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  • ISSN: 2333-6692
    Volume 8, Issue 1
    Research Article
    Salma Alkalbani*
    Background: There is growing evidence that low-carbohydrate diet can positively improve glycemic index in patient with type 2 diabetes mellitus in compare with currently recommended method of low fat, high carbohydrate diet for the same group. However, more researches are needed to prove the effectiveness and safety of this type of diet before starting to implement it to diabetic patients.
    Objective: This study focused on the effectiveness of non-caloric restricted, low-carbohydrate diet in improving glycemic control over 24-week period in active Omani diabetic patients attending primary care setting at North Mawaleh health center in Muscat Government.
    Research design and method: This is prospective descriptive study with longitudinal follow up and pre-test, post- test comparison. Eighty-three patients were recruited. Blood collected at baseline, at 12-week and 24-week. Each patient was advised to follow non-caloric restricted low-carbohydrate regimen (< 80 gm of carbohydrate per day) and exercise recommendations. The patients were seen every alternate week in the first month then monthly to look for reflow measurements, counselling and medication adjustment. The primary outcome was glycated hemoglobin (HbA1c).
    Result: Seventy-one patients were able to complete the study. Non-restrictive low-carbohydrate diet (< 80 gm of carbohydrate/day) showed marked reduction in glycated hemoglobin in 24-week period by 11.58%, from 7.12 (SD1.067) % at week 0 to 6.28(SD1.066) % at week 24, p value < 0.05. This reduction was noticed along with adjustment of diabetic medications. Additionally, the percentage of patients with optimal level of HbA1c (<7%) was improved from 58 % of total patients studied to 79 % by the end of the study. There was significant mean weight reduction by 7.33 % from 82.63(SD14.3) kg to 76.67(SD14.90) kg (p value <0.05). High density lipoprotein increased from 1.30(SD0.297) to 1.40(SD0.468) mmol/l, p value <0.05 and TAG was reduced from 1.47(0.934) to 1.22(0.564) mmol/l value <0.05. The mean eGFR was declined from 86.73 (SD6.21) to 84.92 (SD8.47) ml/minper1.73m2 at the end of the study (p value <0.05). Diabetic medications were stopped in 18 (25.4%) patients, reduced in 7(9.8%) patients, increased in patients 2(2.8%), and unchanged in 44(62.0%) patients. The linear regression failed to show any correlation between reduction in HbA1c and weight changes.
    Conclusion: Non-caloric restricted LCD improved glycemic control in patient with type 2 DM. It also improved lipid profile, BMI and medication requirements. However, it demonstrated adverse effect on eGFR in patient with normal eGFR. Further controlled studies are warranted.
    Ole Lander Svendsen*, Rasmus Bo Jansen, Kasper Foged Guldbrandsen, Tomas Møller Christensen, and Per E. Holstein
    The collapse of bones in the Charcot foot may be caused by other factors than decreased bone mineralization, such as the trabecular structure. The trabecular bone score (TBS) of the lumbar spine can be measured by dual energy x-ray absorptiometry as a measure of trabecular structure and may reflect resistance to fracture beyond that of bone mineral alone.
    Thus, the aim of this study was to investigate whether TBS is lower in diabetes patients with a Charcot foot compared to diabetes patients without a Charcot foot, and to assess changes in TBS and occurrence of fractures over 8.5 years in these patients.
    Methods: 41 patients with type 1 or type 2 diabetes, of which about half had a Charcot foot, were included in 2005-2007 and 21 of these were followed up after 8.5 years.
    TBS and bone mineral density (BMD) of the lumbar spine were measured with Lunar Prodigy DXA-scanner and TBS iNsight software. The occurrence of bone fractures from baseline to follow-up was registered.
    Results: There were no significant differences in TBS between those with and those without a Charcot foot neither at baseline nor at follow-up (p>0.32). Furthermore, there was no significant change in TBS from baseline to follow-up in neither those with nor those without a Charcot foot (p>0.19), and there was no significant difference in the change in TBS between the two groups (p>0.21).
    All fractures had occurred in the diabetes patients with an acute Charcot foot (4 out of 10 patients at follow-up: i.e. 40%), which is statistically significant (p<0.035) compared to no fractures in the diabetes patients without a Charcot foot (11 patients at follow up).
    There were no significant associations between BMD, TBS, and biochemical markers of bone turn over at baseline and later occurrence of fracture in the diabetes patients with Charcot foot.
    Conclusion: There was no association of TBS of the lumbar spine and having a Charcot foot, or not, in diabetes patients, neither at baseline, nor after 8.5 years follows up. Diabetes patients with an acute Charcot foot seem to have an increased risk of fracture, which might not be revealed by measurement of TBS.
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