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Biomedical subjects

B Willms

Publications and source records attributed to B Willms.

At least 73 records · Page 4Linked to original sources
PubMed1976

Urinary cyclic 3',5'-adenosine monophosphate (cAMP) in diabetic subjects with and without symptomatic hypoglycemia and in normal subjects with insulin-induced hypoglycemia.

Urinary cAMP was investigated in diabetic subjects. It was found normal in patients on oral antidiabetics and on insulin in good or poor control. Patients with insulin-induced symptomatic hypoglycemia, however, excreted increased amounts of cAMP in the urine. To demonstrate the significance of hypoglycemia we induced hypoglycemia by i.v.-injection of 0.15 U insulin/kg body weight in six normal subjects. An increase of urinary cAMP was found even during the first 15 minutes with maximal hypoglycemia. Determination of urinary cAMP seems to be helpful in the diagnosis of unrecognized hypoglycemia and counterregulation.

Blood Glucose↗
PubMed1976

Effect of the dopamine receptor blocking agent pimozide on the growth hormone response to arginine and exercise and on the spontaneous growth hormone fluctuations.

Pimozide, a specific blocker of dopamine receptors, was administered orally to 10 diabetics for 2 days before an arginine-hydrochloride infusion. In 8 healthy volunteers and 20 diabetics exercise tests on a bicycle ergometer were performed with a load of 100 Watts and 50 Watts respectively without or after a single dose of pimozide 30 min before the test. In 4 male diabetics day profiles of growth hormone (GH) were estimated without and during treatment with pimozide for 4 days. The arginine and exercise induced GH release was found to be significantly lowered by pimozide, whereas the marked spontaneous fluctuations in the diabetics were even enhanced by pimozide. These data support the concept of the involvement of dopaminergic stimulation in the response of GH to arginine and exercise. The spontaneous fluctuations of GH, however, seem to be regulated by other neuroendocrine mechanisms.

Adolescent↗
PubMed1975

[Insulin allergy and insulin resistance (author's transl)].

The antigenicity of insulin is the cause of the side effects of insulin therapy such as insulin allergy, lipoatrophy at the site of injection and insulin resistance. Factors inherent in the individual patient are decisive for the antigenicity of insulin, as well as species specificity of the insulin,purity and galenical form. Clinical aspects and possibilities for treatment of insulin allergy, lipoatrophy and insulin resistance are discussed in relation to our own cases.

Adrenal Cortex Hormones↗
PubMed1975

[The importance of serum insulin determination in the diagnosis and treatment of diabetes mellitus (author's transl)].

Various types of insulin secretion can be distinguished in diabetics by means of radioimmunological serum insulin determination: Overweight, subclinical diabetics with increased insulin response in the test, adult diabetics with evident insulin response and diabetics with absent insulin response following stimulation. The stimulation or load tests described are an oral glucose tolerance test followed by a sulphonyl urea load test, a "maximum" stimulation test and a glibenclamide-glucose load test. The serum insulin response in these tests is of both diagnostic and prognostic importance to the treatment. By means of serum insulin determination the treatment of diabetes can be set on a rational biochemical basis, and decisions on possibly envisaged modifications of treatment can be facilitated and safeguarded.

Blood Glucose↗
PubMed1975

Lipodystrophy of the extremities. A dominantly inherited syndrome associated with lipatrophic diabetes.

A female patient with the following symptoms has been observed: complete absence of subcutaneous fat on the arms and legs, well developed adipose tissue on the trunk and face, severe hyperlipidemia, eruptive xanthomas, insulin resistant diabetes mellitus with lack of ketoacidosis, hepatomegaly and elevated basal metabolic rate. The patient thus exhibited all characteristics of lipatrophic diabetes (Lawrence type of diabetes). The mother and a sister of the patient were found to have the same peculiar appearance and a slight hyperlipidemia but no diabetes mellitus. The combination of this type of partial lipodystrophy with severe hyperlipidemia, insulin resistant diabetes mellitus without ketoacidosis and elevated basal metabolic rate was further observed in 2 unrelated patients without known familial occurrence. Thus partial lipodystrophy of the extremities is another, previously undescribed, syndrome associated with the Lawrence type of diabetes mellitus. In the 1 family the syndrome of lipodystrophy and hyperlipidemia is dominantly inherited. Besides the autosomal recessively inherited syndrome of congenital generalized lipodystrophy there is a heterogenous group of dominantly inherited syndromes with various types of lipodystrophy.

Adult↗
PubMed1975

[Androgen status of male diabetics. Total testosterone before and following stimulation with HCG, free testosterone, and testosterone binding capacity of patients with and without potency disorders].

In order to investigate the androgen status of diabetics we determined in 39 patients, 18-60 years old, 17 of which suffered from potency disturbances, the basal total plasma testosterone, the free testosterone fraction and the unbound plasma testosterone as well as the testosterone binding capacity. In 39 of these patients we proved the response of Leydig cells to HCG. Between normal persons and patients with and without potency disturbances basal total plasma testosterone did not differ significantly (p greater than 0.10). After a 3-day stimulation with HCG the increase of basal total plasma testosterone was significantly lower in the two diabetic groups in comparison with the normal persons (p less than 0.0005). The group with potency disturbances had significantly lower values for the free testosterone fraction (p less than 0.005) and unbound plasma testosterone (p less than 0.0025) than normal persons whereas diabetics without potency disturbances did not reveal any significant differences (p greater than 0.25 and p greater than 0.40). Further there were significant differences between the patients with and without potency disturbances (p less than 0.025) and (p less than 0.025). Testosterone binding capacity was significantly increased in the group with potency disturbances (p less than 0.0005) and also in the group without potency disturbances (p less than 0.01) as compared with controls. Moreover was it significantly higher in the group with potency disturbances than that without potency disturbances (p less than 0.01). For none of the parameters a functional correlation of age or diabetes duration could be demonstrated. The results are discussed with regard to the causes of potency disturbances in male diabetics.

Adolescent↗