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At least 19 recordsLinked to original sources
PubMed1998

Ambulatory 24-hour blood pressure recordings in patients with Parkinson's disease with or without fludrocortisone.

UNLABELLED: Orthostatic hypotension is often associated with patients suffering from Parkinson's disease. Only few studies have been published about the ambulatory blood pressure in patients with Parkinson's disease. Fludrocortisone has been used in management of orthostatic hypotension. This study was made to determine the Circadian rhythm of blood pressure in healthy elderly people, in Parkinson's disease patients without orthostatic hypotension and Parkinson's disease patients with fludrocortisone medication for orthostatic hypotension. Ambulatory 24-hour blood pressure recordings were made in 20 elderly Parkinson's disease patients and 21 healthy elderly persons. Eight of the Parkinson's disease patients were on fludrocortisone (Florinef) therapy because of orthostatic hypotension. The mean daytime systolic blood pressure of Parkinson's disease patients without fludrocortisone was 123 mmHg and the mean nighttime systolic blood pressure was 121 mmHg. There was no significant difference between daytime and nighttime systolic blood pressure (Figure 1). Diastolic blood pressure in this group was significantly higher during the day (68 mmHg) than at night (63 mmHg) (Figure 2). The daytime blood pressure of control patients was 135/74 mmHg and at night 127/69 mmHg (Figures 1, 2). The blood pressure of Parkinson's disease patients with fludrocortisone was higher at night (156/83 mmHg) than during the day (134/77 mmHg) (Figures 1, 2). The daytime and nighttime systolic and diastolic blood pressure was significantly lower by non-fludrocortisone Parkinson patients than the blood pressure of fludrocortisone Parkinson patients (Figures 1, 2). CONCLUSION: The Parkinson's disease patients were non-dippers and with fludrocortisone the blood pressure was higher at night than on day. On day, the blood pressure of the Parkinson's disease patients with fludrocortisone elevated to the level of controls.

Aged↗
PubMed1984

Evidence that patients with Addison's disease are undertreated with fludrocortisone.

Ten patients with Addison's disease, nine with undetectable plasma aldosterone, were found to be sodium and water depleted with high levels of plasma-renin activity despite receiving 0.05-0.1 mg/day of fludrocortisone and optimum doses of glucocorticoid replacement therapy. Fludrocortisone was withdrawn while patients were in hospital on a fixed sodium intake. There was an immediate natriuresis with a further increase in plasma-renin activity. When a daily dose of 0.3 mg of fludrocortisone was given all patients retained sodium and water and gained weight. There was a fall in plasma-renin activity in all patients and an associated fall in blood urea and plasma potassium, and an increase in plasma volume; oedema developed in some patients. At outpatient follow-up, the dose of fludrocortisone was adjusted according to plasma-renin activity. Most patients required 0.2 mg of fludrocortisone to maintain adequate sodium and water balance. These results suggest that patients with Addison's disease on 0.05-0.1 mg of fludrocortisone with undetectable plasma aldosterone levels are currently being undertreated with fludrocortisone. The best way of assessing sodium balance in these patients and their response to fludrocortisone is by measurement of plasma-renin activity in conjunction with 24 h urinary sodium excretion.

Addison Disease↗
PubMed1994

A sensitive radioimmunoassay for fludrocortisone in human plasma.

Fludrocortisone has been a mainstay of therapy for orthostatic hypotension for many years. Clinical experience suggests that there exists a substantial interindividual variation in responsiveness to the drug. To assess this, we have developed an assay that permits measurement of the low concentrations of fludrocortisone found in human plasma. Fludrocortisone was detected by radioimmunoassay. A polyclonal rabbit antibody, raised against dexamethasone which cross-reacts strongly with fludrocortisone, was reacted with either standard or unknown samples in the presence of [125I]fludrocortisone-3-TyrNH2 (synthesized by coupling tyrosine amide to fludrocortisone-3-oxime and iodinating with chloramine T oxidation). The ED10, ED50, and ED80 were 0.34, 5.0, and 30 ng/mL of plasma, respectively. The cross reactivity with other 9-fluorinated steroids was found as follows: dexamethasone, 340%; betamethasone, 230%; and triamicinolone, 8%. To preclude an erroneous result, subjects who were pregnant or receiving any steroid medication were excluded from the study. The percent cross-reactivity with the main naturally occurring steroids was as follows: 11-desoxycortisol 3.2%, cortisol 1.1%, DOC 0.3%, pregnenolone 0.1%, corticosterone 0.06%, progesterone 0.05%, and aldosterone < 0.05%. The only compound with potential for interference, because of its high level in the circulation in the early morning, was cortisol.(ABSTRACT TRUNCATED AT 250 WORDS)

Fludrocortisone↗
PubMed1975

Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin.

