- Email: [email protected]
Is the sickle cell trait a risk factor in patients with type 2 diabetes mellitus?
European Journal of Internal Medicine 16 (2005) 462 www.elsevier.com/locate/ejim
Letter to the Editor
Is the sickle cell trait a risk factor in patients with type 2 diabetes mellitus? Gabriela Bencaiova *, Alexander Krafft, Roland Zimmermann Department of Obstetrics, University Hospital Zurich, Frauenklinikstr. 10, CH-8091 Zurich, Switzerland Received 31 January 2005; received in revised form 3 February 2005; accepted 3 February 2005
Keywords: Sickle cell trait; Type 2 diabetes; Microvascular diabetic complications
We have read with great interest the paper by Ajayi and Kolawole published in the August 2004 issue of the European Journal of Internal Medicine [1]. The objective of the paper was to determine whether the sickle cell trait may adversely influence the expression of microvascular diabetic complications in Africans with type 2 diabetes. The sickle cell trait has generally been misconstrued as a benign condition. Yet, many isolated cases have shown its role as a co-factor for morbidity and mortality. Normally, in vivo sickling does not occur in sickle cell trait individuals. However, hypoxia, acidosis, dehydration, hyperosmolality, hypothermia, or elevated erythrocyte 2,3diphosphoglycerate levels may transform the sickle cell trait into a syndrome resembling sickle cell disease and, therefore, may contribute to development of a sickle cell crisis. Patients in sickle cell crisis have multiple indicators of an inflammatory response, including elevated white blood cell counts, C-reactive protein levels, and cytokines as well as activated monocytes, neutrophils, platelets, and endothelial cells in the circulation. A previous study showed that the degree of coagulation activation is the most important factor for impairment of this condition and parallels the degree of disease severity [2].
Since diabetic patients have increased blood viscosity, decreased red cell deformability, hyperfibrinogenemia, and increased red blood cell adhesion to vascular endothelium, this condition may transform a sickle cell trait into sickle cell disease with development of sickle cell crisis. This situation is changed with all anti-inflammatory, antiaggregation, and hemorheological therapy administered to diabetic patients. We therefore believe that patients with concurrent type 2 diabetes and sickle cell trait are predisposed to more frequent or severe diabetic microvascular complications. In our opinion, more studies are needed to clarify the role of the sickle cell trait as a risk factor for the development or impairment of diabetic complications.
References [1] Ajayi AA, Kolawole BA. Sickle cell trait and gender influence type 2 diabetic complications in African patients. Eur J Intern Med 2004; 15:312 – 5. [2] Westerman MP, Green D, Gilman-Sachs A, Beaman K, Freels S, Boggio L, et al. Coagulation changes in individuals with sickle cell trait. Am J Hematol 2002;69:89 – 94.
* Corresponding author. Tel.: +41 1 255 5131; fax: +41 1 255 4430. E-mail address: [email protected] (G. Bencaiova). 0953-6205/$ - see front matter D 2005 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2005.02.016
Letter to the Editor
Is the sickle cell trait a risk factor in patients with type 2 diabetes mellitus? Gabriela Bencaiova *, Alexander Krafft, Roland Zimmermann Department of Obstetrics, University Hospital Zurich, Frauenklinikstr. 10, CH-8091 Zurich, Switzerland Received 31 January 2005; received in revised form 3 February 2005; accepted 3 February 2005
Keywords: Sickle cell trait; Type 2 diabetes; Microvascular diabetic complications
We have read with great interest the paper by Ajayi and Kolawole published in the August 2004 issue of the European Journal of Internal Medicine [1]. The objective of the paper was to determine whether the sickle cell trait may adversely influence the expression of microvascular diabetic complications in Africans with type 2 diabetes. The sickle cell trait has generally been misconstrued as a benign condition. Yet, many isolated cases have shown its role as a co-factor for morbidity and mortality. Normally, in vivo sickling does not occur in sickle cell trait individuals. However, hypoxia, acidosis, dehydration, hyperosmolality, hypothermia, or elevated erythrocyte 2,3diphosphoglycerate levels may transform the sickle cell trait into a syndrome resembling sickle cell disease and, therefore, may contribute to development of a sickle cell crisis. Patients in sickle cell crisis have multiple indicators of an inflammatory response, including elevated white blood cell counts, C-reactive protein levels, and cytokines as well as activated monocytes, neutrophils, platelets, and endothelial cells in the circulation. A previous study showed that the degree of coagulation activation is the most important factor for impairment of this condition and parallels the degree of disease severity [2].
Since diabetic patients have increased blood viscosity, decreased red cell deformability, hyperfibrinogenemia, and increased red blood cell adhesion to vascular endothelium, this condition may transform a sickle cell trait into sickle cell disease with development of sickle cell crisis. This situation is changed with all anti-inflammatory, antiaggregation, and hemorheological therapy administered to diabetic patients. We therefore believe that patients with concurrent type 2 diabetes and sickle cell trait are predisposed to more frequent or severe diabetic microvascular complications. In our opinion, more studies are needed to clarify the role of the sickle cell trait as a risk factor for the development or impairment of diabetic complications.
References [1] Ajayi AA, Kolawole BA. Sickle cell trait and gender influence type 2 diabetic complications in African patients. Eur J Intern Med 2004; 15:312 – 5. [2] Westerman MP, Green D, Gilman-Sachs A, Beaman K, Freels S, Boggio L, et al. Coagulation changes in individuals with sickle cell trait. Am J Hematol 2002;69:89 – 94.
* Corresponding author. Tel.: +41 1 255 5131; fax: +41 1 255 4430. E-mail address: [email protected] (G. Bencaiova). 0953-6205/$ - see front matter D 2005 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved. doi:10.1016/j.ejim.2005.02.016