Postarsenical obstructive jaundice complicated by xanthomatosis and diabetes mellitus

Stolzer, Bertrand L.; Miller, George H.; White, William A.; Zuckerbrod, Morris

doi:10.1016/0002-9343(50)90014-3

Cited by 40 publications

(7 citation statements)

References 11 publications

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“…These include the antibiotics chlortetracycline, 93 97 erythromycin estolate, 98 ' 100 and other antimicrobial agents. Most prominent among the latter are triacetyloleandomycin, 99 · 101 · 102 para-aminosalicylic acid, 19 · 22 · 103 · 104 pyrazinamide, 108 organic arsenical preparations, [106][107][108] sulfonamides, 109114 and the sulfones. 115 The effects of antibiotics on the liver are discussed in detail by Ticktin and Robinson in this publication.…”

Section: Antimicrobial Agentsmentioning

confidence: 99%

“…In several instances a reversible syndrome resembling that of primary biliary cirrhosis has been reported to follow arsenical jaundice. 107 The entity of arsenical jaundice is of less immediate clinical importance than it was when first reported, but the report by Hanger and Gutman of the first clearly recognized instance of hepatocanalicular jaundice ap parently caused by drug allergy remains as a model of a careful study of drug hepatotoxicity.…”

Section: · 10°mentioning

confidence: 99%

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Clinical and Laboratory Manifestations of Hepatotoxicity

Zimmerman

1963

Annals of the New York Academy of Sciences

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Section: Antimicrobial Agentsmentioning

confidence: 99%

Section: · 10°mentioning

confidence: 99%

Clinical and Laboratory Manifestations of Hepatotoxicity

Zimmerman

1963

Annals of the New York Academy of Sciences

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“…arsphenamine (Salvarsan) treatment was documented as developing type 2 diabetes (Stolzer et al , 1950). Beginning in the 1990s, epidemiological studies in Bangladesh (Rahman et al , 1998), Taiwan (Lai et al , 1994), Mexico (Coronado-Gonzalez et al , 2007) and Sweden (Rahman and Axelson, 1995; Rahman et al , 1996) have consistently demonstrated a dose-response relationship between exposure to arsenic, (total arsenic or the inorganic arsenicals (Asi) arsenite and arsenate) from contaminated drinking water or in the workplace, and an increased risk of type 2 diabetes.…”

mentioning

confidence: 99%

Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

Hill

Wlodarczyk

Mitchell

et al. 2009

Toxicology and Applied Pharmacology

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Background Epidemiological studies have linked environmental arsenic (As) exposure to increased type 2 diabetes risk. Periconceptional hyperglycemia is a significant risk factor for neural tube defects (NTDs), the second most common structural birth defect. A suspected teratogen, arsenic (As) induces NTDs in laboratory animals. Objectives We investigated whether maternal glucose homeostasis disruption was responsible for arsenate-induced NTDs in a well-established dosing regimen used in studies of arsenic’s teratogenicity in early neurodevelopment. Methods We evaluated maternal intraperitoneal (I.P.) exposure to As 9.6 mg/kg (as sodium arsenate) in LM/Bc/Fnn mice for teratogenicity and disruption of maternal plasma glucose and insulin levels. Selected compounds (insulin pellet, sodium selenate (SS), N-acetyl cysteine (NAC), L-methionine (L-Met), N-tert-Butyl-α-phenylnitrone (PBN)) were investigated for their potential to mitigate arsenate’s effects. Results Arsenate caused significant glucose elevation during an I.P. glucose tolerance test (IPGTT). Insulin levels were not different between arsenate and control dams before (arsenate, 0.55 ng/dl; control, 0.48 ng/dl) or after glucose challenge (arsenate, 1.09 ng/dl; control, 0.81 ng/dl). HOMA-IR index was higher for arsenate (3.9) vs control (2.5) dams (p=0.0260). Arsenate caused NTDs (100%, p<0.0001). Insulin pellet and NAC were the most successful rescue agents, reducing NTD rates to 45% and 35%. Conclusions IPGTT, insulin assay, and HOMA-IR results suggest a modest failure of glucose stimulated insulin secretion and insulin resistance characteristic of glucose intolerance. Insulin’s success in preventing arsenate-induced NTDs provides evidence that these arsenate-induced NTDs are secondary to elevated maternal glucose. The NAC rescue, which did not restore maternal glucose or insulin levels, suggests oxidative disruption plays a role.

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“…This is somewhat surprising because arsenic exposure has been linked to type 2 diabetes since 1950 when a case report documented a patient developing type 2 diabetes after receiving intravenous arsenical treatment for sexually transmitted diseases. 6 However, research efforts on the role of arsenic in diabetogenesis did not intensify until populationbased epidemiologic studies published in the 1990s from Taiwan [7][8][9] and Bangladesh 10 demonstrated that chronic exposure to high levels of arsenic from drinking water is associated with a higher prevalence of type 2 diabetes.…”

mentioning

confidence: 99%

Environmental Arsenic Exposure and Diabetes

2013

Encyclopedia of Metalloproteins

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Postarsenical obstructive jaundice complicated by xanthomatosis and diabetes mellitus

Cited by 40 publications

References 11 publications

Clinical and Laboratory Manifestations of Hepatotoxicity

Clinical and Laboratory Manifestations of Hepatotoxicity

Arsenate-induced maternal glucose intolerance and neural tube defects in a mouse model

Environmental Arsenic Exposure and Diabetes

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