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Biomedical subjects

P H Althoff

Publications and source records attributed to P H Althoff.

At least 19 recordsLinked to original sources
PubMed1992

Gallstones in acromegalic patients undergoing different treatment regimens.

The frequency of gallstones during long-term treatment with the somatostatin analogue octreotide reported in different studies varies from 0% to 50%, the reason for this variation being unknown. Therefore, we examined 58 acromegalic patients undergoing different treatment regimens for the frequency of gallstones. Thirteen were treated with octreotide, 20 with bromocriptine, and 25 had no medical treatment after successful neurosurgery. Also, 58 patients without known gallbladder disease served as controls. The postprandial gallbladder contraction was also investigated in 27 acromegalic patients (10 with octreotide, 10 with bromocriptine, and 7 with no medical therapy). Ten of the 58 acromegalic patients were found to have gallstones, 4 of 25 receiving no medical treatment, 4 of 20 treated with dopamine agonists, and 2 of 13 treated with octreotide. In 9 of the 58 control patients, gallstones were detected. Although in the octreotide group the gallstones were newly formed under therapy, there was no difference in gallstone prevalence between the different treatment regimens and the control group. However, the postprandial gallbladder contraction was significantly more often inhibited during octreotide therapy, and this effect was most pronounced during the first hours following injection. Differences in the timing of injections therefore may be an explanation of the variable incidence of cholelithiasis in the different studies.

Acromegaly↗
PubMed1992

Bromocriptine treatment over 12 years in acromegaly: effect on growth hormone and prolactin secretion.

It is not known whether bromocriptine treatment in acromegaly can be implemented for a life-long period. To elucidate this problem, the secretory GH and PRL states of 12 patients with acromegaly were determined, before bromocriptine treatment, under therapy (15.0 +/- 6.8 mg/day for 12 +/- 3 years; mean +/- SD) and during two-weeks long drug withdrawal after long-term treatment, respectively. Before therapy, all patients showed a non-sufficient GH suppression after oral glucose load (greater than 2 micrograms/l), whereas under dopaminergic treatment the post-glucose GH levels of three patients fell below 2 micrograms/l; normal IGF-I concentrations were found in five patients. However, under bromocriptine, only two patients showed GH suppressions below 2 micrograms/l following glucose, accompanied with normal IGF-I levels. During bromocriptine withdrawal, GH secretion at 60 min in the oral glucose tolerance test increased significantly (17.0 +/- 15.5 vs 5.7 +/- 5.2 micrograms/l; p less than 0.01); the mean IGF-I level rose from 2.1 +/- 0.8 to 4.9 +/- 2.2 kU/l (p less than 0.01). IGF-I was normal during bromocriptine cessation in only one patient; none of the 12 patients showed a GH suppression below 2 micrograms/l after oral glucose load. Under dopaminergic treatment hyperprolactinemia could not be detected. In conclusion, bromocriptine led to a stable suppression of both GH hypersecretion and--if present--concomitantly elevated PRL levels. Severe side effects or a further tumor growth could not be observed. Thus, the data of the longest follow-up investigation that has so far been published indicate that effective life-long bromocriptine therapy seems to be possible in selected patients with acromegaly.

Acromegaly↗
PubMed1992

[Anal incontinence in patients with Addison's disease: a gluco- and mineralocorticoid independent sphincter malfunction?].

Anorectal motor function was evaluated in 15 female patients with Addison's disease and androgen deficiency and 15 age-matched healthy volunteers. Medical history revealed symptoms of faecal incontinence in 5 patients. The patients showed decreased maximum retention volumes (p less than 0.01) in the rectal saline infusion test. Lowered anal sphincter resting (p less than 0.01) and squeeze pressure (p less than 0.01) was demonstrated in patients with adrenocortical insufficiency. No differences between patients and controls were found in respect of perception volume, minimal distension volume for sphincter relaxation and rectal compliance by means of intrarectal balloon distension. Electromyography of the external anal sphincter was performed in 8 patients and showed no evidence for a neurogenic defect. Relevant morphological changes of the anorectum could be excluded endoscopically in 13 of the 15 patients. Therefore impaired anorectal muscular function is responsible for faecal incontinence in patients with Addison's disease and androgen deficiency. Further investigations will show, whether these findings are the consequence of lowered androgen production.

