Diagnosis of arsenicosis relies on both clinical and laboratory criteria, but principally it can be diagnosed on the basis of its cutaneous manifestations. Cutaneous manifestations (melanosis, keratosis, and cutaneous cancers) are essential clues in the diagnosis, and trained dermatologists or arsenic experts are able to clinically confirm a case even without laboratory backup. Although systemic manifestations are not considered as diagnostic hallmarks, yet their presence serves as important telltale signs in arriving at the diagnosis. In countries where laboratory facilities are available, measuring the level of arsenic in drinking water (consumed in the last 6 months), urine, hair, and nails is of immense value. Newer biomarkers of arsenic exposure are being explored to provide early information about arsenic intoxication, of which urinary porphyrin level, blood metallothionein have shown promising results. Controlling the problem of arsenicosis depends on various factors, of which the most important is cessation of intake of arsenic-contaminated water. Deep wells, traditional dug wells, treatment of surface water, rainwater harvesting, and removing arsenic from the contaminated water by arsenic removal plant or arsenic treatment unit are the available options for providing arsenic-free drinking water. The role of nutrition and antioxidants in preventing the onset of symptoms of arsenicosis is also of importance. Nonspecific therapies (e.g., keratolytics for hyperkeratosis) cannot also be ignored and serve as palliative measures. The persons affected need to be followed up at regular intervals to detect the onset of cancers (if any) at the earliest. Role of counseling and education should never be underestimated since absence of public awareness can undermine all efforts of mitigation measures.

Background:Onychomycosis manifests itself in various forms, notably onychodystrophy, onycholysis, subungual hyperkeratosis, or nail-plate discoloration. Not necessarily nail changes mentioned here should always be of fungal origin.Objective:The present study is planned to get an idea about etiological agent and clinical correlation in fingernail onychomycosis.Materials and Methods:Nail-clipping and subungual debris of patients with above mentioned nail changes were subjected to KOH preparation. Culture was done on SDA and SDCCA media. Species identification was done by colony character, pigment production, LCB staining, and some special tests like germ tube test, etc.Results:Out of 85 cases, 44 cases showed the growth of fungus, amounting to 51.76% positivity. Among those 44 cases, the infective fungal agents were predominantly dermatophytes (50%), and the rest were due to yeasts (27.27%) and moulds (22.72%). Among the different species, Trichophyton rubrum (29.54%) accounted for the majority of dermatophytes; Candida albicans (11.78%) was the predominant yeast; and Aspergillus niger (18.18%) the commonest mold. No significant association could be established between the different fungal species and various clinical manifestations. Positive results were found more with fungal culture (95.45%) than KOH preparation (63.64%).Conclusion:The results show that nail changes are not always a reliable marker for predicting the causative organism, and relying only on the clinical manifestation (i.e., pattern of nail changes) in the diagnosis of onychomycosis is often misleading. The present study highlights the need for microbiological confirmation in case of onychomycosis.

Arsenicosis is a multisystem disorder, with virtually no system spared from its vicious claw; though its predominant manifestations are linked to cutaneous involvement. Cutaneous effects take the form of pigmentary changes, hyperkeratosis, and skin cancers (Bowen's disease, squamous cell carcinoma, and basal cell epithelioma). Peripheral vascular disease (blackfoot disease), hypertension, ischemic heart disease, noncirrhotic portal hypertension, hepatomegaly, peripheral neuropathy, respiratory and renal involvement, bad obstetrical outcome, hematological disturbances, and diabetes mellitus are among the other clinical features linked to arsenic toxicity. The effects are mediated principally by the trivalent form of arsenic (arsenite), which by its ability to bind with sulfhydryl groups present in various essential compounds leads to inactivation and derangement of body function. Though the toxicities are mostly linked to the trivalent state, arsenic is consumed mainly in its pentavalent form (arsenate), and reduction of arsenate to arsenite is mediated through glutathione. Body attempts to detoxify the agent via repeated oxidative methylation and reduction reaction, leading to the generation of methylated metabolites, which are excreted in the urine. Understandably the detoxification/bio-inactivation process is not a complete defense against the vicious metalloid, and it can cause chromosomal aberration, impairment of DNA repair process, alteration in the activity of tumor suppressor gene, etc., leading to genotoxicity and carcinogenicity. Arsenic causes apoptosis via free radical generation, and the cutaneous toxicity is linked to its effect on various cytokines (e.g., IL-8, TGF-beta, TNF-alpha, GM-CSF), growth factors, and transcription factors. Increased expression of cytokeratins, keratin-16 (marker for hyperproliferation) and keratin-8 and -18 (marker for less differentiated epithelial cells), can be related to the histopathological findings of hyperkeratosis and dysplastic cells in the arsenicosis skin lesion.

