Early Dinner Improves the Glycemic Profile in Habitual Late Eaters With Uncontrolled Type 2 Diabetes Mellitus in the Short Term.

Background Late dinner (LD) can worsen the glucose profile in type 2 diabetes (T2D). We assessed the short-term effect of early dinner (ED) on glycemic control in habitual late eaters with uncontrolled T2D. Methodology This interventional, single-arm, within-group trial recruited 10 habitual late eaters with uncontrolled T2D (glycosylated hemoglobin: 7-9% and either fasting plasma glucose (FPG): ≥140 mg/dl or post-prandial plasma glucose: ≥200 mg/dl). They had their usual LD (beyond 22:00 hours) on Days 0-3 and ED (before 20:00 hours) on Days 4-10. Continuous glucose monitoring system (CGMS) parameters, two-hour post-dinner, and fasting (10-hour post-dinner) investigations were analyzed. Bedtime hunger was assessed using a Labeled Magnitude Satiety Scale. Results The mean dinner time was reduced from 22:28 hours to 19:29 hours. CGMS revealed that ED lowered the 10-hour post-dinner incremental area under the curve (22,587.9 ± 5,168.3 mg/dl×mins vs. 15,886.3 ± 4,288.7 mg/dl×mins, P < 0.002), 10-hour post-dinner average blood glucose (ABG) (137.5 ± 9.3 mg/dl vs. 125 ± 7.9 mg/dl, P < 0.002), 24-hour ABG (132.2 ± 7.5 mg/dl vs. 124.8 ± 5.4 mg/dl, P = 0.037), and night mean amplitude of glucose excursion (83.7 ± 5.8 mg/dl vs. 69.3 ± 7.5 mg/dl, P = 0.027). ED also reduced FPG (119.8 ± 7.3 mg/dl vs. 105.2 ± 5.7 mg/dl, P = 0.015), fasting insulin (15.0 ± 4.3 µIU/ml vs. 9.7 ± 2.7 µIU/ml, P < 0.002), and HOMA-IR (4.36 ± 1.2 vs. 2.56 ± 0.79, P < 0.002). Post-dinner glucose, insulin, and inflammatory markers were unchanged. Bedtime hunger increased significantly on Days 4 and 5 but returned to baseline by Day 10. Conclusions A simple modification of dinner time in habitual late eaters with uncontrolled T2D improves FPG, glycemic control, and insulin resistance in the short term.

Unrecognized Primary Hypothyroidism As a Possible Cause of Hyperreactio Luteinalis.

Hyperreactio luteinalis (HRL) is characterised by benign enlargement of ovaries in pregnancy associated with hyperandrogenism. A 19-year-old primigravida presented with breathlessness, abdominal distension and vomiting in the thirteenth week of gestation. Abdominal examination revealed distension of abdomen disproportionate to the gestational age. Ultrasound was suggestive of bilaterally enlarged multicystic ovaries with a characteristic "spoke-wheel" pattern and a diagnosis of HRL was made. Laboratory investigations revealed primary hypothyroidism and elevated testosterone. She was initiated on levothyroxine therapy. Her respiratory distress worsened on the third day of admission for which she underwent emergency laparotomy with cyst aspiration. Thyroid function tests normalized within six weeks after the initiation of therapy and remained normal for the remainder of pregnancy. Serum testosterone levels returned to normal six weeks postpartum. The elevated thyroid-stimulating hormone levels could have contributed to development of HRL by cross-reacting with human chorionic gonadotropin and follicle-stimulating hormone receptors. Hyperandrogenism and ovarian enlargement regresses with levothyroxine therapy.

A Lean Lady With Acanthosis Nigricans and Uncontrolled Diabetes Mellitus.

A 47-year-old Asian Indian woman presented with uncontrolled hyperglycaemia and osmotic symptoms despite multiple oral antidiabetic medications and insulin. She had a history of recurrent oral ulcers, profound weight loss, and intermittent fever for one and a half years before the presentation. She had severe acanthosis nigricans, although her body mass index (BMI) was 14.6 kg/m2. Her blood glucose remained uncontrolled despite very large dosages of intravenous insulin (more than 12,000 units daily). Evaluation for possible underlying collagen vascular diseases and malignancies were negative. Her serum insulin levels were high. She tested negative for anti-insulin antibodies but positive for anti-insulin-receptor antibodies. She improved with a pulse dose of intravenous methylprednisolone but relapsed within one month. A second pulse dose was given following which a complete remission of diabetes and regression of acanthosis was observed. Type B insulin resistance, a rare cause of severe insulin resistance, may respond favourably to immunosuppressive therapy with high-dose methylprednisolone.

Current Status of Diagnosis and Management of Functioning Pituitary Tumors: Part II.

Functioning pituitary tumors contribute to significant morbidity and mortality. Proper diagnostic approach and management is essential for optimal outcomes. Prolactinomas, the commonest of these, are the only tumors which can be managed medically. Acromegaly, apart from acral enlargement, can have multiple comorbidities like diabetes, hypertension, and obstructive sleep apnea. The primary treatment is surgical and it can be supplemented by radiotherapy and medications such as somatostatin analogs, growth hormone receptor blockers, or cabergoline. Thyrotropin-secreting tumors are rare and present with hyperthyroidism. Optimal preoperative management followed by surgical resection often leads to cure.