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1.
Indian J Dermatol Venereol Leprol ; 2011 Mar-Apr; 77(2): 238-243
Article in English | IMSEAR | ID: sea-140824
2.
Indian J Dermatol Venereol Leprol ; 2010 Nov-Dec; 76(6): 718-720
Article in English | IMSEAR | ID: sea-140745
3.
Indian J Dermatol Venereol Leprol ; 2010 Mar-Apr; 76(2): 103-115
Article in English | IMSEAR | ID: sea-140564

ABSTRACT

Diet has an important role to play in many skin disorders, and dermatologists are frequently faced with the difficulty of separating myth from fact when it comes to dietary advice for their patients. Patients in India are often anxious about what foods to consume, and what to avoid, in the hope that, no matter how impractical or difficult this may be, following this dictum will cure their disease. There are certain disorders where one or more components in food are central to the pathogenesis, e.g. dermatitis herpetiformis, wherein dietary restrictions constitute the cornerstone of treatment. A brief list, although not comprehensive, of other disorders where diet may have a role to play includes atopic dermatitis, acne vulgaris, psoriasis vulgaris, pemphigus, urticaria, pruritus, allergic contact dermatitis, fish odor syndrome, toxic oil syndrome, fixed drug eruption, genetic and metabolic disorders (phenylketonuria, tyrosinemia, homocystinuria, galactosemia, Refsum's disease, G6PD deficiency, xanthomas, gout and porphyria), nutritional deficiency disorders (kwashiorkar, marasmus, phrynoderma, pellagra, scurvy, acrodermatitis enteropathica, carotenemia and lycopenemia) and miscellaneous disorders such as vitiligo, aphthous ulcers, cutaneous vasculitis and telogen effluvium. From a practical point of view, it will be useful for the dermatologist to keep some dietary information handy to deal with the occasional patient who does not seem to respond in spite of the best, scientific and evidence-based therapy.

4.
Indian J Dermatol Venereol Leprol ; 2009 Jul-Aug; 75(4): 348-355
Article in English | IMSEAR | ID: sea-140382

ABSTRACT

Dermatitis cruris pustulosa et atrophicans (DCPA) is a distinctive type of chronic superficial folliculitis, primarily affecting the lower limbs. It is characterized by symmetrical follicular pustules of both legs, with cutaneous edema, resulting in alopecia, atrophy and scarring. It was first described by Clarke, from West Nigeria, in 1952 and well illustrated in his book "Skin diseases in the African," under the initial label of "Nigerian shin disease." Subsequently, it was described in India as well, in 1964, and continues to be a problem in dermatology clinics across the country. It is predominantly a disease of men and has a high prevalence in some geographical regions; up to 3-4% in Madras, South India. Some unique features that distinguish DCPA from banal pustular folliculitis include its peculiar localization to the legs, extreme chronicity, resistance to therapy and inevitable alopecia and atrophy of the involved skin, with little postinflammatory hyper- or hypopigmentation. Further, even in the presence of extensive lesions, there are no systemic features. Coagulase-positive Staphylococcus aureus is known to have a role in the etiology of DCPA, but the exact etiopathogenesis still needs to be elucidated. Immunological postulates such as hypergammaglobulinemia have been put forward to explain the chronicity of the condition. A number of therapeutic agents have been tried in various studies, including cotrimoxazole, psoralen with ultraviolet A (PUVA) therapy, ciprofloxacin, pentoxifylline, rifampicin, dapsone, minocycline and mupirocin (topical) with variable success rates. Although a well-recognized entity in dermatology clinics in tropical countries, DCPA has received little attention in the dermatological literature and has only a few studies to its credit. Its unique clinical picture, unclear etiopathogenesis and resistance to therapy afford a vast scope for further investigation and study.

5.
Indian J Dermatol Venereol Leprol ; 2009 Mar-Apr; 75(2): 126-35
Article in English | IMSEAR | ID: sea-52818

ABSTRACT

Leprosy is unique in terms of the nature of the causative organism (Mycobacterium leprae), the chronicity of the disease, its prolonged treatment and the definitions of "cure" and "relapse." The principal mode of assessing the efficacy of therapeutic regimens in leprosy is the "relapse rate." There are wide variations in estimates of relapse rates after the World Health Organization (WHO) multidrug therapy in different regions. The important predisposing factors for relapse include the presence of "persister" bacilli, monotherapy, inadequate/irregular therapy, presence of multiple skin lesions/thickened nerves and lepromin negativity. The conventional methods of confirming activity or relapse in an infectious disease (demonstration and/or culture of the etiologic agent) have limited utility in leprosy because of the difficulty in demonstrating bacilli in paucibacillary (PB) cases and absence of a method of in vitro cultivation of M. leprae. Bacteriological parameters are useful in multibacillary (MB) leprosy, whereas in PB leprosy, the criteria for relapse depend primarily on clinical features. Although there are no widely available serologic tests for leprosy other than in a research setting, various immunological tests may be useful for monitoring patients on chemotherapy as well as for confirming suspected cases of relapse. The main differential diagnoses for relapse are reversal reactions, erythema nodosum leprosum and reactivation/resistance/reinfection. The most reliable criteria for making an accurate diagnosis of relapse include clinical, bacteriological and therapeutic criteria. Additional ones that may be used, depending on the setting, are histopathological and serologic criteria. Relapsed cases of leprosy should be identified and put back on chemotherapy as soon as possible to prevent further disability and transmission of infection. Factors that should be considered in choosing an appropriate regimen are the type of leprosy (PB or MB), previous treatment and drug resistance. Occasionally, clinicians may need to use their judgement to modify the standard WHO treatment regimens according to the scenario in each patient.

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