Addison Disease↗
PubMed1991

[Somatomedin C level and stimulation of growth hormone and adrenal cortex function by administration of releasing hormones and physical exertion in patients with obesity].

In a clinical study on potential determinants underlying the impairment of growth hormone stimulation in obese human subjects, we examined in 20 otherwise healthy adult obese subjects (14 females, six males, age 18 to 40 years, body mass index greater than 29 kg/m2) the responses of growth hormone (hGH), adrenocorticotropic hormone (ACTH) and cortisol to releasing hormone stimulation (growth hormone-releasing hormone and corticotropin-releasing hormone) and the responses of hGH, ACTH, cortisol and free fatty acids (FFA) to physical exercise. Subjects with somatomedin-C levels less than or equal to 0.7 U/ml (group 1) were more obese than subjects with somatomedin-C levels greater than 0.7 U/ml (group 2) (p less than 0.01). In group 1, hGH increased by 4.3 +/- 1.2 ng/ml in response to releasing hormone administration and by 0.9 +/- 0.3 ng/ml in response to physical exercise (normal responses, increase by greater than 7 ng/ml), in group 2, hGH increased by 6.7 +/- 1.4, and 2.4 +/- 0.8 ng/ml, respectively (p less than 0.05 vs. group 1). Moreover, FFA stimulation by physical exercise was blunted in group 1 (p less than 0.05 vs. group 2). In contrast, ACTH stimulation was found increased in group 1 in comparison to group 2, particularly in response to physical exercise (p less than 0.01), and resulted in enhanced cortisol stimulation (p less than 0.05). Thus, impaired hGH stimulation in obese human subjects is not explained by an altered relationship between hGH and somatomedin-C levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[The influence of autonomic diabetic neuropathy and human atrial natriuretic peptide on adrenal gland function in postural changes].

To investigate the influence of postural changes on plasma renin activity (PRA), plasma levels of human atrial natriuretic peptide (hANP) and on aldosterone in diabetes mellitus and autonomic neuropathy, ten patients with diabetes mellitus and autonomic neuropathy and ten patients with diabetes mellitus but without autonomic neuropathy were studied. Ten healthy subjects served as controls. Patients and controls were in supine position for 60 minutes, then changed posture sequentially to sitting (90 minutes) and to upright position (15 minutes). In controls, PRA was increased upon sitting and in the upright position, while hANP was decreased. Patients with autonomic neuropathy differed from controls in impaired renin stimulation, whereas in patients without autonomic neuropathy PRA responses to postural changes were only slightly decreased. In both groups of patients, the normal hANP responsiveness to postural changes was lacking. There were no differences in aldosterone levels between patients and controls. In patients with high basal hANP levels due to elevated systolic blood pressure renin responses to postural changes were decreased in comparison to those patients with low basal hANP levels. Thus, in patients with diabetes mellitus increased hANP levels which are not decreased in response to upright standing may contribute to the development of hyporeninism and its sequelae.

Adult↗
PubMed1991

Effect of bromocriptine withdrawal in acromegaly on body composition as assessed by bioelectrical impedance analysis.

To evaluate the effect of bromocriptine withdrawal after dopaminergic long-term treatment (15.0 +/- 6.8 mg/day, mean +/- SD) in 12 acromegalic patients on body composition, bioelectrical impedance was measured before and at the end of two weeks of drug withdrawal. During withdrawal basal hGH and IGF-I increased from 2.5 +/- 1.9 micrograms/l and 2.1 +/- 0.8 kU/l to 9.1 +/- 11.7 micrograms/l and 4.9 +/- 2.2 kU/l, respectively, and the hGH secretion deteriorated significantly both after oral glucose load and in the TRH test, indicating recurrence of active acromegaly. Reactance and resistance decreased by 5 +/- 4 and 23 +/- 19 omega, respectively (p less than 0.01), whereas body weight remained constant (+0.4 +/- 2.1 kg). Bioelectrical impedance analysis indicated evident shifts in body composition, i.e. a significant reduction of body fat (-2.0 +/- 1.7 kg) and a simultaneous increase in both lean body mass (+2.4 +/- 2.2 kg) and total body water (+1.8 +/- 1.6 l). The changes in body composition were related to a combined effect of unsuppressed hypersomatotropism and the lack of bromocriptine actions other than inhibition of hGH secretion (for example stimulation of the renin-angiotensin-aldosterone system by both the recurred hypersomatotropism and the absence of dopaminergic bromocriptine effects). We conclude that bioelectrical impedance analysis is a good additional tool to assess the pathophysiological effects of bromocriptine withdrawal in long-term treated acromegalic patients.

