A 43-year-old female patient is currently being treated by us for a recurrence of adrenal cortical carcinoma associated with Cushing's syndrome and virilization. Despite many relapses of metastatic spread she has not only survived for 25 yr after the removal of the primary tumor but also until now preserved her ability to work in a textile factory.

Adolescent↗

PubMedDate not supplied

Secondary failure to treatment with oral antidiabetic agents in non-insulin-dependent diabetes.

To study the etiopathogenesis of secondary drug failure to treatment with oral antidiabetic agents in patients with non-insulin-dependent diabetes (NIDD) we compared 60 "nonresponders" with 60 "responders" to treatment with oral drugs. Secondary drug failure was defined as mean diurnal blood glucose greater than 12 mmol/L after an initial good response of greater than or equal to 2 yr. The nonresponders were characterized by 50% lower C-peptide concentrations than the responders (P less than 0.001). We could not, however, define a critical C-peptide level to discriminate between patients requiring and not requiring insulin therapy. There was a wide overlap of individual C-peptide values between responders and nonresponders that attenuates the clinical value of single C-peptide measurements in predicting therapy. Only by serial measurements over a period of time was it possible to achieve information about changes in beta cell function. The nonresponders showed increased frequency of islet cell (P less than 0.01), thyroid antimicrosomal (P less than 0.01), and gastric parietal cell antibodies (P less than 0.02). In nonresponders, HLA-antigen B8 was increased (P less than 0.05) and HLA-B7 decreased (P less than 0.01) compared with frequencies of responders. In conclusion, impaired beta cell function is a characteristic feature of many, but not all, NIDD patients who fail on treatment with oral antidiabetic drugs. The presence of islet cell and thyrogastric antibodies can unmask a distinct group of NIDD patients with a high risk of secondary drug failure and subsequent insulin dependency. HLA typing may further help to predict secondary failure in NIDD.

Administration, Oral↗

PubMedDate not supplied

Overnight interruption of wearing insulin pump: substitution dose and injection site of insulin.

Discontinuing wear of the insulin pump for short periods enhances the feasibility of continuous subcutaneous insulin infusion (CSII) therapy. Because insulin requirements differ during pump and injection therapy, we studied the optimal substitution dose and injection site in seven type I diabetic patients to compensate for the overnight (2100-0730 h) interruption of CSII. The missed basal continuous infusion dose was replaced by injecting intermediate-acting insulin subcutaneously in three different ways: 1.5 times the dose in the abdomen, twice the dose in the abdomen, and twice the dose in the buttock. During CSII, glycemia remained unchanged throughout the night. Both 1.5 times and twice the replacement doses injected in the abdomen resulted in an initial decline in blood glucose with hypoglycemia in two patients followed by a rebound rise. When the replacement dose of 1.5 times was used, blood glucose rose by 4.9 +/- 1.2 mM overnight (P less than .02). These changes after abdominal injection were associated with a rapid early absorption of injected insulin with hypoinsulinemia in the morning. With twice the replacement dose injected in the buttock, insulin absorption was slower, fluctuations in nocturnal glycemia were minor, and the blood glucose level at 0730 h was similar to that of the previous night. There was a significant inverse correlation between blood glucose and serum free-insulin levels in the early morning (r = - .60, P less than .01). In conclusion, a substitution dose of 1.5 times to twice the missed basal infusion rate injected in the buttock compensates for the overnight interruption of CSII without risk of major fluctuations in blood glucose levels or nocturnal hypoglycemia.

Abdomen↗

PubMedDate not supplied

Glucose and insulin responses to meals containing milk, lactose, glucose or fructose in subjects with non-insulin-dependent diabetes.

The postprandial blood glucose and serum insulin responses to liquid test meals containing 40 g carbohydrate from milk, lactose, glucose or fructose and equal amounts of energy were compared in 10 non-insulin-dependent (type 2) diabetic patients. The meals were consumed in random order on consecutive days after an overnight fast. Significant differences (p less than 0.001, ANOVA) were observed between the glucose and insulin responses to the meals. The glucose response was significantly higher after the glucose containing meal and lower after the fructose meal as compared with the other meals. The insulin response was significantly higher after the lactose and glucose meals than after the milk and fructose meals. After the milk and lactose meals the blood glucose responses were similar whereas the insulin response was significantly lower after the milk meal. As lactose apparently was similarly absorbed from the two meals the difference in the insulin response was probably due to different insulinogenic effects of the protein components or to differences in the physical properties of the respective meals.

Adult↗