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Biomedical subjects

H Pfüller

Publications and source records attributed to H Pfüller.

At least 19 recordsLinked to original sources
PubMed1998

Albumin, IgG, retinol-binding protein, and alpha1-microglobulin excretion in childhood.

Urine concentrations of two high molecular weight proteins, albumin and IgG, and two low molecular weight proteins, alpha1-microglobulin (A1M) and retinol-binding protein (RBP), were measured in 657 healthy children from birth to 18 years of age. The urinary levels of RBP and A1M suggest an age-dependent decline, whereas the levels of albumin and IgG show an uneven distribution. Reference values for albumin, IgG, A1M, and RBP for each group are reported.

Adolescent↗
PubMed1997

Transient suppression of endogenous cortisol production after intraarticular steroid therapy for chronic arthritis in children.

OBJECTIVE: To assess the effect on endogenous cortisol production of administration of intraarticular steroids for chronic arthritis in children and adolescents. METHODS: We examined 22 children with chronic arthritis who received intraarticular steroid injection. The morning peak cortisol concentration was measured in saliva before and several days to weeks after steroid injection. In 7 children cortisol concentrations were measured at 4 pm and 8 pm as well. In one girl the hypothalamic-pituitary-adrenal axis was tested using the corticotropin releasing hormone stimulation test. RESULTS: After steroid injection there was suppression of endogenous cortisol production that lasted 10 to 30 days. During this period the circadian rhythm of cortisol production and the hypothalamic-pituitary-adrenal axis were disturbed. CONCLUSION: After intraarticular steroid injection children show transient suppression of endogenous cortisol production. It is not known whether this might place them at risk from stress induced acute adrenal insufficiency.

Adolescent↗
PubMed1990

Cholinergic-adrenergic balance: Part 1. Relationship between central and peripheral sensitivities.

Eight healthy volunteers were studied under double-blind conditions after acute challenge with the peripheral beta 2-agonist reproterol, either alone or combined with the peripheral indirect cholinomimetic neostigmine. Their responses were also studied after administration of the centrally active indirect cholinomimetic physostigmine. The beta-adrenergic rise in heart rate was cholinergically suppressed. The beta-adrenergic rise of plasma cyclic adenosine monophosphate (cAMP) was not cholinergically modulated, while that of plasma glucose tended to be cholinergically suppressed. Physostigmine induced an anergic-anhedonic syndrome accompanied by physiological, metabolic, and neuroendocrine stress phenomena. The beta-adrenergic and cholinergic sensitivities, respectively, of the various parameters investigated tended to be nonsignificantly intercorrelated. Only a limited portion of the variance was explained by drug effects. Sensitivity to neostigmine was completely unrelated to sensitivity to physostigmine. Thus, cholinergic sensitivity seems not to be decisive for the fine tuning of the highly complex regulatory systems studied and peripheral sensitivity not to be representative for the central one, at least if unselective drugs like neostigmine and physostigmine are used.

Adult↗
PubMed1990

Cholinergic-adrenergic balance: Part 2. Relationship between drug sensitivity and personality.

Sensitivity to the centrally active cholinomimetic physostigmine varies dramatically among healthy individuals. The elucidation of the reasons for this variability could contribute to the understanding of the pathophysiology of affective disorders where a cholinergic supersensitivity has been demonstrated. Therefore, personality characteristics and habitual stress-coping strategies were related to sensitivity to physostigmine in eight healthy male volunteers. Cardiovascular and behavioral responses tended to be positively correlated with irritability and emotional liability. Passive, "helpless" strategies for coping with stress were positively related to these responses. The metabolic and neuroendocrine responses to physostigmine were generally unrelated to personality. In view of putative beta-adrenergic disturbances in depression, the responses to the peripheral beta 2-adrenergic agonist reproterol were studied. Irritability and emotionality tended to be positively correlated with cardiovascular responses to reproterol as well as with reductions of heart rate by the peripheral cholinomimetic neostigmine.

Adult↗
PubMed1990

Adrenergic-cholinergic imbalances: the physostigmine-syndrome is not antagonized by the MAO-A inhibitor brofaromine.

