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Title of Journal: Diabetologia

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Abbravation: Diabetologia

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Springer Berlin Heidelberg

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DOI

10.1002/chin.200214076

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1432-0428

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Impact of cancer on use of glucoselowering drug t

Authors: Marjolein M J Zanders Harm R Haak Myrthe P P van HerkSukel Lonneke V van de PollFranse Jeffrey A Johnson
Publish Date: 2015/04/03
Volume: 58, Issue: 6, Pages: 1380-1381
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Abstract

To the Editor We thank Frans Pouwer for his comments on our study 1 exploring adherence to glucoselowering drugs following a cancer diagnosis among individuals with diabetes 2 Our findings revealed that there was a significant drop in the medication possession ratio at the time of cancer diagnosis with the largest drops among patients with stage IV disease and gastrointestinal or pulmonary cancers In his letter Pouwer describes two potential mechanisms that could explain these results 1As Pouwer indicates weight loss has been associated with improvements in beta cell function and insulin sensitivity among individuals with diabetes As a result glucose levels decline HbA1c values improve and less glucoselowering drug treatment may be required to obtain optimal metabolic control While weight loss is common among cancer patients especially among those with gastrointestinal lung or advanced cancer as described by Pouwer the impact of weight loss on metabolic control and thus on diabetes treatment among these cancer patients is to our knowledge unknown However according to our research HbA1c values improve before colorectal cancer diagnosis M M J Zanders M P P van HerkSukel R M C Herings L V van de PollFranse H R Haak unpublished data and it is possible that this might be the result of weight loss Although we might expect that the decisions made regarding diabetes treatment are similar for cancer patients and those without cancer ie improvement in HbA1c leads to reductions in glucoselowering drug dose we assume then that the attention of patient and physician is also on metabolic control and diabetes treatment around cancer diagnosis In addition in practice clinical decisionmaking regarding metabolic control is based on anticipating an interplay of factors besides weight loss such as food intake glucose values HbA1c risk of hypoglycaemia diarrhoea and presence of diabetesrelated complications such as kidney dysfunction and foot lesions 3 Finally physicians might decide to not change diabetes treatment among cancer patients if they find that HbA1c values increase ie worsen back to baseline after cancer diagnosis as our research suggests M M J Zanders M P P van HerkSukel R M C Herings L V van de PollFranse H R Haak unpublished data Nevertheless weight loss might be one of the multiple factors that make physicians decide to lower the dose or even discontinue diabetes treatment When weight loss causes physicians to verbally inform patients to change their daily regimen the same amount of treatment already in the patient’s possession might be distributed over a greater number of days giving the impression that adherence has declined when in fact it hasn’t If this was the most plausible and only explanation for the study findings then as suggested by Pouwer we should have used the words ‘medication use’ instead of ‘medication adherence’In our manuscript we briefly described that stress following a major event could have contributed to the observed decline in adherence Depressive symptoms might have a role in this since depression is related to stress and seems also to be associated with lower adherence rates as discussed in the comment of Pouwer 1 Consequently it would be very relevant and interesting to investigate in a future study whether the decline in adherence was modified by the presence of depression or depressive symptoms among patients with cancer and diabetesAs elaborated in our study 2 and in the contribution by Pouwer 1 we can conclude that the association between adherence to glucoselowering treatment and cancer is probably explained by an interplay of factors We thank Pouwer for his valuable additions regarding potential mechanisms to explain the complex association The explanation for the decline in adherence should be studied in more detail taking into account the discussed mechanisms and the type of cancer


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  4. Lack of association between gene variants in the ALMS1 gene and Type 2 diabetes mellitus
  5. Lack of association between gene variants in the ALMS1 gene and Type 2 diabetes mellitus
  6. Low-density-lipoprotein cholesterol concentrations and risk of incident diabetes: epidemiological and genetic insights from the Framingham Heart Study
  7. AMPK phosphorylation of ACC2 is required for skeletal muscle fatty acid oxidation and insulin sensitivity in mice
  8. Effects of fenofibrate on renal function in patients with type 2 diabetes mellitus: the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) Study
  9. Angiotensin-I converting enzyme insertion/deletion polymorphism and its association with diabetic nephropathy: a meta-analysis of studies reported between 1994 and 2004 and comprising 14,727 subjects
  10. Microarray analysis of genes with impaired insulin regulation in the skeletal muscle of type 2 diabetic patients indicates the involvement of basic helix-loop-helix domain-containing, class B, 2 protein (BHLHB2)
  11. Amino acids require glucose to enhance, through phosphoinositide-dependent protein kinase 1, the insulin-activated protein kinase B cascade in insulin-resistant rat adipocytes
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  26. An RBP4 promoter polymorphism increases risk of type 2 diabetes
  27. Müller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products
  28. WNT/β-catenin increases the production of incretins by entero-endocrine cells
  29. Enhanced susceptibility of Cpt1c knockout mice to glucose intolerance induced by a high-fat diet involves elevated hepatic gluconeogenesis and decreased skeletal muscle glucose uptake
  30. Is rs34861192 or rs1862513 a more promising variant for determining plasma resistin in an aged Japanese population?
  31. Environmental pollutants and type 2 diabetes: a review of mechanisms that can disrupt beta cell function
  32. Reply to comment on: Høi-Hansen T, Pedersen-Bjergaard U, Thorsteinsson B (2005) The Somogyi phenomenon revisited using continuous glucose monitoring in daily life. Diabetologia 48:2437–2438
  33. The prevalence of insulin autoantibodies at the onset of Type 1 diabetes is higher in males than females during adolescence
  34. Anaemia in diabetes: is there a rationale to TREAT?
  35. —to: Hales CN, Ozanne SE (2003) For Debate: Fetal and early postnatal growth restriction lead to diabetes, the metabolic syndrome and renal failure. Diabetologia 46:1013–1019
  36. Causal interpretation requires appropriate study design. Reply to Priest PC [letter]
  37. Is type 2 diabetes an amyloidosis and does it really matter (to patients)?
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  47. A longitudinal study of iron status during pregnancy and the risk of gestational diabetes: findings from a prospective, multiracial cohort
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  50. Harry Keen, 1925–2013
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  53. R. Tattersall. Diabetes: the biography. Oxford University Press, Oxford, 2009
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  64. Expression of the enteroviral capsid protein VP1 in the islet cells of patients with type 1 diabetes is associated with induction of protein kinase R and downregulation of Mcl-1
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