IADVL
Indexed with PubMed and Science Citation Index (E) 
 
Users online: 4971 
     Home | Feedback | Login 
About Current Issue Archive Ahead of print Search Instructions Online Submission Subscribe What's New Contact  
  NAVIGATE Here 
    Next article
    Previous article
    Table of Contents

 RESOURCE Links
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
  Related articles
    Citation Manager
    Access Statistics
    Reader Comments
    Email Alert *
    Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed13585    
    Printed330    
    Emailed8    
    PDF Downloaded800    
    Comments [Add]    
    Cited by others 18    

Recommend this journal

 

 SEMINAR: CHRONIC ARSENICOSIS IN INDIA
Year : 2008  |  Volume : 74  |  Issue : 6  |  Page : 559--570

Pathogenesis, clinical features and pathology of chronic arsenicosis


1 Department of Dermatology, IPGMER and SSKM Hospital, Kolkata, India
2 Department of Dermatology, Medical College, Kolkata, India

Correspondence Address:
Nilay Kanti Das
Devitala Road, Majerpara, Ishapore, 24 Pgs (N), West Bengal-743 144
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0378-6323.45097

Rights and Permissions

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-β, TNF-α, 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.






[FULL TEXT] [PDF]*


        
Print this article     Email this article

Online since 15th March '04
Published by Wolters Kluwer - Medknow