Long-term treatment of idiopathic hyperaldosteronim using trilostane

1986 ◽  
Vol 113 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Kaoru Nomura ◽  
Hiroshi Demura ◽  
Nobuo Horiba ◽  
Kazuo Shizume
Keyword(s):  
Antihypertensive Drugs ◽  
Competitive Inhibitor ◽  
Inhibitory Effect ◽  
Term Treatment ◽  
Continuous Treatment ◽  
Steroid Biosynthesis ◽  
Long Term Treatment ◽  
Idiopathic Hyperaldosteronism ◽  
Pre Treatment

Abstract. Three patients with idiopathic hyperaldosteronism were continuously treated with trilostane, a competitive inhibitor of adrenal 3β-hydroxysteroid dehydrogenase (3β-HSDH) (3 to 4⅔ years). Trilostane, in conjunction with antihypertensive drugs, effectively decreased plasma aldosterone levels and improved hyperaldosteronism symptoms without undesirable side effects. Trilostane continued to be effective even when treatment was continuous. Rapid ACTH testing (iv bolus of 0.25 mg α1–24 ACTH) was done on the day without trilostane after long-term treatment, and plasma levels of aldosterone and cortisol were compared to those obtained during a pre-treatment period. Results suggest that the inhibitory effect of trilostane on steroid biosynthesis rapidly disappears following discontinuance of trilostane administration even after long-term treatment, and that continuous treatment causes no significant or irreversible change in steroid biosynthesis. These results suggest that trilostane is a safe, feasible therapeutic agent for long-term treatment of idiopathic hyperaldosteronism.

Role of serotonin in obsessive-compulsive disorder

1998 ◽  
Vol 173 (S35) ◽  
pp. 13-20 ◽  
Author(s):  
H. G. Baumgarten ◽  
Z. Grozdanovic
Keyword(s):  
Obsessive Compulsive Disorder ◽  
Selective Serotonin Reuptake Inhibitors ◽  
Expression Patterns ◽  
Term Treatment ◽  
Continuous Treatment ◽  
Obsessive Compulsive ◽  
Compulsive Disorder ◽  
Long Term Treatment ◽  
Pre Treatment

Background Serotonin may play a role in the pathophysiology of obsessive-compulsive disorder (OCD) because of the anti-obsessional effect of selective serotonin reuptake inhibitors (SSRJs).Method The literature is reviewed on knowledge of the role of serotonergic neurons in brain function, studies on monoamine metabolites in cerebrospinal fluid (CSF), various stress neuropeptides, neuroendocrine and behavioural challenge after administration of direct and indirect serotomimetic compounds, and neuroanatomical data on brain circuits organising behaviour.Results In most of the OCD cases analysed, CSF 5-hydroxyindoleacetic acid and homovanillic acid concentrations do not significantly differ from age-corrected controls. However, a relationship appears to exist between pre-treatment levels of these metabolites and clinical response to drugs acting on the serotonin transporter. Abnormalities in CSF arginine vasopressin, corticotropin-releasing hormone, oxytocin and somatostatin levels have been reported in OCD. Long-term treatment with high-doses of clomipramine, fluvoxamine, and fluoxetine tend to correct these neuropeptide abnormalities.Conclusions We hypothesise that continuous treatment with SSRJs alters serotonin turnover and neuropeptide expression patterns in OCD-entertaining functional forebrain/midbrain circuits.

Twenty-four year spironolactone therapy in an aged patient with aldosterone-producing adenoma

1992 ◽  
Vol 126 (2) ◽  
pp. 186-190 ◽  
Author(s):  
R Takeda ◽  
T Yamazaki ◽  
Y Ito ◽  
H Koshida ◽  
T Morise ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Plasma Renin ◽  
Term Treatment ◽  
Aged Patient ◽  
Steroid Biosynthesis ◽  
Long Term Treatment ◽  
Hypokalemic Alkalosis ◽  
Aldosterone Producing Adenoma ◽  
Subsequent Withdrawal

A case of primary aldosteronism treated with spironolactone therapy has been followed up for 24 years. This is probably the longest case of spironolactone therapy for primary aldosteronism that has ever been reported. Long-term treatment with spironolactone controlled the hypertension and prevented hypokalemic alkalosis in this patient, without any deleterious effects on steroid biosynthesis. Based on data obtained during dose reduction and subsequent withdrawal of spironolactone, it is suggested that the suppressed plasma renin activity associated with adenoma-induced aldosteronism develops prior to hypokalemia and hypertension.