The centrally active cholinesterase inhibitor physostigmine induces a behavioral syndrome which is thought to represent a model of spontaneous depression. In the present acute trial in 6 healthy volunteers, this model depression was accompanied by clearcut cardiovascular, metabolic and neuroendocrine phenomena of stress. The extent of the changes from baseline, however, scarcely correlated between the behavioral and physiologic phenomena. The behavioral and physiological phenomena could not be antagonized by brofaromine, a putative antidepressant reversibly and selectively inhibiting monoamine oxidase A (MAO-A), contrasting to the complete inhibition by the central cholinolytic scopolamine. This is further evidence that antidepressant efficacy depends on long-term adaptive changes secondary to the enhancement of aminergic neurotransmission rather than this enhancement itself.

Adult↗
PubMed1988

Delta sleep-inducing peptide response to human corticotropin-releasing hormone (CRH) in major depressive disorder. Comparison with CRH-induced corticotropin and cortisol secretion.

Twenty-four subjects (12 patients with major depressive disorder and 12 controls matched for sex and age) received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an iv bolus dose. Healthy subjects exhibited a slight, but sustained, increase of plasma delta sleep-inducing peptide (DSIP) concentrations, whereas a marked reduction of DSIP levels was found in depressives. Compared to controls, depressed patients showed a significant attenuation of corticotropin (ACTH) responses, whereas cortisol secretion in response to hCRH was normal. Basal DSIP and cortisol concentrations were highly correlated and were higher in depressives than in controls. Both were negatively correlated with the DSIP responses to hCRH. These findings are compatible with the hypothesis that hypothalamic-pituitary-adrenal (HPA) overactivity in the depressive state is primarily due to central hypersecretion of CRH and support the view of a modulatory function of DSIP in the complex regulatory mechanism of the HPA system and of its pathophysiological significance for aberrant HPA axis function in major depressive disorder.

Adrenocorticotropic Hormone↗
PubMed1988

Growth hormone (GH) responses to GH-releasing hormone in depression: correlation with GH release following clonidine.

Twenty subjects (10 patients with major depressive disorder and 10 controls matched for age, gender, and ovarian status) received 1 microgram/kg synthetic human growth hormone-releasing hormone (GHRH)-44 amide as an i.v. bolus dose. Compared to controls, depressed patients showed a significant attenuation of net growth hormone (GH) responses to GHRH associated with normal basal GH concentrations. The blunted GH responses occurred in the face of significantly higher somatomedin C (Sm-C) concentrations. Comparison of GH responses after GHRH with GH output following the alpha 2-agonist clonidine (CLON) revealed a significant positive correlation. The concordance between GH responses after specific challenges at different levels of the GHRH-GH-somatomedin axis indicates the integrity of the hypothalamic-pituitary-somatotropic system in depression and supports the view that altered GH secretory patterns in depression may primarily be due to a suprapituitary disturbance.

Adult↗
PubMed1988

Corticotropin and cortisol response to human CRH as a probe for HPA system integrity in major depressive disorder.

To explore the integrity of the hypothalamic-pituitary-adrenal (HPA) system in major depressive disorder, 12 patients and normal controls matched for sex, age, and body weight received 100 micrograms synthetic human corticotropin-releasing hormone (hCRH) as an i.v. bolus dose. Compared to controls, depressed patients showed an elevation in baseline cortisol and a significant attenuation of net adrenocorticotropin (ACTH) responses, while cortisol secretion in response to hCRH was normal. These abnormalities in HPA axis function and apparent discordances in the interrelationships of ACTH and cortisol baseline and net stimulation responses between depressed patients and normal controls indicate, at least in part, a derangement of the glucocorticoid-dependent negative feedback circuitry and support the hypothesis that HPA hyperactivity in depression involves neurotransmitter-mediated hypothalamic hypersecretion of CRH.

Adolescent↗
PubMed1988

Growth hormone (GH) and prolactin responses after GH-releasing hormone in major depressive disorder: relationship to somatomedin C levels and dexamethasone suppressibility of cortisol.

