Cases reported "Arsenic Poisoning"

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1/16. Arsenic-related bowen's disease, palmar keratosis, and skin cancer.

    Chronic arsenical intoxication can still be found in environmental and industrial settings. Symptoms of chronic arsenic intoxication include general pigmentation or focal "raindrop" pigmentation of the skin and the appearance of hyperkeratosis of the palms of the hands and soles of the feet. In addition to arsenic-related skin diseases including keratosis, bowen's disease, basal-cell-carcinoma, and squamous-cell carcinoma, there is also an increased risk of some internal malignancies. Arsenic-related diseases are common in areas of the world where the drinking water has a high arsenic content. In this paper, we describe a 35-year-old male patient who had arsenic-related keratosis, squamous-cell carcinoma in the palmar area of his left hand, and bowen's disease on his left thigh. The patient worked in a borax mine for 15 years, so he was exposed to arsenic in drinking water, airborne arsenic in his workplace, and had direct contact. The patient was treated for 11 months for arsenic-related keratosis until an axillary lymph node metastasis occurred; the lesion was excised and diagnosed to be malignant. bowen's disease was detected when the patient was being treated for cancer. No other malignancy was found. The patient is still receiving regular follow-up care.
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2/16. Arsenic toxicity from homeopathic treatment.

    Homeopathic medicine is commonly believed to be relatively harmless. However, treatment with improperly used homeopathic preparations may be dangerous. case reports: Case 1 presented with melanosis and keratosis following short-term use of Arsenic Bromide 1-X followed by long-term use of other arsenic-containing homeopathic preparations. Case 2 developed melanotic arsenical skin lesions after taking Arsenicum Sulfuratum Flavum-1-X (Arsenic S.F. 1-X) in an effort to treat his white skin patches. Case 3 consumed Arsenic Bromide 1-X for 6 days in an effort to treat his diabetes and developed an acute gastrointestinal illness followed by leukopenia, thrombocytopenia, and diffuse dermal melanosis with patchy desquamation. Within approximately 2 weeks, he developed a toxic polyneuropathy resulting in quadriparesis. Arsenic concentrations in all three patients were significantly elevated in integument tissue samples. In all three cases, arsenic concentrations in drinking water were normal but arsenic concentrations in samples of the homeopathic medications were elevated. CONCLUSION: Arsenic used therapeutically in homeopathic medicines can cause clinical toxicity if the medications are improperly used.
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3/16. Hepatic angiosarcoma presenting as hepatic rupture in a patient with long-term ingestion of arsenic.

    Hepatic angiosarcoma (HAS) is a rare primary mesenchymal malignancy of liver with close association to arsenic intoxication. Although the southwest coastal area of taiwan is well known for its prevalence of arsenic intoxication from drinking well water, few cases of HAS associated with arsenic ingestion have been reported. We report a case of HAS complicated by spontaneous hepatic rupture in a 68-year-old female farmer who presented with acute onset of abdominal pain and shock. The arsenic level in her drinking water had been found to be 0.12 ppm at her childhood home and 0.005 ppm at her residence from age 21 to 68 years. The total ingested arsenic was estimated to be 1.9 g, and the latent period was about 25 years with a weighted mean exposure of 0.12 mg/day. We also reviewed data collected by the National Cancer Registry Program from 1981 to 1999 and identified 25 additional reported cases. The median age of these patients was 55 years, and the male-to-female ratio was 1.9 (17:9). Whereas no case was found during this period in the blackfoot disease (BFD) endemic area, a hyperendemic area of arsenic intoxication in taiwan, this case demonstrates the existence of cases of HAS associated with exposure to high levels of arsenic near the BFD area in taiwan.
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4/16. Diphenylarsinic acid poisoning from chemical weapons in Kamisu, japan.

    We noted a new clinical syndrome with prominent cerebellar symptoms in apartment building residents in Kamisu, japan. The well that provided drinking water contained diphenylarsinic acid, a degradation product of diphenylcyanoarsine or diphenylchloroarsine, which were developed for use as chemical weapons, inducing severe vomiting and sneezing. Characteristics of diphenylarsinic acid poisoning include brainstem-cerebellar and cerebral symptoms. Mental retardation associated with brain atrophy in magnetic resonance images was evident in some infants. We must be vigilant to prevent or minimize the effects of further diphenylarsinic acid poisoning in japan or elsewhere.
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5/16. Acute arsenic poisoning in two siblings.

