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Rapid Responses: Rapid Responses published:
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Well structured
- Dr Rajasree Pai (19 March 2008)
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Lowering HbA1c in Type 1 Diabetes
- Subrata K. Mallik (21 March 2008)
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Glycated haemoglobin and red cell deformability.
- Les O. Simpson (24 March 2008)
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More support needed for paediatric diabetes services
- Rachel E Besser, Jacob Eyers (8 April 2008)
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Dr Rajasree Pai, Physician California
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The authors have taken special care to structure the article well especially the statistical methods, conclusion and the limitations of the study. 'What this study adds' is again a good section that helps the viewers to find answers to queries on the topic. However, it has not been clearly stated what the authors meant by ' poor control of microalbuminuria' and what methods do they advocate in preventing the progression of microalbuminuria to macroalbuminura. Competing interests: None declared |
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Subrata K. Mallik, Locum Consultant Endocrinologist Prince Charles Hospital, Merthyr Tydfil CF47 9DT
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I sincerely thank Amin et al for their research article: 'Risk of microalbuminuria and progression to macroalbuminuria in a cohort with childhood onset type 1 diabetes: prospective observational study' in BMJ published 18 March 2008. They concluded that the only modifiable predictor was poor glycaemic control. We in adult diabetes clinic receive patients from transition clinic who rarely have HbA1c of <9.0%. Paediatric diabetologists are in even more difficult situation than we are! For all practical purposes, diabetes cannot be cured and complications cannot be prevented. However, complications can be delayed with adequate control. In a normal person there is constant secretion of a basal level of insulin with bursts of insulin secretion with each meal. We try to mimic this with Basal-bolus regime of insulin therapy which is Physiological Insulin Replacement. Normally insulin is released in portal circulation and about 50% is cleared by liver and rest broken down by kidneys. SC insulin we administer leads to higher level in systemic circulation than portal. There are a number of variables like technique of insulin administration, how much reaches portal circulation, how much is extracted by liver etc in addition to amount of food taken, exercise, infection, comorbidities etc. No wonder it is difficult to get it right. We try to achieve it by trial and error. Problems with young diabetics are: Poor compliance with clinic appointments, sticking to diet, Blood Sugar (BS) monitoring, exercise etc. Other social activities take precedence over diabetes control. They try to avoid hypos during exercise, driving and at night by keeping BS high. The symptoms of hypo are dramatic and can be frightening, therefore they learn about it easily. It becomes dificult for them to appreciate the harmful effects of hyperglycaemia as they don't feel unwell. Education in Diabetes is of paramount importance and the patient has to be willing and cooperative to achieve success. Perhaps our emphasis should be more on preventing hyperglycaemia rather than avoiding hypoglycaemia. It is important to note that hypo is not dangerous as such but if it happens in situations like driving, swimming, operating machinery, the consequences can be devastating. Otherwise, even if patient lapses into coma, there is virtually no risk of death or long- term cerebral damage. Even if left unaided, they almost always recover spontaneously. They have to keep BS rather high during driving and exercise. However, we can try to avoid nocturnal hyperglycaemia which is a major cause of raised HbA1c as the exposure of haemoglobin to raised glucose is longest. If possible, all type 1 diabetic patients should be on Basal-bolus regime. Target BS before bed eg between 6 and 8 mmols. Small bed time snack is taken if it is <6 mmols. Checking 2 am BS will ensure avoidance of nocturnal hypo. During day time they will act on BS results every third day or so to try and achieve a target BS eg 4 to 8 mmols. Providing a supplement insulin scale to the patient is likely to make it easier. The target may be tightened later if appropriate. Minor hypos may be acceptable as long as there is no hypounawareness. We can restrict carbohydrate (CHO) intake as well, particularly in overweight patients. Minimum 100G of CHO is needed to keep urine free of ketones. Metformin may also be considered in obese intelligent patients although there is a risk of lactic acidosis. Even after following all these, in some we may not be able to achieve desirable HbA1c when we should consider adding Ace-inhibitor and Statin to minimise microvascular damage. Competing interests: None declared |
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Les O. Simpson, retired medical research worker Dunedin, New Zealand 9077
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According to Amin et al, (1) poor glycemic control, as assessed by the annual measurement of glycated haemoglobin and the assessment of the albumin/creatinine ratio provides a basis for estimating the risk of progression from micro- to macroalbuminuria in diabetic children. However there was no discussion about the link between HbA1c levels and renal dysfunction. In 1986, Kiesewetter et al (2) reported that in diabetic children, "...there was a significant decrease in erythrocyte deformability," and noted that diabetic children with good stabilisation presented better rheological parameters than the poorly stabilised children. Watala et al (3) reported the results of a study of the intracellular viscosity of red cells from diabetic children and of the effects of erythrocyte membrane glycosylation. They concluded that, "...the alterations in mmembrane lipid-protein interactions together with the increased glycosylation-derived internal viscosity may consequently imply altered viscoelastic properties of erythrocyte membranes and, underlying the impaired deformability of red blood cells in the diabetic state, contribute to the development of late diabetic sequelae." Similar