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/m 2. 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.
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.
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