To explore the growth hormone-releasing hormone (GHRH)-GH-somatomedin axis in major depressive disorder, 12 patients and 12 normal controls matched to the patients on age, sex, ovarian status and body weight received synthetic human GHRH-44 amide (1 microgram/kg) as an intravenous bolus. Compared to controls, the depressed patients showed a reduction in baseline plasma GH and a significant attenuation of net plasma GH responses to GHRH. The blunted GH responses occurred along with significantly increased somatomedin C (Sm-C) concentrations. The impairment of GH responses to GHRH and the increased Sm-C concentrations in patients with depression could have resulted from episodic hypersecretion of GH during the daytime, indicating integrity of the negative feedback circuitry. Normal feedback regulation suggests that diurnal episodic hypersecretion of GH reflects an abnormality at or above the level of the hypothalamus, so that the GHRH-GH-somatomedin axis hyperactivity observed in certain patients with major depressive disorder may be due, at least in part, to hypersecretion of hypothalamic GHRH. Our failure to demonstrate a difference in plasma prolactin (PRL) responses to GHRH between controls and depressed patients indicates that GHRH is not a PRL releaser in patients with major depression and that the altered GH secretory dynamics may not be directly related to the altered circadian PRL secretion linked to depression.

Adult↗
PubMed1988

Insulin-like growth factor I in depressed patients and controls.

To explore the role of the somatomedin-mediated long-loop negative feed-back mechanism in altered growth hormone (GH) secretory dynamics associated with depression, plasma IGF-I concentrations were measured in 34 patients with a major depressive episode and matched healthy subjects. Compared with controls, depressed patients exhibited significantly increased plasma IGF-I concentrations. In the patient group plasma IGF-I concentrations were positively correlated with the maximum post-dexamethasone plasma cortisol concentrations. Our data suggest that increased plasma IGF-I concentration may reflect diurnal GH hypersecretion, contribute to deficient GH responses to dynamic challenges, and indicate an interrelationship between the hypothalamic-pituitary-somatotropic (HPS) and -adrenocortical (HPA) system regulation in depression.

Adult↗
PubMed1987

Growth hormone (GH) response to GH-releasing hormone in depression.

To explore the GHRH-GH-somatomedin axis integrity in major depressive disorder, 11 drug-free patients and normal subjects matched for age, sex, ovarian status, and body weight received 1 microgram/kg synthetic human GHRH-44 amide as an iv bolus dose. Compared to the normal subjects, the depressed patients had reduced mean basal serum GH levels [2.2 +/- 0.5 (+/- SE) vs. 1.1 +/- 0.2 ng/mL (micrograms/L); P less than 0.05] and a significant attenuation of the net GH response to GHRH [1346 +/- 499 vs. 217 +/- 46 ng.min/mL (micrograms.min/L); P less than 0.01]. The blunted GH responses occurred in the face of significantly increased plasma somatomedin C (Sm-C) levels [1.1 +/- 0.2 vs. 0.6 +/- 0.1 U/mL; P less than 0.05]. The magnitude of GH responses to GHRH did not differ between men and women and was not significantly correlated with age, body weight, baseline serum GH levels, or plasma Sm-C levels in either individual groups or both groups combined. The increased plasma Sm-C levels in the depressed patients could have resulted from diurnal hypersecretion of GH, and the diminished GH responses to GHRH may reflect normal Sm-C-mediated feedback at the level of the pituitary. The presumed GH hypersecretion may be due to decreased hypothalamic somatostatin release and/or hyperactivity of GHRH-containing neurons. Thus, the pathological process resulting in abnormal GH secretory patterns associated with depression may occur primarily at a suprapituitary site.

Adult↗
PubMed1987

[Significance of serum fructosamine in the metabolic control of children and adolescents with type I diabetes mellitus].

In 1982 Johnson et al. described a simple colorimetric assay for measuring glycated proteins, termed fructosamine, in the serum of adults with diabetes mellitus and demonstrated this to be a useful index of intermediate glucose control (1-3 weeks). Our study was designed to show this as well in children and adolescents with type I diabetes mellitus. Serum fructosamine was determined in 76 children and adolescents with diabetes mellitus, and 111 age-matched controls. In the controls an age-dependency but not sex-dependency could be demonstrated. In the diabetic patients we found a significant correlation between serum fructosamine and HbA1 values (r = 0.87, p less than 0.001). In 6 patients with newly diagnosed diabetes mellitus serum fructosamine concentrations decreased at a faster rate than HbA1 values. The fructosamine assay is rapid, technically simple and inexpensive, and is at least a useful addition or perhaps an alternative to HbA1 estimation.

Adolescent↗