A 55-year-old man is seen in the clinic for follow-up of type 2 diabetes mellitus. He feels well, has been exercising regularly, and has had good control of his blood glucose on oral metformin, with HgA1c of 6.4%. He has a history of mild hypertension and hyperlipidemia. Which of the following statements is correct regarding routine testing for diabetic patients?
Guidelines for ongoing medical care in diabetic patients recommend that the following screenings or interventions be performed annually: dilated eye examination, lipid profile, and medical nutrition therapy and education. Annual screening for diabetic nephropathy begins with dipstick assessment of urine protein and, if negative, testing of a single voided specimen for albumin/creatinine ratio. Twenty-four-hour urine testing is not recommended. A careful foot examination should be performed yearly by the physician and daily by the patient. Peripheral neuropathy is first suggested by distal loss of sensation to 10 g monofilament testing on clinical examination. HgA1c testing should be performed two to four times a year depending on patient’s diabetes control (if patient’s HgA1c is at goal, twice yearly is adequate). Blood pressure should be measured quarterly. Home glucose measurements are usually performed once daily in well-controlled type 2 diabetics.
A 55-year-old man presents to the office with erectile dysfunction. He has mild diabetes and is on an ACE inhibitor for hypertension. He and his wife enjoy a good relationship, and there is little external stress. He has, however, noted a lessening of sexual desire; they have not had intercourse in the past 6 months. The general physical examination is normal. In particular, his peripheral sensation to monofilament is intact, and vascular examination of the lower extremities is normal. Testicular size is mildly decreased bilaterally. Which of the following is the most appropriate first step in evaluation?
Although the commonest causes of erectile dysfunction are vascular (including small vessel disease), neurological, and psychological, endocrine causes should not be overlooked. Most patients with vascular or neurological causes retain libido, which is driven by testosterone. This patient’s diminished libido, as well as his small testicular size, suggests hypogonadism as a potential cause. The first step in evaluation for endocrine causes of ED is a morning testosterone and prolactin level. Free testosterone is more specific but much more expensive. A testosterone level above 350 effectively excludes hypogonadism. Levels between 200 and 350 are equivocal and should either be repeated or be followed by a free testosterone. If the testosterone level is low, gonadotrophin levels will help determine if the cause is central (low LH) or peripheral (ie, testicular failure with high gonadotrophin level). An elevated prolactin level or evidence of central hypogonadism in a young or middle-aged man should prompt a search for a pituitary tumor. Although peripheral neuropathy and peripheral arterial disease can cause erectile dysfunction, this patient has a normal neurological and vascular examination. Diabetic autonomic neuropathy is usually associated with a distal sensory neuropathy that would be detected on physical examination. In a diabetic with ED and loss of libido, you should not assume that neuropathy is the cause of the ED, as a sight-threatening pituitary tumor may be missed. Psychological factors were once felt to be the leading cause of ED; now organic causes are felt to be more common, although in few areas of life are psychological factors more important than in sexual function. Psychogenic impotence is usually associated with preservation of spontaneous morning erections and is often partner-specific. This patient’s loss of libido should not be ascribed to psychological causes until hypogonadism has been ruled out. Although phosphodiesterase-5 inhibitors are effective treatments for ED, organic causes should be considered first, or important medical diseases might be overlooked.
A 65-year-old diabetic patient is hospitalized because of acute cholecystitis. His diabetes is normally controlled with metformin 850 mg twice daily; a recent hemoglobin A1C level was 6.4. Cholecystectomy is performed, but is complicated by postoperative pneumonia and septic shock. The patient requires endotracheal intubation and ICU care. Blood cultures grow gram-negative rods, and vasopressors are required to maintain peripheral perfusion. What is the best method of controlling blood sugars in this patient?
