Insulin-dependent diabetes mellitus following pentamidine therapy in a patient with AIDS

Liegl, U.; Bogner, Johannes R.; Goebel, Frank-Detlef

doi:10.1007/bf00577749

Cited by 16 publications

(3 citation statements)

References 10 publications

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“…6 The pentamidine mechanisms that cause hypoglycemia are not yet completely understood. 7 Experiments using both mice and rats suggest that pentamidine damages pancreatic β cells, causing hyperglycemia following hypoglycemia.…”

Section: Discussionmentioning

confidence: 99%

Consecutive hypoglycemia attacks induced by co-trimoxazole followed by pentamidine in a patient with acquired immunodeficiency syndrome

Okazaki

Nakamura

et al. 2018

Int J STD AIDS

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Both co-trimoxazole and pentamidine are used for the treatment of pneumocystis pneumonia (PCP) and are known to cause hypoglycemia as an adverse drug reaction. Here, we describe a rare case of a late-diagnosed female patient with acquired immunodeficiency syndrome (AIDS) who developed the first hypoglycemic attack as an adverse effect of co-trimoxazole, followed by a second hypoglycemic attack as an adverse effect of pentamidine. Physicians caring for patients with AIDS and PCP should be aware of possible hypoglycemia in patients with many risk factors.

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Section: Discussionmentioning

confidence: 99%

Consecutive hypoglycemia attacks induced by co-trimoxazole followed by pentamidine in a patient with acquired immunodeficiency syndrome

Okazaki

Nakamura

et al. 2018

Int J STD AIDS

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“…Many compounds have the potential to harm pancreatic beta-cells and disrupt glucose homeostasis in the human organism [ 1 ]. Such compounds include pharmaceuticals like pentamidine [ 2 ], or fluoxetine (SSRI antidepressant) [ 3 ] or saturated fatty acids palmitate [ 4 ], or stearate [ 5 ], and potentially also organochlorine pollutants, such as the now-banned pesticide DDT [ 6 , 7 ]. Even decades after most countries banned its use, DDT and its metabolites persist in the environment [ 8 , 9 ] and represent a threat to living organisms [ 10 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

Markers of acute toxicity of DDT exposure in pancreatic beta-cells determined by a proteomic approach

et al. 2020

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Many compounds have the potential to harm pancreatic beta-cells; organochlorine pollutants belong to those compounds. In this work, we aimed to find markers of acute toxicity of p,p‘-DDT exposure among proteins expressed in NES2Y human pancreatic beta-cells employing 2-D electrophoresis. We exposed NES2Y cells to a high concentration (150 μM, LC 96 after 72 hours) of p,p‘-DDT for 24 and 30 hours and determined proteins with changed expression using 2-D electrophoresis. We have found 22 proteins that changed their expression. They included proteins involved in ER stress (GRP78, and endoplasmin), mitochondrial proteins (GRP75, ECHM, IDH3A, NDUS1, and NDUS3), proteins involved in the maintenance of the cell morphology (EFHD2, TCPA, NDRG1, and ezrin), and some other proteins (HNRPF, HNRH1, K2C8, vimentin, PBDC1, EF2, PCNA, biliverdin reductase, G3BP1, FRIL, and HSP27). The proteins we have identified may serve as indicators of p,p‘-DDT toxicity in beta-cells in future studies, including long-term exposure to environmentally relevant concentrations.

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“…Many compounds have the potential to harm pancreatic beta-cells and disrupt glucose homeostasis in the human organism (1). Such compounds include pharmaceuticals like pentamidine (2), or fluoxetine (SSRI antidepressant) (3) or saturated fatty acids palmitate (4), or stearate (5); and potentially also organochlorine pollutants, such as the now-banned pesticide DDT (6, 7). Even decades after most of the countries banned its use, DDT and its metabolites persist in the environment (8, 9) and represent a threat to living organisms (10, 11).…”

Section: Introductionmentioning

confidence: 99%

Markers of Acute Toxicity in Pancreatic Beta-Cells Exposed to Lethal Doses of the Organochlorine Pollutant DDT Determined by a Proteomic Approach

Pavlíková

Šrámek

Jelínek

et al. 2020

Preprint

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Many compounds have the potential to harm pancreatic beta-cells; organochlorine pollutants belong to those compounds. In this work, we aimed to find markers of acute toxicity of p,p‘-DDT among proteins expressed in human pancreatic beta-cells NES2Y and visible at 2-D electrophoresis. We exposed NES2Y cells to a lethal dose of p,p‘-DDT (150 μM) for 24 hours and 30 hours and determined changes in protein expression using 2-D electrophoresis. We also stained the cells exposed to p,p‘-DDT to visualize the altered phenotype of the exposed cells. Among proteins with changed expression, we identified proteins involved in ER stress (GRP78, and endoplasmin), mitochondrial proteins (GRP75, ECHM, IDH3A, NDUS1, and NDUS3), proteins with potential to change the cell morphology (EFHD2, TCPA, NDRG1, and ezrin), and some other proteins (HNRPF, HNRH1, K2C8, vimentin, PBDC1, EF2, PCNA, biliverdin reductase, G3BP1, FRIL, and HSP27). These proteins can be used as markers of acute DDT toxicity.

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Insulin-dependent diabetes mellitus following pentamidine therapy in a patient with AIDS

Cited by 16 publications

References 10 publications

Consecutive hypoglycemia attacks induced by co-trimoxazole followed by pentamidine in a patient with acquired immunodeficiency syndrome

Consecutive hypoglycemia attacks induced by co-trimoxazole followed by pentamidine in a patient with acquired immunodeficiency syndrome

Markers of acute toxicity of DDT exposure in pancreatic beta-cells determined by a proteomic approach

Markers of Acute Toxicity in Pancreatic Beta-Cells Exposed to Lethal Doses of the Organochlorine Pollutant DDT Determined by a Proteomic Approach

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