Acute diabetic neuropathy following improved glycaemic control: a case series and review.

SUMMARY: We present three cases of acute diabetic neuropathy and highlight a potentially underappreciated link between tightening of glycaemic control and acute neuropathies in patients with diabetes. Case 1: A 56-year-old male with poorly controlled type 2 diabetes (T2DM) was commenced on basal-bolus insulin. He presented 6 weeks later with a diffuse painful sensory neuropathy and postural hypotension. He was diagnosed with treatment-induced neuropathy (TIN, insulin neuritis) and obtained symptomatic relief from pregabalin. Case 2: A 67-year-old male with T2DM and chronic hyperglycaemia presented with left lower limb pain, weakness and weight loss shortly after achieving target glycaemia with oral anti-hyperglycaemics. Neurological examination and neuro-electrophysiological studies suggested diabetic lumbosacral radiculo-plexus neuropathy (DLPRN, diabetic amyotrophy). Pain and weakness resolved over time. Case 3: A 58-year-old male was admitted with blurred vision diplopia and complete ptosis of the right eye, with intact pupillary reflexes, shortly after intensification of glucose-lowering treatment with an SGLT2 inhibitor as adjunct to metformin. He was diagnosed with a pupil-sparing third nerve palsy secondary to diabetic mononeuritis which improved over time. While all three acute neuropathies have been previously well described, all are rare and require a high index of clinical suspicion as they are essentially a diagnosis of exclusion. Interestingly, all three of our cases are linked by the development of acute neuropathy following a significant improvement in glycaemic control. This phenomenon is well described in TIN, but not previously highlighted in other acute neuropathies. LEARNING POINTS: A link between acute tightening of glycaemic control and acute neuropathies has not been well described in literature. Clinicians caring for patients with diabetes who develop otherwise unexplained neurologic symptoms following a tightening of glycaemic control should consider the possibility of an acute diabetic neuropathy. Early recognition of these neuropathies can obviate the need for detailed and expensive investigations and allow for early institution of appropriate pain-relieving medications.

Factors influencing elevated serum apolipoprotein B48 in diabetic and control participants.

Factors influencing the concentration of apolipoprotein B48 (apo B48) at fasting and post-prandial time frames are still being elucidated. This study assesses some possible contributing factors including the presence of type 2 diabetes and gender using an established enzyme-linked immunosorbent assay (ELISA) method. Apo B48 and triglyceride (TG) levels were measured before and for two, four and six hours post-prandially in 49 poorly controlled participants with type 2 diabetes and in 60 apparently healthy participants (controls). Apo B48 levels in the control participants increased post-prandially, peaking at four hours (14.81 ± 7.72 µg/mL) with similar responses demonstrated in TG concentrations. Post-prandial apo B48 levels were significantly higher in male control participants as demonstrated by apo B48 area under the curve (AUC); similar responses were also confirmed in triglyceride AUC. Post-prandial apo B48 concentrations in control participants correlated with HOMA-IR (P < 0.05). Apo B48 continued to increase throughout the six hours in participants with type 2 diabetes (17.73 ± 13.46 µg/mL), when levels were significantly greater than in the control participants (13.04 ± 7.67 µg/mL) (P < 0.05) despite a decrease in accompanying TG levels in participants with type 2 diabetes. Using an ELISA method, this study demonstrated that gender, insulin resistance (as evidenced by HOMA-IR) and diabetes status influence serum apo B48 levels. These effects were only apparent post-prandially.

High-molecular-weight adiponectin is selectively reduced in women with polycystic ovary syndrome independent of body mass index and severity of insulin resistance.

CONTEXT: High-molecular-weight (HMW) adiponectin contributes to insulin resistance (IR), which is closely associated with the pathophysiology of polycystic ovary syndrome (PCOS). Abnormalities in adipocyte function have been identified in PCOS and potentially contribute to lower adiponectin concentrations. OBJECTIVE: Our objective was to determine which variables in plasma and adipose tissue influence HMW adiponectin in a well characterized cohort of women with PCOS. DESIGN: This was a cross-sectional study. SETTINGS AND PARTICIPANTS: A teaching hospital. Women with PCOS (n = 98) and body mass index (BMI)-matched controls (n = 103) (including 68 age-, BMI-, and IR-matched pairs). INTERVENTIONS: A standard 75-g oral glucose tolerance test was performed for each participant. Subcutaneous adipose tissue samples were taken by needle biopsy for a subset of PCOS women (n = 9) and controls (n = 8). MAIN OUTCOME MEASURES: Serum levels of HMW adiponectin and their relation to indices of insulin sensitivity, body composition, and circulating androgens as well as adipose tissue expression levels of ADIPOQ, TNFalpha, PPARgamma, and AR were assessed. RESULTS: HMW adiponectin was significantly lower in women with PCOS compared with both BMI- and BMI- and IR-matched controls (P = 0.009 and P = 0.027, respectively). Although BMI and IR were the main predictors of HMW adiponectin, an interaction between waist to hip ratio and plasma testosterone contributed to its variance (P = 0.026). Adipose tissue gene expression analysis demonstrated that AR and TNFalpha (P = 0.008 and P = 0.035, respectively) but not ADIPOQ mRNA levels were increased in PCOS compared with controls. CONCLUSIONS: HMW adiponectin is selectively reduced in women with PCOS, independent of BMI and IR. Gene expression analysis suggests that posttranscriptional/translational modification contributes to reduced HMW adiponectin in PCOS.