Metabolic control and educational status in children with type 1 diabetes: effects of a summer camp and intensive insulin treatment

2005 ◽  
Vol 42 (4) ◽  
pp. 156-161 ◽  
Author(s):  
G. Karagüzel ◽  
İ. Bircan ◽  
S. Erişir ◽  
R. Bundak
2018 ◽  
Vol 14 (2) ◽  
pp. 73 ◽  
Author(s):  
S Pinar Bilir ◽  
Richard Hellmund ◽  
Beth Wehler ◽  
Huimin Li ◽  
Julie Munakata ◽  
...  

Flash glucose monitoring – an alternative to traditional self-monitoring of blood glucose (SMBG) – prevents hypoglycaemic events without impacting glycated haemoglobin (HbA1c).21Given the potential benefits, this study assessed the cost-effectiveness of using flash monitoring versus SMBG alone in patients with type 1 diabetes (T1D) receiving intensive insulin treatment in Sweden.Methods:This study used the IQVIA CORE Diabetes Model (IQVIA CDM, v9.0) to simulate the impact of flash monitoring versus SMBG over 50 years from the Swedish societal perspective. Trial data informed cohort data, intervention effects, and resource utilisation; literature and Tandvårds-Läkemedelförmånsverket (TLV) sources informed utilities and costs. Scenario analyses explored the effect of key base case assumptions.Results:In base case analysis, direct medical costs for flash monitor use were SEK1,222,333 versus SEK989,051 for SMBG use. Flash monitoring led to 0.80 additional quality-adjusted life years (QALYs; 13.26 versus 12.46 SMBG) for an incremental cost effectiveness ratio (ICER) of SEK291,130/QALY. ICERs for all scenarios remained under SEK400,000/QALY.Conclusion:Hypoglycaemia and health utility benefits due to flash glucose monitoring may translate into economic value compared to SMBG. With robust results across scenario analyses, flash monitoring may be considered cost-effective in a Swedish population of T1D intensive insulin users.


2004 ◽  
Vol 7 (2) ◽  
pp. 14-19
Author(s):  
CAMILLO RICORDI

The discovery of insulin changed the course of history in the treatment of diabetes. However, despite tremendous progress in insulin formulations and treatment strategies, insulin treatment still cannot fully prevent chronic complications and intensive insulin treatment to improve metabolic control, has often paralleled an increased risk of severe hypoglycemia. A cure for Type 1 diabetes should include: ? Restoration of self tolerance, to prevent recurrence of autoimmunity ? Restoration of physiologic metabolism by replacement of the biologic function (insulin producing cells) that was partially of completely impaired as a result of the disease process. ? Prevention of destruction of the new insulin producing cells by the recipient immune system in the absence of any treatment that could introduce an additional risk to the patient, which could be comparable to, or higher than the risk imposed by disease progression under exogenous insulin treatment. Pancreatic islets could be considered an ideal and more physiologic alternative to insulin, as they can restore metabolic control after transplantation, preventing the development of chronic complications. In fact, islets are capable of perfectly timed insulin release and can keep glucose levels in the normal range, functioning for an entire lifetime, if they are not destroyed by the recipient's immune system. Significant progress has been recently reported in the translational research approach towards the development of a cure for Type 1 diabetes. There is now strong evidence for the technical feasibility of human islet isolation and purification procedures. Proof of function of isolated human islets has been clearly established both in animal models and in pilot clinical trials of human islet allotransplantation in patients with surgical and Type 1 diabetes. Additional research in now needed to improve the current clinical results in terms of long term prevention of rejection and recurrence of autoimmunity, the development of safe, non diabetogenic immunomodulation strategies and ultimately the achievement of donor specific immune tolerance. If success will be achieved in these areas, then we will face the critical challenge of identifying sufficient and suitable sources of insulin producing tissue to treat the increasing number of patients who could benefit from this form of therapy and which would not be limited to Type 1 diabetes. That is why the work on xenogeneic islets, embryonic and adult stem cells, islet regeneration and proliferation, as well as engineering of insulin producing cells must be continued, to identify the most ideal source of insulin producing tissue that could be utilized on a large scale once the impediments and limitations of immunosuppression will be resolved.


2013 ◽  
Vol 12 (1) ◽  
pp. 15 ◽  
Author(s):  
Alina C R Feitosa ◽  
Gilson S Feitosa-Filho ◽  
Fatima R Freitas ◽  
Bernardo L Wajchenberg ◽  
Raul C Maranhão

2008 ◽  
pp. 709-716
Author(s):  
J Ždychová ◽  
J Veselá ◽  
L Kazdová ◽  
R Komers

Akt kinase regulates numerous cell functions including glucose metabolism, cell growth, survival, protein synthesis, and control of local hemodynamics. mTOR is one of down-stream effectors of Akt involved in the initiation of protein translation. However, renal Akt signaling in Type 1 diabetes (DM) in vivo, in particular under the conditions reflecting differences in metabolic control, has received less attention. Renal cortical activity and expression of Akt and mTOR (kinase assay, western blotting) were determined in streptozotocin-diabetic rats (D) with different levels of glycemic control (blood glucose 22.0±1.0, 13.4±1.5, 8.1±0.4 mmol/l, p<0.05 between the groups), achieved by varying insulin treatment (0, 4 and 12 IU/day), and in control rats with (C4) or without (C) chronic insulin administration. Renal Akt activity was reduced in D rats without insulin treatment and severe hyperglycemia (D-0, -62 %, p<0.01 vs. C), partially restored in moderately hyperglycemic rats (D-4, -30 %, p<0.05 vs. C), and normalized in D rats with intensive insulin and tight metabolic control (D-12). Expression of active mTOR paralleled Akt activity in D-0 (-51 %, p<0.01 vs. C), but not in D-4 and D12 that demonstrated increases in active mTOR (+55 %, +80 % resp., p<0.05) as compared to C. Moreover, insulin activated renal Akt (+82 %, p<0.01), but not mTOR in C4. In conclusion, glycemic control and intensity of insulin treatment are important modulators of renal Akt and mTOR activity in diabetes. While Akt activity is reversible by tight metabolic control, combination of hyperglycemia and insulin treatment resulted in enhancement of mTOR activity. In addition to Akt, other signaling pathways likely contribute to regulation of renal mTOR activity in diabetes.


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