Opposite Effects of Captopril on Angiotensin I-Converting Enzyme ‘Activity’ and ‘Concentration’; Relation between Enzyme Inhibition and Long-Term Blood Pressure Response

1981 ◽  
Vol 60 (5) ◽  
pp. 491-498 ◽  
Author(s):  
F. Boomsma ◽  
J. H. B. de Bruyn ◽  
F. H. M. Derkx ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Blood Pressure ◽  
Enzyme Activity ◽  
Inhibitory Effect ◽  
Enzyme Concentration ◽  
Term Treatment ◽  
Converting Enzyme ◽  
Control Value ◽  
Long Term Treatment

1. The relationship between the antihypertensive action of captopril and its inhibitory effect on angiotensin I(ANG I)-converting enzyme has been investigated. Converting enzyme was measured in plasma by its ability to generate hippuric acid from the synthetic substrate hippuryl-l-histidyl-l-leucine. Inhibition by captopril appeared transient on storage of the plasma samples at −20°C, so that measurements in such samples were not a valid index of the effect in vivo. 2. Rapid reversal of captopril's inhibitory effect on ANG I-converting enzyme in plasma was achieved by the addition of N-ethylmaleimide (0.1 mmol/l). In this way an estimate of converting enzyme ‘concentration’ was obtained both in stored and in freshly prepared plasma samples. Measurements of converting enzyme ‘activity’ in freshly prepared samples, in the absence of N-ethylmaleimide, were used as an index of inhibition in vivo. 3. In eight hypertensive subjects ANG I-converting enzyme ‘concentration’ did not change after a single oral 100 mg dose of captopril. Long-term treatment of 10 hypertensive subjects with captopril was associated with a gradual increase in converting enzyme ‘concentration’ from 29 ± 2 to 47 ± 3 m-units/ml (mean ± sem) over a period of several weeks. In contrast, captopril caused a rapid fall of converting enzyme ‘activity’. 4. Abrupt withdrawal of captopril after long-term treatment caused a gradual decrease in ANG I-converting enzyme ‘concentration’ to the control value. In contrast, converting enzyme ‘activity’ rose rapidly and became equal to enzyme ‘concentration’ 2 days after the drug had been stopped. 5. The concentration of enzymatically active renin in plasma rose from 13 ± 3 to 81 ± 34 μ-units/ml during long-term captopril treatment (mean ± sem). Blood pressure fell from 168 ±4/108 ± 3 to 140 ± 3/90 ± 3 mmHg and had not returned to the control value in the first week after the drug had been stopped, despite the fact that circulating active renin and ANG I-converting enzyme ‘activity’ were elevated. 6. It is concluded that long-term inhibition of ANG I-converting enzyme by captopril is associated with an increased plasma concentration of this enzyme. The results also suggest that the level of converting enzyme ‘activity’ in plasma is not the only factor that determines the long-term effect of captopril on blood pressure.

A STUDY OF THE ANTITHYROID EFFECT OF TOLBUTAMIDE

1962 ◽  
Vol 25 (3) ◽  
pp. 343-350 ◽  
Author(s):  
G. HANNO ◽  
H. K. AWWAD
Keyword(s):  
Thyroid Function ◽  
Mode Of Action ◽  
Salivary Secretion ◽  
Inhibitory Effect ◽  
Drug Dose ◽  
Term Treatment ◽  
Antithyroid Drugs ◽  
Total Drug ◽  
Long Term Treatment

SUMMARY The mechanism of the antithyroid effect of tolbutamide was investigated by studying its effect on thyroid iodine trapping, the salivary secretion of 131I and the organic binding of thyroid 131I. No inhibitory effect was noted on iodine trapping. After prolonged therapy a defect in the organic binding of 131I was observed in some cases. There was a significant correlation between thyroid function as measured by the 2 hr. neck:thigh ratio and the total drug dose in patients on long-term treatment. Recovery of the gland from this defect after withdrawal of the drug seemed to be slower than the recovery from other antithyroid drugs having the same mode of action.

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