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  • 1
    ISSN: 1432-1440
    Keywords: Diabetes mellitus ; Hypertension ; Sodium homeostasis ; Human atrial natriuretic peptide ; Kidney function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Potential impairment of the efficacy of human atrial natiuretic 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 µg hANP (Bissendorf peptide) or placebo. At base-line, patients differed from controls in elevated creatinine clearance (P〈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〈0.01); hANP resulted in increased plasma protein concentrations only in controls (P〈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〈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.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Critical care ; Severe non-thyroidal illness ; Free fatty acids ; Thyroid function tests
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 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 proteines must be questioned because of the results.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Critical care ; Aldosterone ; Plasma renin activity ; Cortisol ; Prolactin ; Dopamine treatment
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To investigate the influence of critical illness on plasma renin activity and aldosterone levels and to examine potential inhibitory effects of dopamine therapy on aldosterone responsiveness, we measured plasma renin activity, and potassium and creatinine in serum, as well as the responses of aldosterone, cortisol and prolactin levels to TRH 200 µg i.v. + Synacthen 0.25 mg i.v. in 63 unselected, critically ill patients (32 females, 31 males, aged 18–84 years). Of the patients 19 received dopamine treatment (3–13 µg/kg/min i.v.); 21 of the patients died in the further course of their disease. Plasma renin activity was increased in 66.7% of the patients and aldosterone levels were elevated in 90.5% of the patients. There were correlations (P〈0.05) of lethality with plasma renin activity and cortisol levels and correlations (P〈0.01) of aldosterone concentrations with plasma renin activity and cortisol levels. Whereas dopamine treatment had no inhibitory effect on aldosterone levels before and after stimulation, prolactin stimulation was decreased in dopamine-treated patients. Thus, dopamine does not generally lose its potency of hormone inhibition in critically ill patients, but has no influence on the secondary aldosteronism developing regularly in the early phase of critical illness, which is apparently mainly due to the stimulatory effect of ACTH (or ACTH-related pituitary peptides) and is considered an epiphenomen of the stress mechanisms acting upon the patients in this condition.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Keywords: Gonadotropins ; Hypogonadism ; Pituitary hormone releasing hormones
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A patient (19 years old) with Kallmann's syndrome was treated with gonadotropin-releasing hormone (2.5–16 µg) administered subcutaneously every 2 h using a portable infusion pump. During 42 weeks of treatment testosterone levels and testicular size did not increase sufficiently although no reasons for this insufficient response were detectable. Therefore the regime of controlling and changing the catheter system was intensified. By this means partial occlusions of the catheter were detected and could be corrected. Afterwards testosterone levels increased immediately and persistently to normal values.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1041
    Keywords: captopril ; congestive heart failure ; plasma aldosterone ; plasma prolactin ; metoclopramide ; dexamethasone suppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary After long-term captopril treatment, an inappropriate increase in aldosterone levels has been observed in hypertensive patients. It is not known, whether a similar change would occur in patients with severe congestive heart failure, and whether it is due to a decrease in endogenous dopaminergic inhibition of aldosterone secretion or to aldosterone stimulation by ACTH or an ACTH-related peptide. Therefore, the aldosterone and prolactin responses to metoclopramide have been studied in 10 patients with severe congestive heart failure (NYHA Class III or IV) after 6 months of captopril treatment, before and 11 h after pretreatment with dexamethasone. 7 placebo-treated patients served as double-blind controls. In captopril-treated patients, the supine aldosterone levels exceeded the normal range and were as high as in placebo-treated patients. The responsiveness of aldosterone and prolactin to metoclopramide was not influenced by captopril. Only in the placebo group were the aldosterone levels decreased by dexamethasone. Captopril increased plasma renin activity and serum potassium, and decreased supine epinephrine and norepinephrine and serum sodium. Thus, previous reports of inappropriately high aldosterone levels after long-term captopril treatment were confirmed in patients with severe congestive heart failure. It is concluded that increased aldosterone is due neither to a decrease in endogenous dopaminergic inhibition nor to dexamethasone-suppressible stimulation of aldosterone secretion.
    Type of Medium: Electronic Resource
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