The best way to maintain glucose control in the critically ill patient is to use continuous glucose infusion with frequent fingerstick blood glucose measurements and dosage adjustments. Although initial studies suggested the benefit of “tight” glucose control (especially in septic or postoperative patients), subsequent trials showed that a more modest target (140-180) leads to better outcomes and prevents complications (especially adverse cardiac events and severe hypoglycemia). Once stabilized and taking enteral nutrition, the patient can often be easily transitioned to a basal-bolus regimen (ie, a long-acting insulin supplemented by pre-meal boluses of a short-acting insulin). Although metformin is usually the initial oral agent chosen for the outpatient management of type 2 diabetes, it should not be used in the setting of critical illness, where fluctuations in renal perfusion and GFR increase the risk of lactic acidosis. Metformin should be withheld around the time of surgery and radiographic procedures involving the use of IV contrast agents for the same reason. “Sliding scale” insulin has fallen out of favor in this setting as well; it is reactive rather than proactive and often leads to wide fluctuations and inadequate glucose control. Although continuous insulin infusion using a subcutaneous pump may be employed as an outpatient for tight glucose control, its use in the critical care setting has not been well studied and is probably inferior to IV insulin.
A 58-year-old postmenopausal woman presents to your office on suggestion from a urologist. She has passed three kidney stones within the past 3 years. She is taking no medications.
Her basic laboratory work shows the following:
A repeat calcium level is 11.4 mg/dL; PO4 is 2.3 mmol/L (normal above 2.5).
Which of the following tests will confirm the most likely diagnosis?
Hypercalcemia must first be confirmed since misleading laboratory values can be caused by hemoconcentration of the serum sample. Ninety percent of hypercalcemia is attributed either to hyperparathyroidism or to malignancy. Almost all patients with malignancy-associated hypercalcemia have previously diagnosed cancer or symptoms (weight loss, anorexia, cough, hemoptysis) to suggest this diagnosis. In this otherwise healthy patient, confirmed hypercalcemia should lead to measurement of intact parathyroid hormone (iPTH). Other causes of hypercalcemia include familial hypocalciuric hypercalcemia, vitamin D intoxication, sarcoidosis and other granulomatous diseases, hyperthyroidism, prolonged immobilization, and milk-alkali syndrome. Thyroid studies and liver enzymes (to evaluate for granulomatous hepatitis) might be ordered if the iPTH level is suppressed. Urine calcium excretion is assessed before parathyroidectomy to rule out familial hypocalciuric hypercalcemia, which can otherwise mimic hyperparathyroidism. Urine calcium determination, however, would not be the first test obtained in the assessment of hypercalcemia. Osteoporosis should be considered in this postmenopausal woman with hyperparathyroidism and appropriate screening for osteoporosis performed with central dual x-ray absorptiometry (DXA).
A patient comes to your office for a new-patient visit. He has moved recently to your city due to a job promotion. His last annual examination was 1 month prior to his move. He received a letter from his primary physician stating that laboratory workup had revealed an elevated alkaline phosphatase and that he needed to have this evaluated by a physician in his new location. On questioning, his only complaint is pain below the knee that has not improved with over-the-counter medications. The pain increases with standing. He denies trauma to the area. On examination you note slight warmth just below the knee, no deformity or effusion of the knee joint, and full ROM of the knee without pain. You order an x-ray, which shows cortical thickening of the superior fibula and sclerotic changes. Laboratory evaluation shows an elevated alkaline phosphatase of 297 mg/dL with an otherwise normal metabolic panel. In particular, the liver transaminases and gamma glutamyl transpeptidase (GGT) levels are normal. Which of the following is the treatment of choice for this patient?
The radiographs and elevated alkaline phosphatase suggest Paget disease of the bone. Most patients with Paget disease do not require treatment, as they are asymptomatic. Bone pain, hearing loss, bony deformity, congestive heart failure, hypercalcemia, and repeated fractures are all indications for specific therapy beyond just symptomatic treatment for pain. Bisphosphonates bind to hydroxyapatite crystals to decrease bone turnover; they are now recommended as the treatment of choice for symptomatic Paget disease. Newer bisphosphonates such as alendronate and risedronate have replaced etidronate because they are more potent and do not produce mineralization defects. The recommended dose in Paget disease is higher than the bisphosphonate dose used to treat osteoporosis. Subcutaneous injectable calcitonin is still used in patients who cannot tolerate the GI side effects of bisphosphonates. Melphalan and prednisone can be used to treat multiple myeloma, but myeloma causes osteolytic (rather than sclerotic) changes and does not cause elevation of the serum alkaline phosphatase. Ursodeoxycholic acid (UDCA) is utilized in the treatment of primary biliary cirrhosis (which can also present with elevated alkaline phosphatase) but has no effect on bone mineralization.
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