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.

Adolescent↗
PubMed1987

Effects of fludrocortisone withdrawal on plasma angiotensin II, ACTH, vasopressin, and potassium in patients with Addison's disease.

UNLABELLED: We attempted to answer to the question whether excessive rises in endogenous plasma angiotensin II (AII) stimulate ACTH secretion by measuring PRA, AII, AVP, ACTH, and cortisol in 8 patients with Addison's disease before and after withdrawal of fludrocortisone substitution. Blood was drawn at 14.30 h, exactly 6 1/2 h after the morning dose of hydrocortisone had been taken. PRA and AII were initially higher than normal in 4 patients. After withdrawal of fludrocortisone for 1 or 2 weeks, PRA and AII rose markedly in 4 patients (up to 260 ng/l) without concomitant changes in plasma ACTH levels (r = -0.081, AII vs ACTH). Changes in plasma cortisol could not have obscured a stimulatory effect of AII on ACTH by variable feedback inhibition of ACTH release. The increase in plasma AII levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. In all patients, hyperkalaemia developed after fludrocortisone withdrawal, independent of changes in PRA and AII. Rises in PRA, AII, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Plasma AVP remained in the normal range after fludrocortisone withdrawal, but was slightly elevated after increasing salt intake without fludrocortisone administration. CONCLUSIONS: Rises of endogenous plasma AII to levels tenfold higher than normal do not stimulate ACTH release. AII is probably not a physiological modulator of ACTH secretion. Mineralocorticoid substitution in Addison's disease should be monitored by plasma potassium measurement. Hyperkalaemia may coexist with normal PRA.(ABSTRACT TRUNCATED AT 250 WORDS)

Addison Disease↗
PubMed1998

A preliminary placebo-controlled crossover trial of fludrocortisone for chronic fatigue syndrome.

OBJECTIVE: To provide a preliminary assessment of the efficacy and safety of fludrocortisone acetate treatment of chronic fatigue syndrome. DESIGN: A placebo-controlled, double-blind, random-allocation crossover trial of 6 weeks of fludrocortisone. SETTING: An outpatient clinical trials unit. PATIENTS: Twenty-five participants with chronic fatigue syndrome (mean age, 40 years; 19 [76%] women; mean duration of illness, 7.0 years) were recruited from a research and clinic registry. Five patients withdrew from the trial. INTERVENTIONS: All participants were scheduled to receive fludrocortisone acetate (0.1-0.2 mg) or a placebo for 6 weeks in each treatment. MAIN OUTCOME MEASURES: Self-administered questionnaires were completed at the beginning and end of each treatment arm that asked patients to rate the severity of their symptoms on a visual analogue scale. The Medical Outcomes Study 36-Item Short-Form Health Survey, a reaction time test, and a treadmill exercise test were used to assess functional status. Blood pressure, heart rate, and plasma norepinephrine levels were obtained at baseline. Blood pressure and heart rate were recorded at the end of the exercise test and monitored at all subsequent visits. RESULTS: At baseline, the study participants reported symptom severity greater than 5 for most symptoms, and all had evidence of marked functional impairments. No improvement was observed in the severity of any symptom or in any test of function for the 20 participants who completed both arms of the trial. Blood pressure and heart rate readings were unaffected by treatment, and plasma norepinephrine levels did not differ from those of a healthy control group. The incidence of adverse experiences was similar in the fludrocortisone and placebo arms of the trial. CONCLUSION: Low-dose fludrocortisone does not provide sufficient benefit to be evident in a preliminary blinded trial of unselected patients with chronic fatigue syndrome.

