Diabetes mellitus (DM) is a global epidemic causing significant morbidity and mortality. The most occurring DM is type 2 diabetes mellitus (T2DM) which has similar symptoms as type 1 diabetes mellitus (T1DM). However, it is less marked, making it difficult to diagnose during the early stages. The management of T2DM is usually based on weight and glycemic control, which can be achieved through dietary interventions such as intermittent fasting (IF) and the ketogenic diet (KD). Therefore, this systematic review and meta-analysis aim to demonstrate the role of IF and KD in glycemic and weight control among patients with T2DM.Two methods, including an electronic database search through ScienceDirect, Google Scholar, PubMed, Scopus, Embase, and Web of Science, and a manual search were used to identify relevant studies published between 2000 and 2022. The search yielded 1299 articles, of which only 12 met the inclusion criteria. In addition, study quality appraisal was performed using Review Manager software (RevMan 5.4.1).The pooled results have shown that IF had a similar effect on HBA1c reduction as control interventions (standardized mean differences [SMD]: 0.36%; 95% CI; -0.37, 1.10; P = 0.33, I2 = 87%). Similarly, an insignificant difference in weight reduction between IF and control interventions was recorded (SMD: -1.05%; 95% CI; -2.29, 0.19; P = 0.10, I2 = 96%). On the other hand, KD significantly reduced body weight compared with control diets (SMD: -1.91 kg; 95% CI; -2.96 kg, -0.85 kg; P = 0.0004, I2 = 96%). Similarly, KD had a better effect on the HBA1c percentage reduction than control diets (SMD: -2.00%; 95% CI; -3.76, -0.25; P = 0.03, I2 = 97%).IF and KD have shown reductions in HBA1c and body weight among patients with T2DM. However, the interventions are subject to side effects and should be used with caution and under the supervision of a health professional.
Background: - Diabetes-related complications result from cumulative exposure to hyperglycemia. Hence, achieving and maintaining adequate glycaemic control is critical. Insulin is a necessary treatment in DM-2 patients who did not achieve glycaemic targets on oral agents. Inertia in starting insulin has been reported in many populations. Aim:- To assess the degree of inertia related to insulin initiation and intensification in patients with DM-2. Methods:- We performed a retrospective longitudinal cohort study and followed DM-2 two years before and two years after the start of insulin. The primary outcome was the proportion of patients who achieved glycaemic targets ( HbA1c ≤ 7.5%) at 6 months, 1 year and 2 years. Results:- We included 374 patients who were predominantly males (62%). The mean age was 55.3 ± 11.3 years, the mean duration of DM-2 was 12.0 ± 7.3 years, the mean age of DM-2 onset was 41.2 ± 9.6 years, 64.4 % were obese,47.6% had a microvascular disease, and 24.3% had a macrovascular disease. The mean HbA1c at (-2 years) and (-1 year) were 9.2±2.1% and 9.3±2.0%, respectively. The mean HbA1c at the time of insulin initiation was 10.4 ±2.1%. The mean HbA1c at 6,12 months and 2 years was 8.5±1.8% %, 8.4±1.8% % and 8.5±1.7%, respectively. The proportion of patients who achieved HbA1c targets at 6, 12 months and 2 years were 32.9%, 31.0%, and 32.9%. According to the multivariate regression analysis ; for every unit increase in BMI, HbA1c at (-1 year), and HbA1c at the start of inulin , the HbA1c levels at 6 months increase by 0.05% (p 0.023), 0.17% (p0.017), and 0.19% (p=0.011), respectively; while it is reduced by 0.03% (p=0.013).for every 1-year increase in the age of DM-2 onset. Multivariate logistic regression analysis showed that the achieving HbA1c targets at 6 months and 1 year increases the odds of achieving HbA1c targets at 2 years ; (OR 4.87(2.4-9.6) p<0.001) and ( OR 6.2 (3.2-12.0), p<0.001) respectively. Conclusion: - In patients with DM-2, there was an alarming delay in starting and titrating insulin. The reduction in HbA1c plateaued at 6 months. Earlier initiation and intensification of insulin therapy are critical to achieving glycaemic targets. More studies are needed to examine the causes of therapeutic inertia from physicians, patients, and systems point of view.
Background: Adrenal crisis (AC) is a life-threatening condition that occurs either as the initial presentation of adrenal insufficiency or in patients who are known to have hypoadrenalism, when a precipitating acute stressor outweighs the mineralocorticoid and glucocorticoid supply. It is known that exposure to high levels of thyroid hormones in the presence of hypoadrenalism may precipitate AC.Graves’ disease (GD), as a precipitant of AC in patients with congenital adrenal hyperplasia (CAH), has been rarely described in the literature. Clinical Case: A 15-year-old male with classic CAH diagnosed since birth when he had vomiting and darkly pigmented skin. He was on regular follow-up with his endocrinologist in his home country. For an unclear reason, he was on hydrocortisone 40 mg daily in divided doses. The patient presented to the emergency department with nausea, vomiting, loose stool, dizziness, and fatigue for 5 days. On examination, he was conscious and oriented but looked tired. He had a temperature of 36.8°C, blood pressure (supine) 132/78 mmHg (standing blood pressure could not be taken because the patient was dizzy), pulse rate 130/minute, and respiratory rate 17/minute. Otherwise, the physical exam was unremarkable. Initial laboratory investigations showed sodium 114 (136–145 mmol/L), potassium 6.0 (3.5–5.1 mmol/l), chloride 83 (102–104 mmol/L) and Bicarbonate 14 (22–29 mmol/L). Serum creatinine, complete blood count, C-reactive protein (CRP) and procalcitonin levels were within normal. He was treated for AC with stress doses of hydrocortisone intravenously, and normal saline intravenous infusion. He showed a gradual improvement of his symptoms with normalization of the electrolytes. Thus, he was switched to oral hydrocortisone replacement 15 mg am and 10 mg in the afternoon. Nevertheless, his pulse rate was 105 -110 / min. Therefore, thyroid function test (TFT) was done and revealed TSH 0.3 (0.5–4.3 mIU/L) and FT4 30.6 (12.9–20.6 pmol/L). Thyroid uptake scan showed a mildly enlarged thyroid gland with homogeneous and slightly increased radiotracer uptake suggestive of GD. Thus, propranolol and carbimazole were prescribed in addition to hydrocortisone. Then, the patient was discharged after proper education about precipitating factors of AC. Later on, the patient appeared for his clinic appointment, he was clinically well with normal vital signs, serum electrolytes, and TFT. Propranolol was stopped, carbimazole dose was adjusted, and he was maintained on hydrocortisone. Conclusion: Unrecognized Graves’ disease was the precipitating factor of the adrenal crisis in this patient with CAH. Despite the rarity of the association, a high index of clinical suspicion for unusual acute stressors is very important for proper management of AC and to prevent future recurrence.
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