was beef-pork ultralente insulin. In our experience, fasting morning hyperglycemia is best prevented by the administra- tion of human ultralente insulin at ...
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was beef-pork ultralente insulin. In our experience, fasting morning hyperglycemia is best prevented by the administration of human ultralente insulin at bedtime. We switch all of our new patients to this insulin and find dramatic improvements in morning glycemia. For some reason, human NPH and animal lente and ultralente insulins appear to result in higher fasting blood glucose than does human ultralente. Could it be that animal insulins are inactivated in humans more rapidly than is human insulin? If this were true, then human NPH might qualify as an animal insulin because it is complexed with protamine, a protein that is not native to humans. Most of our adult IDDM patients require 4-6 U human ultralente at bedtime to achieve morning blood glucose that matches bedtime blood glucose. Nevertheless, some patients require as much as three times the lente dose at bedtime than they require in the morning. Furthermore, this larger dose is usually more predictable if administered in two separate injections rather than as one injection of 12-18 U. In addition, some patients on our regimen may arise with normal blood glucose (e.g., 90 mg/dl) yet discover 1 h later that their blood glucose had increased by 50% while still fasting. For such individuals, we recommend a small amount of human regular insulin on arising. This is injected separately from the morning human ultralente insulin and is frequently added to the prebreakfast regular insulin. We call it the "dawn phenomenon dose." In our experience, it has never exceeded 1.5 U. Some patients require as little as 0.5 U to maintain a normal fasting blood glucose throughout the morning hours. Sherwin et al. (1) neglected to point out that a common cause of elevated morning blood glucose is delayed gastric emptying due to gastroparesis diabeticorum. Patients suffering from this neuropathic condition may frequently and unpredictably fail to achieve full emptying of their evening meal before bedtime. While they are sleeping, the stomach may therefore empty further, resulting in blood glucose elevation on arising. We find that ~50% of such patients respond favorably to metaclopromide syrup administered 30 min before the evening meal. We try to avoid the use of this medication before other meals, where possible, because of the high incidence of adverse side effects.
developed cataracts. Their IDDM had been diagnosed at age 3 wk to 14 yr and the cataracts at age 6-16 yr. In 2 children, cataracts were noted at the onset of diabetes. These 2 children had had symptoms of diabetes for 2 and 6 mo, respectively. In the remainder, cataracts were noted 3.5 mo to 10 yr after the diagnosis of IDDM. One child appeared to develop cataracts while coming out of her "honeymoon" phase. The chief complaint in the 8 children who had diffuse subcapsular cataracts was the sudden onset over a few days or gradually over a few weeks of blurred vision. Two children had a snowflake or punctate appearance to their cataracts but did not have visual complaints. Metabolic control in the 10 patients was considered average to poor. The HbA|c in 3 children at the time the cataracts were diagnosed was 8.0, 9.0, and 14-0% (mean ± SD for our clinic 9.0 ± 1.5%). In the 7 children whose HbA|c levels were not measured, metabolic control was considered poor in 5, as judged by history of recurrent ketoacidosis. We sought associations with other microangiopathic complications of diabetes. None of the children had evidence of diabetic retinopathy by ophthalmoscopy, nor did any of the children have proteinuria. One child had limited joint mobility. Another child had hypothyroidism and was being treated with L-thyroxine. Another child subsequently developed hyperthyroidism. In each case, a period of intensified control was instituted to see if the density of the cataracts could be reversed or improved with improved glucose homeostasis. Although improvement occurred in the eyes of some children, it was insufficient in 8 of them, all of whom required some surgery. Only the 2 children with punctate cataracts did not require surgery. This represents the largest reported experience with cataracts in children with IDDM. Klein et al. (1) reported 9 cases of cataracts in 266 patients