Acromegaly↗
PubMed1991

[Comparison of ischemic pain threshold and reactive hyperemia in autonomic diabetic neuropathy and silent myocardial ischemia].

31 patients with coronary artery disease (11 patients with diabetes mellitus and autonomic neuropathy. 10 patients with diabetes without neuropathy, and 10 patients with asymptomatic myocardial ischemia) participated in a study designed to investigate whether there is a difference in forearm skeletal muscle ischemia and pain threshold. The degree of ischemia was determined by plethysmographically measured reactive hyperemia. There was no difference in maximum reactive hyperemia after passive forearm ischemia of 5-min duration in the three groups. After symptom-limited ischemic work, there was significantly more reactive hyperemia in patients with silent myocardial ischemia as compared to diabetic patients. Exercise time was longer in patients with silent myocardial ischemia (153 +/- 51 s) than in patients with diabetic neuropathy (139 +/- 45 s) and diabetics without neuropathy (120 +/- 45 s). Pain as a cause of termination of symptom-limited ischemic forearm exercise occurred less frequently in patients with diabetic neuropathy (2/11) and patients with silent myocardial ischemia (3/10) as compared to patients with diabetes without neuropathy. Patients with silent myocardial ischemia had a higher ischemic tolerance in the ischemic working forearm than did diabetic patients with and without neuropathy. In patients with neuropathy, however, ischemic pain occurred less frequently at the same ischemic work level compared to diabetics without neuropathy. Therefore, diabetic neuropathy appears to facilitate the occurrence of silent myocardial ischemia. The data presented here suggest that there is a qualitative difference in ischemic tolerance between patients with silent myocardial ischemia and patients with diabetic neuropathy.

Angina Pectoris↗
PubMed1990

[Long-term treatment of acromegaly with the somatostatin analog octreotide (Sandostatin). On the predictive significance of acute tests].

Twelve acromegalic patients were treated (mean +/- SD) 26 +/- 15 months with daily doses of 440 +/- 330 micrograms of the somatostatin analogue octreotide acetate (SMS 201-995, Sandostatin). The levels of somatomedin-C (Sm-C) decreased by 63% from 8.1 +/- 7.7 U/ml to 3.0 +/- 1.3 U/ml. Before starting therapy a long oral glucose tolerance test (oGTT) and a TRH test were performed both without and after s.c. injection of 100 micrograms octreotide. Under long-term treatment with octreotide four of twelve patients reached normal Sm-C-values. The GH levels of all of these patients were continuously suppressed to less than 2 ng/dl in an oGTT after a test dose of 100 micrograms octreotide s.c. till the end of the test (5 1/2 hours after octreotide injection). The other eight patients had a relief of acromegalic symptoms and five had a decrease of their Sm-C-levels, but none of them reached normal Sm-C-values. None of these patients had a continuous suppression of GH after a test dose of octreotide in an oGTT. Hyperprolactinemia (n = 4) was observed only in those patients with an insufficient response to octreotide. The GH-response to TRH showed neither without nor after injection of octreotide a correlation with the results of long-term treatment. Thus it is concluded that GH-suppression in a long oGTT after administration of a test dose of 100 micrograms octreotide acetate s.c. allows to identify those acromegalic patients who will benefit from long-term treatment with the somatostatin analogue octreotide acetate.

Acromegaly↗
PubMed1990

[The morphology and clinical significance of pathologic changes of the adrenals and hypophysis in AIDS].

