatologists ego”1. In this article an attempt is made to know the disease, its evolution through ages and its treatment as understood by a modern medicine doctor.
The name \’psoriasis\’ from the Greek word ‘psora’ means itch 2 Hippocrates (460 – 377 BC) writing on skin diseases, grouped many dry, scaly, disfiguring dermatoses and described them as lopoi 3 . The word lopoi is derived from the Greek words lopos (the epidermis) and lepo ( to scale) 2. From that day onwards till recently , started the confusion between psoriasis and leprosy as the different manifestations of same diseases, it continued till recently. The Bible also did not differentiate between psoriasis and leprosy. In the Old testament many skin diseases including psoriasis, scabies and leprosy were described as a single disease and described using the term traract or zaraath 3. Similar classification of skin disease as Kustha is seen in Cakara Samhitha 4. This classification broadly encompasses many skin diseases of dissimilar etiology and pathomechanism . To put in shortly ‘psoriasis’ of today was considered as ‘ leprosy’ of yesterday. The implication of this misclassification was painful as patients were ostracized and cruelty was imposed upon those who suffered from psoriasis and leprosy alike 5.
In the four hundred years from Hippocrates to Galen there was a gradual accumulation of clinical knowledge. In Alexandria the emphasis was placed on the appearances of diseases 5. Many important clinical observations were added in dermatology during this time. Notable were the writings of first century physicians , Dioskorides, Archigenes and Kriton. Kriton wrote four books on cosmetics in which he considered more than fifty subjects covering “every sort of thing from bad odours in axilla to psoriasis of nails” 5.
Galen (133 – 200AD) first utilized the term psoriasis, but his description was not consistent with the present day psoriasis 3. For centuries psoriasis was mistaken as leprosy and the society imparted the same cruel treatment to these patients also. They were to carry a bell or clapper to announce their appearance and had to wear a special dress 3. In 1313, Philip the fair of France ordered that they be burned at the stake 1.
In 1809, it was Robert Willan who gave the classic description of psoriasis as we know it today. Unfortunately he described it under the term lepra vulgaris , which further perpetuated the confusion between psoriasis and leprosy 3. Lepra vulgaris, as described by Robert Willan , was enlarging, sharply marginated erythematous plaques with silvery – white scales that occurred most frequently on the knees, and were associated with nail pitting 6. For decades after the description by Willan , some authors favoured using the term psoriasis , while others choose the term lepra 7. Finally , Gilbert and Hebra matched Willan’s description with the term psoriasis, ending much confusion 3.
With the establishment of distinct disease status of psoriasis , renewed enthusiasm set in to study the disease . This has led to description of bleeding spots on removal of scales by Heinrich Auspitz (1835 -1886), later known as ‘Auspitz sign’ 8. Auspitz sign forms one of the diagnostic parameters of psoriasis . Koebner phenomenon described by Kobner in 1876, formation of isomorphic lesions along the line of trauma , along with Auspitz sign, forms another characteristic features of psoriasis. The identification of this feature in psoriasis lead to the understanding of vascular component in the disease production 3. Later in 1898 described microabscess in epidermis. These micro abscesses are collection of neutrophils in stratum spinosum, presently known as Munro’s abscess 3. As days passed, new subsets of psoriasis were described such as generalized pustular psoriasis of pregnancy by Hebra (1872) and generalized pustular psoriasis by Leo Van Zumbusch (1910).
The search for the cause of a disease is from time immemorial; psoriasis is no exemption. As in any skin disease earlier theories were based on certain observations. Accordingly various theories were put forth such as environmental theory, nutritional theory , change in body humors , etc. There is a detailed description of skin diseases and its causes in ancient Ayurvedic books such as Sushruta Samhita and Caraka Samhita.
