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Tyrosine kinase inhibitors can cause significant hypoglycemia in patients with diabetes on other antihyperglycemic medications. These patients should be monitored, and their medications adjusted accordingly.

Causes of hypercalcemia can be categorized into parathyroid-dependent (PTH-mediated) and parathyroid-independent (non-PTH-mediated) disorders. Parathyroid-independent hypercalcemia encompasses hypercalcemia of malignancy, granulomatous disorders, endocrinopathies, medications, and other disorders.

K.D., a 20-year-old white female college student was brought by her parents for evaluation of hypoglycemia. She had experienced multiple episodes of palpitations, blurred vision, and left facial paresthesias for a year, progressively worsening and occurring more frequently in the 2 months just before her appointment. Usually the episodes occurred between 3:00 and 7:30 p.m. The symptoms occurred without regard to meals and were relieved with food or juice. Her most severe witnessed episode, which occurred while she was at college, happened a few days before the consultation, while K.D. was working, 2 hours postprandially. Observers reported that she appeared confused, agitated, and diaphoretic. Her glucose via fingerstick by paramedics was 35 mg/dl. She received intravenous dextrose, and subsequently her glucose rose to 217 mg/dl with resolution of her symptoms. She had several episodes with neuroglycopenic symptoms and glucose levels of 35-45 mg/dl. There was no history indicating diabetic medications in her home. She also complained of a 25-lb weight gain during the past year. A year before her visit, K.D. was diagnosed with diabetes by oral glucose tolerance test (OGTT). The results were: View this table: At that time, she had a normal hemoglobin A1c, and she was instructed in diet and exercise. No antidiabetic medications had been prescribed. K.D. had a psychiatric evaluation, was diagnosed with depression, and was started on sertraline. In the month before the consultation, she also had a neurological work-up with negative computed tomography scans of the head and normal electroencephalogram. Her family history was significant only for diabetes of a maternal aunt. She denied allergies or use of cigarettes, alcohol, or illicit drugs. She was taking sertraline, 50 mg daily for the past year; ethinyl estradiol/norgestimate, one daily for the past 2 years; and oxcarbazepine, 175 mg twice daily for the …

Neuropathy as a complication of diabetes is common and presents in a wide variety of clinical scenarios. Often the work-up is one of exclusion tempered with monitoring the response of symptoms to treatment options. The collaboration of a neurologist is often crucial to determining the best course of action for the patient. This review will address proposed pathogenic mechanisms and potential therapeutic interventions, both pharmacologic and nonpharmacologic.

Neuropathies related to diabetes mellitus can affect 60-70% of patients with diabetes. These can include peripheral polyneuropathies, mononeuropathies, and autonomic neuropathies. Control of glucose, lipids, and hypertension and cessation of smoking can limit onset and progression of these neuropathies. Besides control of the above listed risk factors, we do not have effective medications to treat the pathophysiologic mechanisms of diabetic neuropathies. Treatment is limited to ameliorating pain and correcting the end organ consequences of the neuropathic processes.