Adult↗
PubMed1988

The effect of fludrocortisone acetate on plasma volume and natriuresis in patients with aneurysmal subarachnoid hemorrhage.

In order to prevent hypovolemia fludrocortisone acetate treatment was started on admission in 39 consecutive patients with CT evidence of subarachnoid hemorrhage. In 28 patients an aneurysm was proven or probable, and in 21 of these the effects of fludrocortisone acetate on sodium balance and on plasma volume could be studied. In the first five days plasma volume decreased more than 10% in four patients, decreased less than 10% in five and increased in 12. The cumulative sodium balance measured over five days was negative in seven of the 21 patients. Plasma renin values were measured in 15 of the 21 patients and also in stored samples of 18 patients who were not treated with fludrocortisone acetate. Plasma renin values were less high in patients treated with fludrocortisone acetate, regardless of the presence of a negative sodium balance. In three of the 39 patients signs of pulmonary edema developed, and low serum potassium values were observed in four of the 21 patients. In comparison with previous studies, these findings suggest that fludrocortisone acetate is an effective method of decreasing the incidence of volume depletion and negative sodium balance.

Blood Volume↗
PubMed1993

Benefits of fludrocortisone in the treatment of symptomatic vasodepressor carotid sinus syndrome.

OBJECTIVE: To assess treatment with fludrocortisone in vasodepressor carotid sinus syndrome. PATIENTS AND METHODS: Eleven patients, mean (SD) age 83 (5) years, with daily dizzy episodes and a median of five (range two to 20) syncopal episodes over a median of one year were studied. All had vasodepressor carotid sinus syndrome (> 50 mm Hg fall in systolic blood pressure during carotid sinus massage independent of bradycardia). Carotid sinus massage was carried out while the patient was supine and upright (tilt table) before and after 600 micrograms intravenous atropine. Phasic heart rate and blood pressure recordings were monitored throughout. The study was repeated after 100 micrograms of fludrocortisone daily by mouth for two weeks. Patients continued to take fludrocortisone for a six month follow up period. RESULTS: Baseline systolic blood pressure was (mean (SD)) 169 (31) mm Hg and the RR interval was 770 (150) ms. After carotid sinus massage, systolic blood pressure fell to 113 (27) mm Hg (p < 0.01) and RR was 1060 (210) ms (NS). The vasodepressor response was 56 (12) mm Hg. Baseline systolic blood pressure after two weeks of fludrocortisone treatment was 171 (37) mm Hg (NS); but the fall in systolic blood pressure during carotid sinus massage was significantly reduced (32 (14) mm Hg; p < 0.01). At six months follow up, two patients complained of intermittent dizziness and no patients had syncope. CONCLUSION: Fludrocortisone effectively reduces the vasodepressor response and relieves the symptoms of vasodepressor carotid sinus syndrome.

Aged↗
PubMed1994

Effects of fludrocortisone on sympathetic nerve activity in humans.

Fludrocortisone reduces plasma norepinephrine in healthy humans, but forearm vascular and pressor responses to norepinephrine are potentiated. The effects of fludrocortisone on sympathetic nerve activity in healthy humans are not known. To investigate these effects we evaluated muscle sympathetic nerve activity, heart rate, and arterial pressure in 11 healthy volunteers during three protocols: (1) before and on day 7 of fludrocortisone (0.4 mg/d) treatment with ad libitum diet (n = 6); (2) before and on day 7 of fludrocortisone (0.4 mg/d) or placebo with a 150 mmol/24 h (mEq/24 h) sodium diet (n = 7); and (3) before and on day 2 of fludrocortisone (0.4 mg/d) or placebo with a 150 mmol/24 h (mEq/24 h) sodium diet (n = 4). Placebo did not alter any parameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Effect of fludrocortisone acetate in patients with subarachnoid hemorrhage.