With the advent of microscopy , there appeared renewed interest in psoriasis. Under microscope the structural changes are viewed and found out that there is increase in the layers of epidermis. In 1963, Van Scott noted a significant increase in mitoses of psoriatic epidermis. This led to the concept that psoriasis is a hyperproliferative disease. With the cell cycle studies we reached much clarity to the hyperproliferative hypothesis. The studies of Van Scott and Weinsten proved the reduced sojourn of keratinocytes . This knowledge logically led to the use of cytostatic agents in the treatment of psoriasis. However, the use of methotrexate in the treatment of psoriasis had occurred by chance. Gubner treated rheumatoid arthritis in 1951 with folic acid antagonist aminopterin and noted clearing of skin lesions in patients with psoriasis 10. He might have treated psoriatic arthritis as ‘rheumatoid arthritis’ as there is a subset of psoriatic arthritis mimicking rheumatoid arthritis.
Another chance finding of the clearance of psoriatic lesions in transplant patients treated with cyclosporine by Muller led to better understanding of the pathomechanism of psoriasis11. This provided further insight into the pathogenesis of psoriasis. The subsequent studies to understand the mechanism of action of cyclosporine in psoriasis shifted the emphesis from the proliferation theory to immunological theory . Hence the major player was identified as T cells and macrophages. The immunohistochemical studies led to the understanding of roles played by the various proinflammatory and inflammatory mediators in the pathogenesis of psoriasis.
Recently the term psoriatic disease was introduced in an attempt to provide a new perspective on psoriasis 12. This concept is based on the newer understanding of the pathogenesis of psoriasis and its extracutaneous manifestations. People had observed arthritis in psoriatic patients. But it was Wright who proposed the term psoriatic arthritis 13. Initially psoriatic arthritis was considered only as a variability of psoriasis severity . Later the knowledge of the familial occurrence and the significant association of HLA – CW6 in psoriatic arthritis resulted in the understanding of genetic factors operating in the pathogenesis of the disease. The advances in molecular biology also helped to further understand the pathogenesis of psoriasis. The available data suggests that psoriasis is an inflammatory disease. For the initiation and maintenance of the inflammation, there should be an altered immune response. With the help of molecular biology techniques, the inflammatory cascade has been characterized. According to the model proposed by Ritchlin 14 which was modified further 15 the major events start in the skin and subsequently expand to the joints. It is also observed that patients with psoriatic arthritis show microscopic inflammatory changes of colonic mucosa even in the absence of bowel symptoms. This probably prompt one to think that bowel could be another site where inflammatory process begins 15.
It has been observed in psoriatics that there is significantly higher rate obesity, insulin resistance, type 2 diabetes mellitus and metabolic syndrome 16. These patients also show an increased occurrence of hypertensions, hyper lipidaemia and cardiovascular diseases 17. If these diseases are taken together one common feature evolve ie. the basis of all these manifestations can be seen as global inflammation. The end result of inflammation is varied in different systems. So it is hypothesized that inflammation in various organs lead to diseases like diabetes mellitus, hypertension, liver disease, kidney disease, etc which are known to be associated with psoriasis. All these informations put together will lead to the new concept of ‘psoriatic disease’ instead of psoriasis. This new concept will help us to see psoriasis in a wider perspective and hence to reduce various adverse events occurring in patients with psoriatic and to improve the quality of life of them.

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2. Fox H . Dermatology of ancients . JAMA 1915; 65 :469.
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14. Ritchin C. Psoriatic arthritis , B . Pathology and pathogenesis. In Klippel J A eds. Primer on the Rheumatic Diseases. Springer Ed, New York 2008 : 178 -184.
15. Scarpa R, Altomare G, Marchesoni A, Balato N, Cerininc M M, Lotti T, Oliveri I, Vena GA, Salvasani C, Valesini G, Giannetti A. Psoriatic disease : concepts and implications JEADV 2010; 24 : 627 630.
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17. Henseler T, Christophers E. Disease concomitance in psoriasis . J Am Acad Dermatol 2006; 32 : 982 -986.
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