comments regarding reduced erythrocyte deformability in diabetic children in comparison with the situation in healthy children were reported in 1999 by Linderkamp et al (4). More recently, Negrean et al (5) described a, "...direct correlation between the decrease of erythrocyte deformability and the severity of diabetic microangiopathy." The authors noted that, "...impaired blood rheology does depend on the quality of glycemic control." However, Le Devehat et al(6)reported that after 15 years, even if there is good glycemic control "..haemorheological impairments appear to be inevitable." Therefore it seems that high levels of HbA1c are accompanied by a reduction in red cell deformability which will have an adverse affect on capillary blood flow. It is possible that poorly deformable red cells may influence both the quality and quantity of the glomerular filtrate. Furthermore, because of the haemoconcentrating effect of glomerular filtration, blood flow in the efferent arteriole would be compromised. As a result, the flow rate in the peritubular plexus will be reduced and impair tubular reabsorption. In such circumstances, maybe it is time to recognise the implications of the findings from a four-year long study of pentoxifylline on the vascular complications of diabetic patients. (7) Pentoxifylline has been shown to reduce blood viscosity and to improve red cell deformability. The authors reported, among other beneficial changes, that there was a significant decrease in albumiuria and proteinuria and an increase in creatinine clearance. Perhaps it is time to evaluate the effects of pentoxifylline in diabetic children. References. 1. Amin R, Widmer B, Prevost AT, et al. Risk of microalbuminuria and progression to macroalbuminuria in a cohort with childhood onset type 1 diabetes: prospective observational study. BMJ.doi.10.1136. 2. Kiesewetter H, Jung F, Korber N, et al. Microcirculation and hemorheology of children with type 1 diabetes. Klin Wochenschr 1986;64:962-8. 3. Watala C, Witas H, Olszowska L, et al. The association between erythrocyte internal viscosity, protein non-enzymatic glycosylation and erythrocyte membrane dynamic properties in juvenile diabetes mellitus. Int J Exp Pathol 1992;73:655-63. 4. Linderkamp O, Ruef P, Zilow EP, et al. Impaired deformability of erythrocytes and neutrophils in children with newly diagnosed insulin- dependent diabetes mellitus. Diabetologia 1999;42:865-9. 5. Negrean V, Suciu I, Sampelean D, et al. Rheological changes in diabetic microangiopathy. Rom J Intern Med 2004;42:407-13. 6. Le Devehat C, Vimeux M, Khodabandehlou T. Blood rheology in diabetic patients. Clin Hemorheol Microcirc 2004;30:297-300. 7. Ferrari E, Fioravanti M, Patti AL, et al. Effects of long-term treatment (4 years) with pentoxifylline on haemorheological changes and vascular complications in diabetic patients. Pharmatherapeutica 1987;5:26 -39. Competing interests: None declared |
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Rachel E Besser, Specialist Paediatric Registrar Queen Mary's Hospital, Frognal Avenue, Sidcup, Kent DA14 6LT, Jacob Eyers
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Amin et al's study identifying mean HbA1c as a strong predictor for microalbuminuria and progression to macroalbuminuria (1) was necessary but comes as no surprise. The Diabetes Control and Complications Trial (2) demonstrated that a lower HbA1c decreases development of complications. However it should not be forgotten that the improved HbA1c levels in the intensively treated group (mean HbA1c 7%) compared with the conventional group (9%) was achieved through intensive support by monthly clinic visits and frequent telephone calls. This is unavailable to the majority of diabetes units across the country who make do with three monthly clinic visits, such as were available to patients in the DCCT conventionally treated group. Paediatric diabetes services are overstretched in the UK and unable to achieve set targets, with an average caseload of more than 100 children for every paediatric diabetes specialist nurse despite current recommendations of a maximum ratio of one nurse to 70 children (3). In addition, many clinics do not have access to psychological support despite Diabetes National Service Framework standards (4). In the 2005-2006 National Diabetes Audit for children and young people (0-16 years) with diabetes in England and Wales (5), the median HbA1c was 8.7% and 8.8% respectively, with 25% having an HbA1c around 10%. Whilst we welcome and acknowledge Carel’s call for tight diabetes control in the accompanying editorial (6), given the limited resources available to most paediatric diabetes clinics in the UK, these results reflect the hard work and dedication of medical staff who often compensate shortfalls in service provision. If Making Every Young Person with Diabetes Matter (7) does indeed matter to the Department of Health, more money for paediatric diabetes services is needed urgently if the patients with sub optimal HbA1c's we see in today's clinics are not to become the dialysis patients of tomorrow. Rachel Besser Specialist Paediatric Registrar, Queen Mary’s Hospital, Frognal Avenue, Sidcup, Kent DA14 6LT rachelbesser@hotmail.com Jacob Eyers Consultant Paediatrician with an interest in diabetes. Queen Mary’s Hospital, Sidcup. jacob.eyers@qms.nhs.uk 1. Amin R, Widmer B, Prevost AT, Schwarze P, Cooper J, Edge J, et al. Risk of microalbuminuria and progression to macroalbuminuria in a cohort with childhood onset type 1 diabetes prospective observational study. BMJ 2008;336:697-701 2. The DCCT research Group. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. NEJM 1993;329:977-986 3.Diabetes UK (2005) Your Local care - a survey of diabetes services. 4. Department of Health (2001), National Service Framework for Diabetes: Standards. 5. The Information Centre. National Diabetes Audit. Key findings about the quality of care for children and young people with diabetes in England and Wales. Report for the audit period 2005-2006. Healthcare commission, Diabetes UK, National Diabetes Support Team, YHPHO, BSPED,RCN. 6.Carel J, Levy-Marchal C. Renal complications of childhood type 1 diabetes BMJ 2008;336:677-8 7. DH Diabetes Policy Team. Making Every Young Person with Diabetes Matter:Report of the Children and Young People with Diabetes Working Group (2007) Competing interests: None declared |
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