Insulin therapy adverse effects

The most common adverse effects of indinavir are indirect hyperbilirubinemia and nephrolithiasis due to crystallization of the drug. Nephrolithiasis can occur within days after initiating therapy, with an estimated incidence of approximately 10%. Consumption of at least 48 ounces of water daily is important to maintain adequate hydration. Thrombocytopenia, elevations of serum aminotransferase levels, nausea, diarrhea, insomnia, dry throat, dry skin, and indirect hyperbilirubinemia have also been reported. Insulin resistance may be more common with indinavir than with the other Pis, occurring in 3-5% of patients. There have also been rare cases of acute hemolytic anemia. 

In 33 patients with type 2 diabetes treated with sulfo-nylureas and insulin who took miglitol 50 mg bd for 1 week and then over the next month increased the dose to 50 mg tds, 15% developed adverse effects (6% diarrhea, 6% abdominal distension), which disappeared within 3 weeks of continuing therapy (42). 

In a post-marketing surveillance study of 1142 patients in whom acarbose was added to insulin therapy for type 2 diabetes mellitus, HbAlc improved by 0.9% and there were 108 adverse effects in 6.9% of the patients (45). Most of the complaints were gastrointestinal (flatulence, abdominal pain, diarrhea) and more than half were reported in the first week of acarbose therapy. 

Hypoglycaemia is the most common adverse effect with sulphonylureas, but is less common than with insulin therapy. It can be severe, and prolonged (for days), and may be fatal in 10% of cases, especially in the elderly and in patients with heart failure. Erroneous alternate diagnoses such as stroke may be made. 

Insulin edema is a rare complication, more often seen in the earlier years of insulin therapy (SEDA-11, 364). It is mostly seen when dysregulated patients with progressive weight loss are treated with relatively high amounts of insulin. Reduced sodium excretion (88), sodium reabsorption, and water retention by a possible direct action of insulin on the kidney may be involved (89). The role of aldosterone or of inhibition of the renin-angiotensin-aldosterone system in insulin edema is unclear. Insulin edema is a specific adverse effect, but it can aggravate pulmonary edema, congestive heart failure, and hypertension. Treatment consists of reduction of the insulin dose, after which the edema resolves within 3 days. 

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