Systemic manifestations in chronic arsenic toxicity in absence of skin lesions in West Bengal.

BACKGROUND & OBJECTIVE: Pigmentation and keratosis are the prerequisites to diagnose arsenicosis. However, many systemic manifestations occur in association with pigmentation and keratosis in people exposed to chronic drinking of arsenic contaminated water. The present study aim to find out whether systemic manifestations occur in significant number of cases in arsenic exposed people in the absence of skin lesions in an affected district in West Bengal, India. METHODS: A cross-sectional study was carried out in South 24 Parganas, an arsenic affected district of West Bengal, India. Both dermatological and systemic manifestations were recorded and water samples collected for arsenic analysis from 7683 participants. A correlation of systemic manifestations in relation to arsenic exposure was carried out in subjects having no arsenical skin lesion. Prevalence odds ratio (POR) was calculated for each outcome comparing those with high arsenic exposure with those with lowest exposure. RESULTS: The frequency of occurrence of various clinical manifestations like weakness, anaemia, diarrhoea, hepatomegaly and lung disease was found to be significantly higher among participants drinking water having arsenic concentration > or = 50 microg/l in comparison to those taking water with arsenic content below this level. Further, there was increased occurrence of these manifestations with increasing concentration of arsenic level in drinking water, and this followed a dose-response relationship. INTERPRETATION & CONCLUSION: It appears that it is worthwhile to include people with systemic manifestations in absence of skin lesions with evidence of arsenic exposure as suspected cases of arsenicosis for case detection and in surveillance programme.

Chronic arsenic toxicity & human health.

Chronic arsenic toxicity (arsenicosis) due to drinking of arsenic contaminated ground water is a major environmental health hazard throughout the world including India. A lot of new information is emerging from extensive research on health effects of chronic arsenic toxicity (CAT) in humans during the last two decades. Available literature has been reviewed to highlight the problem including its malignancies. Pigmentation and keratosis are the specific skin lesions characteristics of CAT. CAT also produces various systemic manifestations over and above skin lesions, important ones being chronic lung disease like chronic bronchitis, chronic obstructive pulmonary disease and bronchiectasis, liver disease like non-cirrhotic portal fibrosis and other diseases like polyneuropathy, peripheral vascular disease, hypertension and ischeamic heart disease, diabetes mellitus, non-pitting oedema of feet/hands, weakness and anaemia. Cancer of skin, lung and urinary bladder are important cancers associated with chronic arsenic toxicity. Stoppage of drinking of arsenic contaminated water is the main stay in the management of arsenicosis as specific chelation therapy has limited value. Early skin cancer, detectable by regular active surveillance, is curable. In addition to dermatological features, CAT produces protean clinical manifestations. Treatment of arsenicosis is unsatisfactory and is mostly symtomatic.

Arsenic and liver disease.

The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognised. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. The nature and degree of liver involvement are reported on the basis of hospital based studies in patients who consumed arsenic contaminated drinking water for one to 15 years. Two hundred forty-eight patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examination including liver function tests and hepatitis B surface antigen (HBsAg) status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. Hepatomegaly was present in 190 of 248 patients (76.6%). Non-cirrhotic portal fibrosis was the predominant lesion (91.3%) in liver histology. The maximum arsenic content in liver was 6 mg/kg (mean 1.46 [0.42], control value 0.16 [0.04]; p <0.001); it was undetected in 6 of 29 samples studied. The largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic contaminated water are reported. Non-cirrhotic portal fibrosis is the predominant lesion in this population. Hepatic fibrosis has also been demonstrated due to long term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferases elevated at 12 months and hepatic fibrosis at 15 months.

Hepatic manifestations in chronic arsenic toxicity.

OBJECTIVE: The hepatotoxic action of arsenic, when used as a therapeutic agent, has long been recognized. Data on liver involvement following chronic exposure to arsenic-contaminated water are scanty. We report the nature and degree of liver involvement on the basis of hospital-based and cohort follow-up studies in patients who consumed arsenic-contaminated drinking water for 1 to 15 years. METHODS: 248 patients with evidence of chronic arsenic toxicity underwent clinical and laboratory examinations including liver function tests and HBsAg status. Liver biopsy was done in 69 cases; in 29 patients, liver arsenic content was estimated by neutron activation analysis. A cohort follow up of 23 patients who took arsenic-free water for 2-12 years was also carried out. RESULTS: Hepatomegaly was present in 190 of 248 patients (76.6%). Noncirrhotic portal fibrosis (91.3%) was the predominant lesion in liver histology. The maximum arsenic content in liver was 6 mg/Kg (mean 1.46 [0.42], control value 0.16 [0.04]; p < 0.001); it was undetected in 6 of 29 samples studied. Cohort follow-up studies showed elevation of globulin in four cases and development of esophageal varices in one case. CONCLUSION: We report the largest number of patients with liver disease due to chronic arsenicosis from drinking arsenic-contaminated water. Noncirrhotic portal fibrosis is the predominant lesion in this population.

Objective evaluation of psychological abnormality in irritable bowel syndrome.

BACKGROUND: Irritable bowel syndrome (IBS) is frequently regarded as a psychological disorder. Data on objective evaluation of psychological abnormalities among IBS patients and control subjects are scanty in our country. We therefore objectively studied patients with IBS. METHODS: 42 patients satisfying the Manning's criteria and Munich workers' for diagnosis of IBS underwent psychological evaluation using the following tests: a) Eyesenck personality questionnaire. b) State and trait anxiety inventory according to Speilberger's method. c) Hamilton depression rating scale for detection of depression. d) Whitely index of hypochondriasis and discriminant function by Pilowsky's illness behavior questionnaire. RESULTS: Neuroticism was detected in 76% of IBS patients compared to 9% in control population (p < 0.01). State and trait anxiety scores were 44.5 +/- 17.1 and 49.0 +/- 15.3 respectively in IBS patients; these were higher than those in controls (35.5 +/- 7.5 and 41.2 +/- 6.1 respectively; p < 0.01). Severe depression was observed in 26% of IBS patients and 6% of control subjects (p < 0.05). Significantly higher hypochondriasis score was observed in IBS patients as compared to controls (p < 0.001). CONCLUSION: Neuroticism, hypochondriasis and depression were significantly more prevalent in IBS patients attending a clinic, compared to control population.

Histological changes in hamster liver by ES antigen of Ascaris suum.

Polyacrylamide gel electrophoresis with SDS (PAGE-SDS) of the ES antigens of A. suum revealed several protein molecules which differed from those obtained in ES antigens of A. lumbricoides. Nature of liver damage caused by ES antigens of A. suum was studied in hamsters to find out the nature of damage and to compare with those caused by ES antigens of A. lumbricoides. Feeding of ES antigens of A. suum was carried out in 7 hamsters for 75 days. After such feeding gross hepatic damage was noticed. This was characterized by pericentrivenular degeneration and necrosis of liver parenchyma, the lesions being different and much more severe than those observed in hamster challenged by ES products of A. lumbricoides. The lesions appear to be immune mediated.