In this study with randomized controls, we administered fludrocortisone acetate to 46 of 91 patients with subarachnoid hemorrhage in an attempt to prevent excessive natriuresis and plasma volume depletion. Fludrocortisone significantly reduced the frequency of a negative sodium balance during the first 6 days (from 63% to 38%, p = 0.041). A negative sodium balance was significantly correlated with decreased plasma volume during both the first 6 days (p = 0.014) and during the entire 12-day study period (p = 0.004). Although fludrocortisone treatment tended to diminish the decrease in plasma volume, the difference was not significant (p = 0.188). More patients in the control group developed cerebral ischemia (31% vs. 22%) and, consequently, more control patients were treated with plasma volume expanders (24% vs. 15%), which may have masked the effects of fludrocortisone on plasma volume. Fludrocortisone therefore reduces natriuresis and remains of possible therapeutic benefit in the prevention of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.

Clinical Trials as Topic↗
PubMed1986

Adverse effect of phenytoin on mineralocorticoid replacement with fludrocortisone in adrenal insufficiency.

Two patients with longstanding adrenal insufficiency developed severe mineralocorticoid deficiency during concomitant phenytoin treatment. A 64-year-old man with primary adrenal insufficiency of 41 years duration was treated with phenytoin for an acute seizure disorder. He subsequently developed mineralocorticoid insufficiency despite taking his customary dosages of cortisone acetate and fludrocortisone. This responded to volume repletion and increased fludrocortisone requirement from 0.05 mg to 0.4 mg daily, which decreased to the former amount following discontinuation of phenytoin. A 42-year-old woman with primary adrenal insufficiency of 3 years duration and a lifelong seizure disorder treated with phenytoin incurred multiple, life-threatening episodes of mineralocorticoid insufficiency. Her fludrocortisone requirement was ultimately established as 2.0 mg daily with a normal hydrocortisone requirement and clearance rate. Fludrocortisone thus appears to be another synthetic steroid whose metabolism is sensitive to drugs that increase hepatic 6-beta-hydroxylation, such as phenytoin. Treatment with these inducing drugs may markedly alter mineralocorticoid requirements in patients with primary adrenal insufficiency.

Adrenal Insufficiency↗
PubMed1979

The pressor actions of noradrenaline, angiotensin II and saralasin in chronic autonomic failure treated with fludrocortisone.

1 Treatment of postural hypotension due to chronic autonomic failure with fludrocortisone increased the pressor sensitivity to intravenous noradrenaline. Fludrocortisone increased the blood pressure in the standing but not the lying position. These effects of fludrocortisone may be the result of increased sensitivity of vascular receptors to noradrenaline. 2 The pressor action of angiotensin II, to which patients were supersensitive, may have involved the stimulation of alpha-adrenoceptors since it was partially antagonised by phentolamine. 3 Saralasin had a marked, paradoxical, pressor effect. This may have been mediated by vascular alpha-adrenoceptors because log dose-response curves of saralasin-induced increases in systolic pressure were shifted to the right in a parallel fashion after phentolamine. 4 Fludrocortisone treatment increased the pressor sensitivity to intravenous saralasin but not to angiotensin-II.

Aged↗
PubMed1976

Therapeutic experience with fludrocortisone in diabetic postural hypotension.

Fourteen patients with diabetic postural hypotension were treated with fludrocortisone for a mean 12 months (range 6-30 months). The mean daily dose of fludrocortisone was 0.2 mg (range 0.1 mg-0.4 mg). Standing systolic and diastolic blood pressures increased significantly (P less than 0.001) after treatment with fludrocortisone and the postural hypotension decreased significantly (P less than 0.001). Thirteen patients noted considerable symptomatic improvement. Fludrocortisone should be used cautiously in patients with congestive cardiac failure or the nephrotic syndrome.

Adult↗
PubMed1996

Fludrocortisone in the treatment of hypotensive disorders in the elderly.

OBJECTIVE: To evaluate tolerance of fludrocortisone in older patients with hypotensive disorders. DESIGN: Prospective case series. SETTING: Syncope clinic. PATIENTS: 64 Consecutive patients over 65 years (mean age 80 years) with one or more hypotensive disorders (orthostatic hypotension, vasodepressor carotid sinus syncope, and/or vasodepressor neurocardiogenic syncope. INTERVENTIONS: Fludrocortisone in daily doses of 100 micrograms [corrected] (72%), 50 micrograms [corrected] (27%), and 200 micrograms [corrected] (one patient). MAIN OUTCOME MEASURES: Adverse events, treatment withdrawal. RESULTS: During follow up 13 patients died of unrelated causes. Of the remainder 33% discontinued fludrocortisone at a mean of five months. Reasons for discontinuing treatment were hypertension, five; cardiac failure, four; depression, three; oedema, three; and unspecified, two. In those who continued treatment supine systolic and diastolic blood pressure did not differ significantly from baseline (follow up two to 21 months). Hypokalaemia developed in 24% at a mean of eight months; in no case was treatment withdrawn because of hypokalaemia. CONCLUSION: Fludrocortisone, even in low doses, is poorly tolerated in the long term in older patients with hypotensive disorders.

