Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic arsenic toxicity due to drinking arsenic-contaminated water has been one of the worst environmental health hazards affecting eight districts of West Bengal since the early eighties. Detailed clinical examination and investigation of 248 such patients revealed protean clinical manifestations of such toxicity. Over and above hyperpigmentation and keratosis, weakness, anaemia, burning sensation of eyes, solid swelling of legs, liver fibrosis, chronic lung disease, gangrene of toes, neuropathy, and skin cancer are some of the other manifestations. A cross-sectional survey involving 7683 participants of all ages was conducted in an arsenic-affected region between April 1995 and March 1996. Out of a population of 7683 surveyed, 3467 and 4216 people consumed water containing As below and above 0.05 mg/L, respectively. Except pain abdomen the prevalence of all other clinical manifestations tested (e.g., pigmentation, keratosis, hepatomegaly, weakness, nausea, lung disease and neuropathy) were found to be significantly higher in As exposed people (water As > 0.05 mg/L) compared to control population (water As level < 0.05 mg/L). The prevalence of pigmentation and keratosis, hepatomegaly, chronic respiratory disease and weakness rose significantly with increasing arsenic concentrations in drinking water. The respiratory effects were most pronounced in individuals with high arsenic water concentrations who also had skin lesion. Therapy with chelating agent DMSA was not found to be superior to placebo effect. However, therapy with DMPS caused significant improvement of clinical condition of chronic arsenicosis patients as evidenced by significant reduction of total clinical scores from 8.90 +/- 2.84 to 3.27 +/- 1.73; p < 0.0001. Efficacy of specific chelation therapy for patients suffering from chronic As toxicity has further need to be fully substantiated. However, supportive treatment could help in reducing many symptoms of the patients. Treatment in hospital with good nutritious diet has been found to reduce symptom score in a subset of placebo treated patients in West Bengal during the course of DMSA and DMPS trial. People should be advised to stop drinking As contaminated water or exposure to As from any other source. The various clinical manifestations should be treated symptomatically.
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PMID:Chronic arsenic toxicity: clinical features, epidemiology, and treatment: experience in West Bengal. 1263 24

We present a case history of a 24 years old male who developed autonomic dysfunction, intestinal pseudo-obstruction and anemia due to lead poisoning. Concomitant recording of blood levels of lead and autonomic function showed a gradual decline in blood lead level (98.8 microg/dL at week 0, 56 microg/dL at week 6, and 40 microg/dL at week 52) and gradual improvement in autonomic functions. Decrease in blood lead levels with DMSA (Meso-2, 3-dimercaptosuccinic acid) therapy showed improvement in autonomic functions. At week 0, the patient had severe loss of autonomic tone and autonomic reactivity which improved at week 6. At the 52nd week, most of the autonomic parameters had normalized except for the persistence of mild loss of parasympathetic reactivity.
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PMID:Autonomic dysfunction due to lead poisoning. 1711 13

We describe a case of lead poisoning in a worker after hand and forearm trauma with fracture of radius and multiple fractures of metacarpal bones and hand phalanges and tissue infiltration of lead oxide (PbO) paste. Orthopedic surgery was immediately performed. After 20 days the patient had abdominal colic pain episodes and severe stipsis and blood lead level (BLL) was 60 mcg/mL with urinary lead level (ULL) of 238 mcg/24 h. After mobilization test with calcium disodium edetate were observed a high increase of BLL (180 mcg/dL) and UBL (17,000 mcg/24h). An initial anemia was observed and became severe (Hb 7.6 g/dL). A NMR exam and echography showed forearm subcutaneous lead paste infiltration and the patient underwent to a second surgical debridement with local low temperature (5 degrees C) irrigation of saline and CaNa2EDTA made the removal of the hardened lead paste. The day after, oral succimer (DMSA) chelation treatment was started with recovery of lead poison.
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PMID:[A peculiar lead poisoning: a concern of team achievement]. 2340 45