Evaluation of hypoglycemia in a patient with known diabetes mellitus, although usually straightforward, can at times be challenging. We present the case of an 8 year-old Latina girl initially diagnosed with type 1 diabetes mellitus in the setting of multiple autoimmune disorders, including dermatomyositis and lupus nephritis. She subsequently developed signs of insulin resistance and severe hypoglycemia, which was found to be due to insulin-receptor autoantibodies. This condition, known as type B insulin resistance, is a rare, heterogeneous metabolic disease that may feature hypoglycemia in the setting of extreme insulin resistance and hyperinsulinemia and, in this case, masqueraded as type 1 diabetes mellitus. The presence of hypoglycemia in the setting of multiple autoimmune disorders should prompt consideration of autoimmune-mediated hypoglycemia. In addition to immunologic modifying therapies, advances in diabetes care in the form of continuous glucose monitoring have provided an additional tool to manage recurrent hypoglycemia.

A 12-year-old Caucasian female was admitted for evaluation of severe headaches progressively increasing in intensity, radiating to neck for the past 1 month. The history was significant for decreased energy level, difficulty in concentrating for past 6 weeks, slow linear growth, and excessive weight gain (4 inches increase in height and 30 pounds of weight gain over the past 3 years) and intermittent bilateral knee pain. There was no history of fever, rash, vomiting, and changes in bowel habits, temperature intolerance, or difficulty in vision. One week prior to admission, she came to emergency room with the complaint of headaches, was sent home on pain relieving medications after ensuring computed tomography of the brain was negative for intracranial bleed.Family history included type 1 diabetes mellitus and hypothyroidism in mother since she was a child and paternal grandfather had hyperthyroidism. Physical exam revealed height of 145.4 cm (14th percentile), weight of 66 kg (96th percentile) and obesity with a body mass index of 31.5 kg/m 2 . She had a heart rate of 70 beats per minute, respiratory rate of 16 per minute, blood pressure of 93/64 mm Hg, and oxygen saturation of 100%. She had normal visual fields. Her skin was dry and there was loss of lateral third of eye brows bilaterally. Abdominal examination did not reveal liver enlargement. Both breasts and pubic hair were Tanner stage 1. There were no signs of meningeal irritation, normal strength in all 4 limbs with normal gait and coordination.On admission, initial computed tomography of the brain revealed a mass in the pituitary region. This was confirmed with contrast-enhanced magnetic resonance imaging, demonstrating homogeneous enlargement of the pituitary gland measuring 17 mm × 14 mm × 9 mm with compression of optic nerves bilaterally. Laboratory testing done for evaluation of intracranial mass, showed an elevated α-fetoprotein 7.6 ng/mL (normal 0.6-5.6 ng/ mL), prolactin 67.6 ng/mL (normal 4.6-49.1 ng/mL), and a normal quantitative β-human chorionic gonadotropin( < 1.20 mIU/mL). She also had mildly elevated liver functions with aspartate aminotransferase of 42 U/L (normal 17-33 U/L) and alanine aminotransferase of 49 U/L (normal 6-35 U/L). Cerebrospinal fluid analysis showed mildly elevated protein level of 70 mg/dL, normal glucose and negative for α-fetoprotein.Additional testing showed very elevated thyroid-stimulating hormone (TSH > 1000 µIU/mL), low free T4 (<0.40 ng/dL), and positive thyroid peroxidase antibodies. She had a delayed bone age on hand radiograph and normal bilateral hip radiograph. Ultrasound of abdomen showed increased echogenicity of the liver with diminished periportal visualization suggestive of fatty infiltration and ultrasound pelvis revealed multiple ovarian cysts.In view of elevated TSH, low free T4, and positive thyroid autoantibodies, she was diagnosed with profound primary hypothyroidism secondary to Hashimoto's thyroiditis and pituitary hyperplasia due to hypothyroidism. Elevated α-fetoprotein and prolactin, fatty liv...

Some studies have shown the correlation between E4 type of Apolipoprotein E gene and diabetic neuropathy, however, there are contradicting results in recent studies. The aim of this meta-analysis was to investigate the association between APOE4 gene and diabetic neuropathy. Database of Pubmed, Wuhan University Library, and Google were searched. A total of 56 studies were screened and 5 studies were selected for quantitative meta-analysis. This meta-analysis was performed to assess heterogeneity and combine results by using software RevMan 5.2. Strength and relationship were calculated as the odds ratio (OR) with a confidence interval (CL) of 95% using generic inverse variance data. Sensitivity analysis and Publication Bias analysis was conducted. A total of 5 studies were included for quantitative analysis with total of 914 patients (498 diabetic patients with neuropathy as case and 416 diabetic patients without neuropathy as controls). The result of our study indicated that APOE4 carriers were likely to have high risk of diabetic neuropathy. (E4 vs. others; pooled OR with 95% confidence interval 1.80 (1.28, 2.53), p< 0.05 (p =0.0007)). In conclusion, this meta-analysis suggests that there is significant association between APOE4 gene and occurrence of diabetic peripheral neuropathy. However, further studies are needed for more detailed analysis.