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Follow-up Visit
When SW returns to his PCP for a regular exam in 2 months, his blood pressure is 144/88 mm Hg, and a fasting blood glucose is now 122 mg/dL. His lipid profile has worsened (total cholesterol: 200 mg/dL; triglycerides: 240 mg/dL; HDL cholesterol: 17 mg/dL; LDL cholesterol: 136 mg/dL; microalbumin/creatinine ratio: 40).
Q: How do you explain SW’s worsening lipid profile and fasting glucose levels?
A: There are several possible reasons for this disease progression. First, SW’s level of insulin resistance may have increased. Second, the degree of beta cell function may have decreased to the point that his insulin production is no longer able to keep up with his plasma glucose levels. Third, thiazide diuretics (ie, hydrochlorothiazide) can sometimes cause biochemical alterations, such as hypokalemia, hyperuricemia, hyperglycemia, and hypercholesterolemia in individual patients.
Even though the initial choice of a diuretic is supported by clinical trial data and was a reasonable selection, this patient appears to be sensitive to the metabolic effects of the diuretic, and changing to a different drug class would be appropriate at this point.
SW is switched from hydrochlorothiazide to ramipril (10 mg per day) and started on atorvastatin (10 mg per day at bedtime). One month later his blood pressure is 142/86 mm Hg. His lipid values are: total cholesterol, 170 mg/dL; triglycerides, 200 mg/dL; HDL-C, 31 mg/dL; and calculated LDL-C, 99 mg/dL. His fasting glucose is 116 mg/dL and the microalbumin/creatinine ratio is 20.
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