Background:Lupus erythematosus (LE) is an autoimmune disorder with diverse clinical manifestation ranging from mild cutaneous disorder to life-threatening systemic illness (SLE). In some patients, it remains to persist in the skin-limited form while in others it evolves into SLE. Here comes the role of identifying the markers of systemic involvement, which could determine the course and prognosis of the disease.Aim:To identify those manifestations that could be used to identify the activity of the disease SLE.Materials and Methods:An institution based, descriptive, cross-sectional study carried out over 1 year period. Sixty patients (male : female 1 : 4) with cutaneous LE were recruited for the study. The patients were classified in two groups depending on the presence or absence of ARA criteria of SLE. Detailed account of LE-specific and nonspecific lesions were noted. Statistical significance of the results was compared between the two groups using the chi-square test.Results:Among the different cutaneous manifestations, highly significant (P value <0.001) was found between SLE and nonscarring alopecia, photosensitivity, oral ulcer, malar rash (in decreasing order of odds favoring the association with SLE). Dimorphic skin lesions (P value=0.0326) also showed significant association where as discoid lesion (especially localized variant) predicted toward a skin limited form of the disease with high probability of not developing SLE (P value <0.0001). No significant association was found between SLE and papulosquamous lesions, Raynaud's phenomenon or scarring alopecia.Conclusion:Identification of lesions with high degree of association with SLE can alert the physician of the unfavorable prognosis and allow timely intervention and institution of appropriate management strategies.

Arsenicosis is a global problem but the recent data reveals that Asian countries, India and Bangladesh in particular, are the worst sufferers. In India, the state of West Bengal bears the major brunt of the problem, with almost 12 districts presently in the grip of this deadly disease. Recent reports suggest that other states in the Ganga/Brahmaputra plains are also showing alarming levels of arsenic in ground water. In West Bengal, the majority of registered cases are from the district of Nadia, and the maximum number of deaths due to arsenicosis is from the district of South 24 Paraganas. The reason behind the problem in India is thought to be mainly geogenic, though there are instances of reported anthropogenic contamination of arsenic from industrial sources. The reason for leaching of arsenic in ground water is attributed to various factors, including excessive withdrawal of ground water for the purpose of irrigation, use of bio-control agents and phosphate fertilizers. It remains a mystery why all those who are exposed to arsenic-contaminated water do not develop the full-blown disease. Various host factors, such as nutritional status, socioeconomic status, and genetic polymorphism, are thought to make a person vulnerable to the disease. The approach to arsenicosis mitigation needs be holistic, sustainable, and multidisciplinary, with the 2 main pillars being health education and provision of 'arsenic-free water.' In the state of West Bengal, the drive for arsenic mitigation has been divided into 3 phases using various methods, including new hand pumps/tube wells at alternative deep aquifers, dug wells, arsenic removal plants, arsenic treatment units, as well as piped and surface water supply schemes. The methods have their own limitations, so it is intended that a pragmatic approach be followed in the arsenicosis prevention drive. It is also intended that the preventive measures be operationally and economically feasible for the people living in the affected areas.