Arsenic Intoxication Presenting with Macrocytosis and Peripheral Neuropathy, without Anemia

Heaven, Ralph; Duncan, Max; Vukelja, Svetislava J.

doi:10.1159/000204205

Cited by 16 publications

(6 citation statements)

References 5 publications

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“…Various case reports and studies have revealed that exposure to As has resulted in various forms of cancer and peripheral neuropathy. 7,17,18 Acute and chronic exposure to As Acute A single exposure to a high dose may lead to severe reactions such as diarrhea, vomiting, pain, dehydration and weakness. Nowadays, acute intoxication rarely occurs in western European countries; if it occurs, it is usually the result of intentional (suicide or homicide) or accidental poisoning.…”

Section: Introductionmentioning

confidence: 99%

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Arsenic neurotoxicity — A review

2007

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Arsenic (As) is one of the oldest poisons known to men. Its applications throughout history are wide and varied: murder, make-up, paint and even as a pesticide. Chronic As toxicity is a global environmental health problem, affecting millions of people in the USA and Germany to Bangladesh and Taiwan. Worldwide, As is released into the environment by smelting of various metals, combustion of fossil fuels, as herbicides and fungicides in agricultural products. The drinking water in many countries, which is tapped from natural geological resources, is also contaminated as a result of the high level of As in groundwater. The environmental fate of As is contamination of surface and groundwater with a contaminant level higher than 10 particle per billion (ppb) as set by World Health Organization (WHO). Arsenic exists in both organic and inorganic species and either form can also exist in a trivalent or pentavalent oxidation state. Long-term health effects of exposure to these As metabolites are severe and highly variable: skin and lung cancer, neurological effects, hypertension and cardiovascular diseases. Neurological effects of As may develop within a few hours after ingestion, but usually are seen in 2—8 weeks after exposure. It is usually a symmetrical sensorimotor neuropathy, often resembling the Guillain—Barré syndrome. The predominant clinical features of neuropathy are paresthesias, numbness and pain, particularly in the soles of the feet. Electrophysiological studies performed on patients with As neuropathy have revealed a reduced nerve conduction velocity, typical of those seen in axonal degeneration. Most of the adverse effects of As, are caused by inactivated enzymes in the cellular energy pathway, whereby As reacts with the thiol groups of proteins and enzymes and inhibits their catalytic activity. Furthermore, As-induced neurotoxicity, like many other neurodegenerative diseases, causes changes in cytoskeletal protein composition and hyperphosphorylation. These changes may lead to disorganization of the cytoskeletal framework, which is a potential mechanism of As-induced neurotoxicity. Human & Experimental Toxicology (2007) 26, 823— 832

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Section: Introductionmentioning

confidence: 99%

“…Various case reports and studies have revealed that exposure to As has resulted in various forms of cancer and peripheral neuropathy. 7,17,18…”

Section: Introductionmentioning

confidence: 99%

Arsenic neurotoxicity — A review

2007

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“…Chronic arsenic toxicity is characterized by macrocytosis, pancytopenia, hyperkeratotic lesions noted on the extremities, hyperpigmented melanosis described as "raindrops in the dust", bronze pigmentation, GI symptoms, anemia, and liver disease [6,27,28]. In addition, Mees' lines -transverse white striae on the fingernails (Fig.…”

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confidence: 99%

“…In addition, Mees' lines -transverse white striae on the fingernails (Fig. 1), a sensation of a metallic taste [6] and peripheral neuropathy have all been characterized in chronic arsenic exposure [27].…”

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confidence: 99%

Heavy metal poisoning: management of intoxication and antidotes

Rusyniak

Arroyo

Acciani

et al. 2010

Experientia Supplementum

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Abstract. Of the known elements, nearly 80% are either metals or metalloids. The highly reactive nature of most metals result in their forming complexes with other compounds such oxygen, sulfide and chloride. Although this reactivity is the primary means by which they are toxic, many metals, in trace amounts, are vital to normal physiological processes; examples include iron in oxygen transport, manganese and selenium in antioxidant defense and zinc in metabolism. With these essential metals toxicity occurs when concentrations are either too low or too high. For some metals there are no physiological concentrations that are beneficial; as such these metals only have the potential to cause toxicity. This chapter focuses on four of these: arsenic, mercury, lead and thallium.

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“…Previous studies found that cutaneous papillomatosis in camels and cattle resulted in substantial alterations in the hematological parameters, including a significant decrease in total erythrocytes count, Hb concentration, and PCV [ 8 , 23 ]. The development of anemia associated with papillomatosis may be attributed to the marked off-food as disease sequelae or due to the variety of cytokines involved in the chronic inflammatory process [ 29 ]. BP causes neutropenia, lymphopenia, and consequently, the development of leucopenia due to its action to form the circulating leucocytes and/or release endogenous corticosteroids in response to stress [ 30 ].…”

Section: Discussionmentioning

confidence: 99%

Regression of bovine cutaneous papillomas via ivermectin-induced immunostimulant and oxidative stress

Saied

2021

J Adv Vet Anim Res

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Objective: Ivermectin (IVM) could be used effectively to treat bovine cutaneous papillomatosis, a widespread viral skin disease that causes major economic losses in cattle. This study aimed to evaluate the regression of bovine cutaneous papillomas induced by IVM by estimating oxidative stress markers, besides clinicopathological and hematological findings. Materials and Methods: Twenty naturally infected animals with cutaneous papillomatosis were chosen randomly and diagnosed clinically and histopathologically. All the infected animals were divided into groups: Group I ( n = 10), which received no treatment and was considered the control group. In Group II ( n = 10), the animals were subcutaneously injected at 0.2 mg/kg of IVM 2 weeks apart during the 90-day experimental period. Papilloma regression was tracked clinically, papilloma biopsies were taken for histopathological analysis, and blood samples were taken for hematological and oxidative parameter testing. Results: From the 15th to 45th day after receiving IVM, papillomas began to fade. Necrotic areas, ulcerations, and lymphocytic infiltration were found in the histopathological studies, besides a decrease in papilloma epidermal proliferation. total erythrocytes count, packed cell volume, total leucocytes count, and lymphocytes values were increased significantly, and a large decrease in glutathione peroxidase and glutathione reduced was identified as signs of IVM-induced oxidative stress. Conclusion: IVM has oxidative and immunostimulatory properties, and it can be used against cutaneous papillomatosis.

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Arsenic Intoxication Presenting with Macrocytosis and Peripheral Neuropathy, without Anemia

Cited by 16 publications

References 5 publications

Arsenic neurotoxicity — A review

Arsenic neurotoxicity — A review

Heavy metal poisoning: management of intoxication and antidotes

Regression of bovine cutaneous papillomas via ivermectin-induced immunostimulant and oxidative stress

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