Reversal of the carpal tunnel syndrome after change of insulin injection sites.
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Adult↗
Biomedical subjects
R S Clements
Publications and source records attributed to R S Clements.
Acuphobia in a long-standing insulin-dependent diabetic patient cured by hypnosis.
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Adult↗
The use of human insulin derived from baker's yeast by recombinant DNA technology.
Human insulin has gradually replaced animal insulin as the therapeutic agent of first choice among insulin-dependent and insulin-requiring patients with diabetes. Like animal insulin, human insulin manufactured by several different methods is available in Regular, NPH, Lente, and 70/30 (NPH/Regular) formulations. The most recently developed method of manufacturing human insulin uses recombinant DNA technology with baker's yeast as the host cell [rDNA HI (BY)], offering potentially limitless supplies of insulin structurally identical to that made by the human pancreas. Clinical studies have demonstrated that the extent of insulin absorption, the glucose-lowering effects, and the clinical effects on glycemic control and on incidence of hypoglycemia with rDNA HI (BY) are similar to those observed when patients are treated with semisynthetic human insulin (ssHI). Dose-for-dose transfer of patients from ssHI to rDNA HI (BY) is therefore appropriate. It is standard practice to recommend that any change in insulin be conducted under medical supervision.
Blood Glucose↗
Insulin antibodies in non-insulin-dependent diabetes mellitus: effect of treatment with semisynthetic human insulin.
This multicenter study of patients with non-insulin-dependent diabetes mellitus (NIDDM) was undertaken (1) to determine the incidence of insulin antibody formation in such patients before exposure to exogenous insulin; (2) to assess the long-term immunologic response to semisynthetic human insulin (ssHI) in new insulin users and in patients transferred from animal insulin; and (3) to document the efficacy and safety of ssHI in both new and transfer patients. In addition, a substudy at one participating center was designed to compare the effects of a twice-daily versus a once-daily regimen in initiating ssHI therapy in new patients with uncontrolled NIDDM. Among the 37 new patients, only one had detectable insulin antibody levels before administration of insulin. After ssHI therapy was begun, this patient's antibody levels rapidly fell below the assay's limit of detection. Detectable levels of antibodies to human insulin were found in only 36% of 28 new patients after 12 months of therapy. As expected, the prevalence of insulin antibodies among animal-insulin users was high: 82% of the 17 transfer patients had detectable insulin antibody levels (mean, 2.27 mU/ml) at baseline. After six months of treatment with ssHI, antibody levels decreased significantly (mean, 0.75 mU/ml; P less than 0.05). Control of glycemia was assessed by measurement of glycosylated hemoglobin. Values decreased significantly (P less than 0.01) in the new patients after the introduction of ssHI and remained stable in the transfer group after initiation of ssHI therapy. Hypoglycemic episodes were infrequent in both groups. In initiating ssHI therapy in new patients hospitalized with uncontrolled NIDDM, a twice-daily regimen resulted in a more rapid normalization of glycemia and earlier discharge than did the standard once-daily regimen. In conclusion, the results of this study provide further evidence that NIDDM and insulin-dependent diabetes mellitus (IDDM) are immunologically different disorders, with the immune system probably not involved in the pathogenesis of NIDDM. The data also indicate that ssHI is less immunogenic than animal insulin and that it is effective and safe in the management of NIDDM both in first-time insulin users and in patients transferred from animal-species insulin. Thus ssHI would appear to be useful in treating NIDDM, especially in patients who require intermittent insulin therapy.
Diabetes Mellitus, Type 2↗
Increased responsiveness to exogenous insulin administration in the hyperglycemic obese person with type II diabetes.
This study was undertaken to investigate whether obese persons with type II diabetes mellitus showed less of a response to the hypoglycemic effect of insulin treatment than did lean type II diabetic patients. Forty-three patients (lean, n = 17; obese, n = 22; obese on hypercaloric diets, n = 4) were treated with insulin and placed on a diet calculated to maintain ideal body weight. A rapid decrease in the mean serum glucose concentration was seen in both the lean and obese groups following the initiation of insulin therapy. The glucose concentration of the lean patients plateaued after the second day of insulin treatment, whereas the obese patients' levels continued to fall after the third and fourth days. A difference was noted in the caloric intake of the two groups. Lean patients ingested 28 kCal/kg/day; obese patients ingested 17 kCal/kg/day. An additional group of four obese diabetic patients who ingested 28 kCal/kg/day was studied to determine if the hypocaloric intake of the first group of obese patients had altered their responsiveness to insulin. Despite the higher caloric intake, the mean serum glucose concentration of this group of patients fell more rapidly than did that of the lean patients. Caloric intake during the initiation of insulin therapy does not seem to influence the increase in insulin responsiveness of obese insulin-requiring type II diabetic patients.
C-Peptide↗
Evolution of renal function abnormalities in the db/db mouse that parallels the development of human diabetic nephropathy.
The db/db mutant mouse is a rodent model of genetic diabetes that develops renal glomerular lesions with striking mesangial matrix accumulation by the age of 16 weeks, after 8-10 weeks of sustained hyperglycemia. However, abnormalities in renal function that antedate or accompany the appearance of these pathologic changes, which resemble those found in human diabetes, have not been delineated. We therefore examined renal function in young db/ db mice and their nondiabetic db/m littermates from the age of 8 through 15 weeks. Serum creatinine and blood urea nitrogen concentrations at the onset of diabetes in db/db mice did not differ significantly from mean concentrations in db/m controls. An elevated creatinine clearance, due in large part to increased body weight, and increased urinary albumin excretion were observed in db/db compared with db/m mice soon after establishment of sustained hyperglycemia. A relative reduction in creatinine clearance was demonstrable in db/db mice at the age of 15 weeks, coincident with the appearance of overt compromise in renal function manifested by frank increases in the serum creatinine and blood urea nitrogen. The findings indicate that the well-documented glomerular pathology in db/db mice is accompanied by definable alterations in renal function, which are similar in chronology and nature to those found in human diabetes.
Aging↗