Aged↗
PubMed1981

The treatment of idiopathic orthostatic hypotension: a combined fludrocortisone and flurbiprofen regime.

We report our experience in the management of idiopathic orthostatic hypotension using the prostaglandin synthetase inhibitor, flurbiprofen. In five subjects with proven autonomic failure the effect on blood pressure of the addition of flurbiprofen (or fludrocortisone) to the previous drug regime was assessed. Both lying and standing blood pressure were seen to rise with fludrocortisone treatment although the change in standing blood pressure was not statistically significant. Flurbiprofen, in contrast, produced no change in lying blood pressure but a significant rise in standing blood pressure. Digital blood flow measurements were made on three subjects before and after flurbiprofen and a dose-related reduction in post-occlusive reactive hyperaemia was demonstrated suggesting an effect of this drug on precapillary smooth muscle tonus. Two patients failed to maintain a long-term response to treatment with flurbiprofen and fludrocortisone but have been helped by the addition of I) ephedrine or II) tyramine an monoamine oxidase inhibitor (phenelzine). We recommend a stepwise approach to treatment in this condition commencing with flurbiprofen and adding fludrocortisone later if necessary. This approach would appear to offer the maximum benefit with a minimum of side effects.

Adolescent↗
PubMed1975

Levodopa-induced postural hypotension. Treatment with fludrocortisone.

Six parkinsonian patients with symptomatic postural hypotension secondary to levodopa therapy were treated with 0.05 to 0.2 mg of fludrocortisone acetate daily for six to ten months. Severe orthostatic light-headedness and frequent syncope had previously been alleviated only be reducing the dosage of levodopa to levels producing less than optimal antiparkinsonian benefits. In all six patients, symptoms were alleviated satisfactorily, and supine and upright blood pressures returned to normal levels during treatment with fludrocortisone acetate. There were no adverse reactions. Fludrocortisone acetate is an effective and safe drug for the treatment of severe and otherwise intractable postural hypotension secondary to therapy with levodopa.

Aged↗
PubMed1983

Fludrocortisone suppression of sympathetic nervous activity.

Fludrocortisone depressed plasma norepinephrine in normal subjects but to a lesser degree than it depressed renin activity or urinary aldosterone excretion. Sympathetic nervous reactivity (defined as upright/supine plasma norepinephrine) was decreased more than supine plasma norepinephrine. Pretreatment supine plasma norepinephrine (but not plasma renin activity or aldosterone excretion) correlated with blood pressure changes during fludrocortisone dosing, which suggests participation of the sympathetic nervous system in the blood pressure elevations reported during exogenous steroid administration or primary aldosteronism. Suppression of sympathetic nervous activity and reactivity by fludrocortisone tends to explain its limited usefulness in patients with autonomic dysfunction and postural hypotension.

Adolescent↗
PubMed1975

Response of plasma aldosterone to fludrocortisone in primary hyperaldosteronism and other forms of hypertension.

The response of plasma aldosterone to fludrocortisone administration (400 mug 12-hourly for 3 days) was studied in twenty-two patients with primary hyperaldosteronism. No difference was observed in the response between those patients with an adrenal adenoma and those with bilateral adrenocortical hyperplasia, there being no significant change in plasma aldosterone levels across the test period. No separation between the groups was seen when basal plasma renin concentration was related to the aldosterone level following fludrocortisone. It is concluded that the test is of little value in the pre-operative differentiation of these conditions. Twenty-three patients with no demonstrable cause for their hypertension and four with elevated levels of plasma deoxycorticosterone were similarly studied for comparison. These groups demonstrated a normal fall in plasma aldosterone levels following fludrocortisone.

Adenocarcinoma↗