Lee Ling Lim

Place of sodium-glucose cotransporter-2 inhibitors in East Asian subjects with type 2 diabetes mellitus: Insights into the management of Asian phenotype

The burden of type 2 diabetes (T2DM) in East Asia is alarming. Rapid modernization and urbanization have led to major lifestyle changes and a tremendous increase in the prevalence of obesity, metabolic syndrome, and diabetes mellitus. The development of T2DM at a younger age, with lower body mass index, higher visceral adiposity, and more significant pancreatic beta-cell dysfunction compared to Caucasians are factors responsible for the increased prevalence of T2DM in East Asians. Sodium-glucose Cotransporter-2 (SGLT2) inhibitors (canagliflozin, dapaglifozin, empagliflozin, etc.) reduce renal glucose reabsorption, leading to favorable effects on glycemic, blood pressure, and weight control. The insulin-independent mechanism enables their use as monotherapy or combination therapy with insulin and other oral antidiabetic agents. The role of SGLT2 inhibitors in the management of T2DM among East Asians is an interesting area of research, given that East Asians have been proven to be uniquely different from Caucasians. This review provides comprehensive coverage of the available literature not only on the efficacy and safety, but also on the recent cardiovascular and renal outcomes of SGLT2 inhibitors, focusing among East Asians.

Asymmetrical bone loss in a patient with poliomyelitis: an indication for anti-osteoporotic therapy.

BACKGROUND Poliomyelitis survivors suffer from post-myelitic complications including osteoporosis that are often overlooked. METHODS We report a case of a 49-year-old lady with history of poliomyelitis with resultant flaccid paralysis of the involved limb. RESULTS The bone mineral density revealed asymmetrical severe osteoporosis in the poliomyelitic limb. Given the risk of falls and fractures, she was commenced on oral bisphosphonate therapy. CONCLUSION Poliomyelitis is an important acquired risk factor for regional osteoporosis. This condition should be detected and treated in this cohort of patients who are clearly at higher risk of fractures.

Association between serum 25-hydroxyvitamin D and glycated hemoglobin levels in type 2 diabetes patients with chronic kidney disease

Vitamin D is suggested to influence glucose homeostasis. An inverse relationship between serum 25‐hydroxyvitamin D (25[OH]D) and glycemic control in non‐chronic kidney disease (CKD) patients with type 2 diabetes was reported. We aimed to examine this association among type 2 diabetes patients with CKD.

Relationship of glycated hemoglobin, and fasting and postprandial hyperglycemia in type 2 diabetes mellitus patients in Malaysia

Studies on the relative contributions of fasting and postprandial hyperglycemia (FH and PPH) to glycated hemoglobin (HbA1c) in patients with type 2 diabetes have yielded inconsistent results. We aimed to assess the relationship by using continuous glucose monitoring in a multi‐ethnic cohort.

Primary hyperparathyroidism: a rare cause of genu valgus in adolescence.

A 15-year-old girl presented with a history of progressive genu valgus of both lower limbs. She had no other skeletal deformities or fractures. There was no significant family history, in particular none to suggest multiple endocrine neoplasia syndrome. Radiographs of the lower limbs confirmed severe bilateral genu valgus (Figure 1). Investigations revealed a markedly elevated serum corrected calcium of 12.4 mg/dL (normal, 8.8–10.4), phosphate of 2.8 mg/dL (normal, 3.4–5.8), alkaline phosphatase of 1136 IU/L (normal, 50–136), intact PTH of 1649 pg/ml (normal, 10–68), 25-hydroxyvitamin D of 28 ng/ml (normal, 9–52), and 24-hour urinary calcium of 196 mg/d (normal, 88–300). Further radiographs of the hand re-

