Insulin resistance and hyperinsulinemia in homozygous β-thalassemia

Cavallo‐Perin, P.; Pacini, Giovanni; Cerutti, Fránco; A, Bessone; Condo, Carmen; Sacchetti, L; Piga, Antonio; Pagano, Gianfranco

doi:10.1016/0026-0495(95)90155-8

Cited by 80 publications

(51 citation statements)

References 22 publications

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“…Insulin resistance may come from iron deposition in both liver (where iron deposits may interfere with insulin's ability to suppress hepatic glucose production) and muscle (where iron deposits may decrease glucose uptake because of muscle damage) (12). Persistent insulin resistance along with a progressive reduction in circulating insulin levels may lead to glucose intolerance and overt diabetes (36).…”

Section: Risk Factors For Abnormal Glucose Tolerancementioning

confidence: 99%

Abnormal Glucose Tolerance in Transfusion-Dependent β-Thalassemic Patients

Chern

Lin

et al. 2001

Diabetes Care

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OBJECTIVE -To study the prevalence of and risk factors for abnormal glucose tolerance in transfusion-dependent ␤-thalassemic patients.RESEARCH DESIGN AND METHODS -A total of 89 transfusion-dependent ␤-thalassemic patients were interviewed. Diabetes was previously diagnosed in 14 of them. In the remaining 75 patients, 68 participated in an oral glucose tolerance test. Potential risk factors were identified using the independent t test, 2 test, and Fisher's exact test. Logistic regression analysis was used to select the independent risk factors that best predicted abnormal glucose tolerance. A two-tailed P value of Ͻ0.05 was considered to be statistically significant.RESULTS -The prevalence of impaired glucose tolerance was 8.5% (7 of 82) and that of diabetes was 19.5% (16 of 82). Presentation with diabetic ketoacidosis was 31.1% (5 of 16). The risk factors for abnormal glucose tolerance found in transfusion-dependent ␤-thalassemic patients were serum ferritin concentration and hepatitis C infection.

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Section: Risk Factors For Abnormal Glucose Tolerancementioning

confidence: 99%

Abnormal Glucose Tolerance in Transfusion-Dependent β-Thalassemic Patients

Chern

Lin

et al. 2001

Diabetes Care

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“…Dmochowski et al (25) reported that serum concentrations of ferritin were negatively correlated with insulin sensitivity (r ϭ Ϫ0.58) in subjects with hemosiderosis. Cavallo-Perin et al (26) reported that insulin sensitivity, which correlated closely with iron overload (r ϭ Ϫ0.70), was reduced by 40% in thalassemia patients. Insulin resistance also appeared to be closely linked to total body iron stores in the general population (21).…”

mentioning

confidence: 96%

“…Insulin resistance itself, assessed by either the euglycemic clamp (24) or the minimal model (25,26), was found to be associated with total body iron stores, even in the presence of normal glucose tolerance. Dmochowski et al (25) reported that serum concentrations of ferritin were negatively correlated with insulin sensitivity (r ϭ Ϫ0.58) in subjects with hemosiderosis.…”

mentioning

confidence: 97%

Cross-Talk Between Iron Metabolism and Diabetes

Fernández‐Real¹,

López‐Bermejo²,

Ricart³

2002

Diabetes

581

411

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Emerging scientific evidence has disclosed unsuspected influences between iron metabolism and type 2 diabetes. The relationship is bi-directional-iron affects glucose metabolism, and glucose metabolism impinges on several iron metabolic pathways. Oxidative stress and inflammatory cytokines influence these relationships, amplifying and potentiating the initiated events. The clinical impact of these interactions depends on both the genetic predisposition and the time frame in which this network of closely related signals acts. In recent years, increased iron stores have been found to predict the development of type 2 diabetes while iron depletion was protective. Iron-induced damage might also modulate the development of chronic diabetes complications. Iron depletion has been demonstrated to be beneficial in coronary artery responses, endothelial dysfunction, insulin secretion, insulin action, and metabolic control in type 2 diabetes. Here, we show that iron modulates insulin action in healthy individuals and in patients with type 2 diabetes. The extent of this influence should be tested in large-scale clinical trials, searching for the usefulness and cost-effectiveness of therapeutic measures that decrease iron toxicity. The study of individual susceptibility and of the mechanisms that influence tissue iron deposition and damage are proposed to be valuable in anticipating and treating diabetes complications. Diabetes 51:2348 -2354, 2002

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“…Patients with thalassemia may have insulin sensitivity reduced by 40%, with a close correlation ( r = −0.70) with iron status 24. Oxidative stress induced by iron may be partly responsible.…”

Section: Discussionmentioning

confidence: 99%

Acute cardiac decompensation in a patient with beta‐thalassemia and diabetes mellitus following cessation of chelation therapy

Lioudaki

Whyte

2016

Clinical Case Reports

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Key Clinical MessagePatients with higher liver iron stores are likely to have a worse cardiac outcome following noncompliance with chelation. Cardiovascular magnetic resonance identifies myocardial siderosis allowing optimization of iron chelation regimes. Diabetes puts thalassemic patients at increased risk of myocardial fibrosis. Dual chelation therapy with deferoxamine and deferiprone offers improved cardiac outcomes.

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Insulin resistance and hyperinsulinemia in homozygous β-thalassemia

Cited by 80 publications

References 22 publications

Abnormal Glucose Tolerance in Transfusion-Dependent β-Thalassemic Patients

Abnormal Glucose Tolerance in Transfusion-Dependent β-Thalassemic Patients

Cross-Talk Between Iron Metabolism and Diabetes

Acute cardiac decompensation in a patient with beta‐thalassemia and diabetes mellitus following cessation of chelation therapy

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