A semiquantitative morphometric technique (point counting) was applied to the pituitary and adrenals taken at necropsy from 130 AIDS patients (4 women, 126 men, mean age 39 [22-71] years) to ascertain the nature, extent and location of the pathological lesions. Abnormalities were found in 32% of the pituitaries and 76% of the adrenals. Only 17 patients had normal findings in both organs. The predominant lesions were due to opportunistic infections or infiltration by Kaposi's sarcoma or non-Hodgkin lymphoma. The commonest finding was necrotizing cytomegalovirus adrenalitis (n = 68); in one third of the cases this had caused severe destructive lesions involving over 50% of the parenchyma. The almost total destruction of the adrenals noted in some cases suggests that cytomegalovirus adrenalitis may run a progressive course; its clinical significance has hitherto been underestimated.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Abnormalities in cholesterol metabolism cause peripheral neuropathy and dementia in AIDS--a hypothesis.

The AIDS dementia complex and peripheral neuropathy in AIDS are considered to be direct or indirect manifestations of HIV infection, yet the pathogenesis in unclear. There are parallels between AIDS and Tangier disease clinically and histopathologically and in lipid metabolism. The neurological disorders in AIDS may be caused by dysfunction of cellular cholesterol transport. Substitution of high density lipoprotein is recommended in the treatment of severe polyneuropathy and dementia in AIDS.

AIDS Dementia Complex↗
PubMed1990

Thyroid hormone binding inhibition in critically ill patients--who is the inhibitor?

In 31 severely ill patients of our intensive care unit an increased thyroid hormone binding inhibition detected by quantitative measurement of the effect of ether extracts of patients' sera on thyroxine tracer binding to TBG was found. As free fatty acids in serum were diminished in these patients, their postulated role as binding inhibitors in the "low T4 syndrome" of critically ill patients must be questioned. It cannot be excluded that THBI assays demonstrating this inhibition measure artefacts caused by heparine-induced in vitro lipolysis.

Acute Disease↗
PubMed1988

Impaired renal responsiveness to human atrial natriuretic peptide (hANP) in normotensive patients with type 1 diabetes mellitus.

Potential impairment of the efficacy of human atrial natriuretic peptide (human ANF-(99-126), hANP), the most potent endogenous natriuretic agent in healthy subjects, was examined in eight male normotensive patients with uncomplicated type 1 diabetes mellitus (aged 22-37 years). After giving informed consent, patients and eight male control subjects (aged 22-28 years) received in a random double-blind study design i.v. bolus injections of 100 micrograms hANP (Bissendorf peptide) or placebo. At base-line, patients differed from controls in elevated creatinine clearance (P less than 0.05) and in mild postprandial hyperglycemia. Whereas the responses of urinary cyclic guanosine monophosphate, the second messenger of hANP, were found to be normal in patients, the diuretic and natriuretic effects of hANP were grossly impaired when compared to controls (P less than 0.01); hANP resulted in increased plasma protein concentrations only in controls (P less than 0.05 vs patients). In both groups, creatinine clearance remained uninfluenced by hANP. There were similar decreases in plasma renin activity, aldosterone, levels, and blood pressure (systolic more than diastolic) in both groups (P less than 0.05 vs placebo). Heart rate and blood glucose remained unchanged. Thus, there is evidence for a decreased responsiveness to hANP exclusively of renal fluid, sodium, and chloride excretion in uncomplicated type 1 diabetes mellitus. The mechanisms responsible for this phenomenon remain obscure, neither a down regulation at the hANP receptor sites nor an hANP-induced shift from intra- to extravascular fluid volume are likely to be involved in its probably diabetes-specific pathogenesis.

Adult↗
PubMed1988

[Free fatty acids in the serum in critical diseases: do they play a role in the protein binding of thyroid hormones?].

As a contribution to the question if the elevated concentrations of free fatty acids in sera of critically ill patients described in literature play a role in the decrease of thyroid hormone levels in these patients, serum levels of the important free fatty acids were measured in 31 patients of our intensive care unit in the course of their disease using gas chromatography. After admission to the ward, only palmitoleic acid was significantly increased compared with 174 control persons, arachidonic acid was not different from the controls, palmitic, stearic, linoleic and linolenic acid were significantly decreased. In the course of the disease, no relevant changes were observed. The 21 patients not surviving their disease showed significantly lowered levels of palmitic, stearic and linoleic acid before death compared with the surviving patients at the end of the observation period. The hypothetical role of single free fatty acids as inhibitors of the binding of thyroid hormones to their transport proteins must be questioned because of the results.

Adolescent↗