    We report a case series of acute arsenic poisoning of 2 siblings, a 4-month-old male infant and his 2-year-old sister. Each child ingested solubilized inorganic arsenic from an outdated pesticide that was misidentified as spring water. The 4-month-old child ingested a dose of arsenic that was lethal despite extraordinary attempts at arsenic removal, including chelation therapy, extracorporeal membrane oxygenation, exchange transfusion, and hemodialysis. The 2-year-old fared well with conventional therapy.
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6/16. Porocarcinoma in a patient with chronic arsenism and multiple bowen's disease: case report.

    BACKGROUND: Chronic arsenism with bowen's disease is often seen in patients who drink water containing a high level of arsenic. Inorganic arsenic has demonstrated an increased risk of skin cancer. OBJECTIVE: We present a rare case of porocarcinoma in a patient with chronic arsenism and multiple bowen's disease. methods: Report of a case and review of the literature. RESULTS: A case of porocarcinoma arising in a patient with chronic arsenism is presented. The tumor was completely excised by means of wide excision with a 5 mm free margin. The surgical defect was reconstructed with a rhombic flap. CONCLUSION: Chronic arsenism can induce various skin neoplasms, possibly including porocarcinoma.
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7/16. Persistent neuropathy and hyperkeratosis from distant arsenic exposure.

    The purpose of this case series is to assess long-term sequelae of arsenic exposure in a cohort acutely exposed to arsenic in drinking water from a well dug into a landfill containing arsenical pesticides. Ten of the 13 individuals (or next of kin) in the initial study agreed to participate in the follow-up study. Next of kin provided questionnaire data and released medical information on the three individuals who had died. The remaining seven cohort members were assessed by an interview, questionnaire, detailed physical examination and sensory nerve testing. Available medical records were obtained and reviewed. Sensory testing was performed using an automated electrodiagnostic sensory Nerve Conduction Threshold (sNCT) evaluation. Sensory complaints and electrodiagnostic findings consistent with polyneuropathy were found in a minority (3/7) of subjects 28 years after an acute toxic arsenic exposure. Two of the seven patients examined (1 of 3 with neuropathic findings) also had hyperkeratotic lesions consistent with arsenic toxicity and one of the patients had hyperpigmentation on their lower extremities possibly consistent with arsenic toxicity.
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8/16. Acute lead arsenate poisoning.

    Three cases of acute lead arsenate poisoning which occurred in south australia during a 12 month interval are described. The case reports demonstrate a number of features of the characteristic clinical syndrome which may follow ingestion of lead arsenate. The recommended management is immediate gastric lavage and subsequent chelation therapy with calcium EDTA and dimercaprol. Early gastric lavage may prevent significant lead absorption. However, arsenic acid (produced in the stomach when lead arsenate reacts with hydrochloric acid) is relatively water soluble and prompt gastric lavage is unlikely to prevent extensive arsenic absorption. It remains controversial as to whether chelation with dimercaprol prevents arsenical neuropathy.
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9/16. Acute arsenic intoxication from environmental arsenic exposure.

    Reports of acute arsenic poisoning arising from environmental exposure are rare. Two cases of acute arsenic intoxication resulting from ingestion of contaminated well water are described. These patients experienced a variety of problems: acute gastrointestinal symptoms, central and peripheral neurotoxicity, bone marrow suppression, hepatic toxicity, and mild mucous membrane and cutaneous changes. Although located adjacent to an abandoned mine, the well water had been tested for microorganisms only and was found to be "safe." Regulations for testing of water from private wells for fitness to drink are frequently nonexistent, or only mandate biologic tests for microorganisms. Well water, particularly in areas near mining activity, should be tested for metals.
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10/16. Acute arsenic intoxication.

    The diagnosis of acute arsenic poisoning should be considered in any patient presenting with severe gastrointestinal complaints. signs and symptoms include nausea, vomiting, colicky abdominal pain and profuse, watery diarrhea. hypotension, fluid and electrolyte disturbances, mental status changes, electrocardiographic abnormalities, respiratory failure and death can result. Quantitative measurement of 24-hour urinary arsenic excretion is the only reliable laboratory test to confirm arsenic poisoning. Treatment includes gastric emesis or lavage, chelation therapy, electrolyte and fluid replacement, and cardiorespiratory support.
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