Sleep and Obesity

Rising global prevalence and incidence of obesity lead to increased cardiovascular-renal complications and cancers. Epidemiological studies reported a worldwide trend towards suboptimal sleep duration and poor sleep quality in parallel with this obesity epidemic. From rodents and human models, it is highly plausible that abnormalities in sleep, both quantity and quality, impact negatively on energy metabolism. While excess dietary intake and physical inactivity are the known drivers of the obesity epidemic, promotion of healthy sleep habits has emerged as a new target to combat obesity. In this light, present review focuses on the existing literature examining the relationship between sleep physiology and energy homeostasis. Notably, sleep dysregulation perturbs the metabolic milieu via alterations in hormones such as leptin and ghrelin, eating behavior, neuroendocrine and autonomic nervous systems. In addition, shift work and trans-meridian air travel may exert a negative influence on the hypothalamic-pituitary-adrenal axis and trigger circadian misalignment, leading to impaired glucose tolerance and increased fat accumulation. Amassing evidence has also suggested that uncoupling of the circadian clock can increase the risk of adverse metabolic health. Given the importance of sleep in maintaining energy homeostasis and that it is potentially modifiable, promoting good sleep hygiene may create new avenues for obesity prevention and treatment.

Continuous glucose monitoring results in lower HbA 1c in Malaysian women with insulin-treated gestational diabetes: a randomized controlled trial

To determine if therapeutic, retrospective continuous glucose monitoring (CGM) improves HbA1c with less hypoglycaemia in women with insulin‐treated gestational diabetes mellitus (GDM).

PRKAR1A-negative familial Cushing’s syndrome: two case reports

IntroductionDetermining the etiology of Cushing’s syndrome is very challenging to endocrinologists, with most of the difficulty arising from subtype differentiation of adrenocorticotropic hormone–dependent Cushing’s syndrome. We present the pitfalls of evaluating a rare cause of adrenocorticotropic hormone–independent Cushing’s syndrome in the transition period between adolescence and adulthood.Case presentationA sibling pair with familial isolated primary pigmented nodular adrenocortical disease is described. The index case, a 20-year-old Chinese woman, presented with premenopausal osteoporosis with T12 compression fracture and young hypertension. Biochemical analysis confirmed adrenocorticotropic hormone–independent Cushing’s syndrome (elevated 0800 h plasma cortisol 808 nmol/L with suppressed adrenocorticotropic hormone level <5 pg/ml). Computed tomography of her adrenal glands revealed a 0.7-cm left adrenal hypodense nodule. After a left adrenalectomy, she had residual hypercortisolism (progressive weight gain, new T10 compression fracture, and not glucocorticoid-dependent postoperatively). Completion of contralateral adrenalectomy was performed upon recognition of typical histologic characteristics of primary pigmented nodular adrenocortical disease found in an initial left adrenalectomy specimen. Similarly, her younger brother developed adrenocorticotropic hormone–independent Cushing’s syndrome at age 18 years, with typical cushingoid habitus, but no osteoporosis or hypertension. His adrenal computed tomographic scans showed micronodularities over bilateral adrenal glands. He was successfully treated with bilateral adrenalectomy. Screening for Carney’s complex and PRKAR1A gene mutation was negative. Signs and symptoms of Cushing’s syndrome resolved after bilateral adrenalectomy for both patients. They were placed on lifelong glucocorticoid and mineralocorticoid replacement therapy and long-term surveillance for Carney’s complex.ConclusionsThe cases of these two patients illustrate the difficulties involved in diagnosing primary pigmented nodular adrenocortical disease, a variant of adrenocorticotropic hormone–independent Cushing’s syndrome that is managed with bilateral adrenalectomy. A high index of suspicion for this disease is needed, especially in adolescents with adrenocorticotropic hormone–independent Cushing’s syndrome who have a significant family history, features of Carney’s complex, and no resolution of Cushing’s syndrome after unilateral adrenalectomy. Patients with primary pigmented nodular adrenocortical disease can either have bilateral/multiple adrenal nodules or normal adrenal glands visualized by computed tomography. Long-term surveillance is imperative in patients with confirmed Carney’s complex and in those who have not undergone complete genetic testing to exclude this hereditary disorder.