Use Of Fludrocortisone Research Articles

Impact of fludrocortisone on the outcomes of subarachnoid hemorrhage patients: A retrospective analysis

BackgroundWhether the use of fludrocortisone affects outcomes of patients with aneurysmal subarachnoid hemorrhage (aSAH). MethodsWe conducted a retrospective analysis of 78 consecutive patients with a ruptured aSAH at a single academic center in the United States. The primary outcome was the score on the modified Rankin scale (mRS, range, 0 [no symptoms] to 6 [death]) at 90 days. The primary outcome was adjusted for age, hypertension, aSAH grade, and time from aSAH onset to aneurysm treatment. Secondary outcomes were neurologic and cardiopulmonary dysfunction events. ResultsAmong 78 patients at a single center, the median age was 58 years [IQR, 49 to 64.5]; 64 % were female, and 41 (53 %) received fludrocortisone. The adjusted common odds ratio, aOR, of a proportional odds regression model of fludrocortisone use with mRS was 0.33 (95 % CI, 0.14-0.80; P = 0.02), with values <1.0 favoring fludrocortisone. Organ-specific dysfunction events were not statistically different: delayed cerebral ischemia (22 % vs. 39 %, P = 0.16); cardiac dysfunction (0 % vs. 11 %; P = 0.10); and pulmonary edema (15 % vs. 8 %; P = 0.59). ConclusionsThe risk of disability or death at 90 days was lower with the use of fludrocortisone in aSAH patients.

FRI254 Unconventional Pre-operative Management Of Congenital Adrenal Hyperplasia

Abstract Disclosure: M.A. Ortiz-Rivera: None. L.N. Madera Marin: None. A. Rosado-Burgos: None. L. El Musa Penna: None. W. Medina-Torres: None. L.R. Sepulveda-Garcia: None. L.A. Gonzalez-Rodriguez: None. M. Ramirez-Vick: None. M. Alvarado-Santiago: None. A.J. Grana Santini: None. M. Feliciano-Emmanuelli: None. Management of classic salt-wasting congenital adrenal hyperplasia [CAH] warrants suppression of the hypothalamic-pituitary-adrenal axis through glucocorticoid and mineralocorticoid supplementation. Preferred glucocorticoid replacement is generally hydrocortisone [HC] 3 times daily but caring for these patients often involves unconventional choices of glucocorticoid preparation regimens tailored to meet patient needs. A 41-year-old female with history of long-standing poorly controlled classic salt-wasting CAH associated to secondary amenorrhea and hypothyroidism, presenting with bilateral myelolipomas was consulted to our service for pre-op optimization. She underwent evaluation by Urology due to worsening right-sided back pain for which an abdominal-pelvic CT was performed showing large bilateral adrenal gland lesions (left mass measuring 11.5 x 10.3 x 10.6 cm and right mass measuring 8.1 x 10.4 x 7.7 cm) consistent with adrenal myelolipomas. Endocrine surgeon favored adrenalectomy due to mass effect brought about by massive adrenal growth secondary to inadequate therapeutic regime. Patient had been lost to follow-up after transitioning from pediatric to adult Endocrinology and was managed by her primary care physician who kept her on an unmodified therapeutic regime. During a pharmacy shortage of HC, she was switched from HC 25 mg TID to 5 mg daily. Furthermore, use of fludrocortisone 0.1 mg daily had been inadvertently halted in the past year. There had been progressive skin hyperpigmentation since the age of 20, significant hirsutism and salt cravings which made her add soy sauce to meals. At the age of 12 a vaginoplasty was performed, with menstrual periods ceasing at age 15. Physical examination was remarkable for grave voice, broad shoulders, bronze skin and coarse terminal hairs on chin, upper lip, sides of face and upper back. Hormonal workup revealed a direct renin &amp;gt; 300 pg/mL (nl 3.6 – 81.6), ACTH 463 pg/mL (nl 0.00 – 46.00), androstenedione &amp;gt; 10 ng/mL (nl 0.6 – 3.10), total testosterone [TT] 419 ng/dL (nl 13 – 53) and 17-hydroxyprogesterone [17-OHprog] &amp;gt; 20 ng/mL (nl 0.20 – 2.6). Frequent increases in medication dosing, up to HC 20mg TID and fludrocortisone 0.1mcg BID, did not attain adequate hormonal control. Dexamethasone 0.25 mg was then added at bedtime and the patient was finally able to achieve restoration of menses, resolution of salt cravings and hormonal profile control with decreases in renin to 23.02 pg/mL, androstenedione to &amp;lt; 0.30 ng/mL, TT to 11 ng/dL and 17-OHprog to 3.15 ng/mL. Alternative treatment strategies are sometimes warranted to achieve control of CAH. In this patient with prominent androgen excess and amenorrhea who failed to meet goals on high doses of hydrocortisone and fludrocortisone, combination therapy with a small dose of long-acting glucocorticoid at bedtime achieved the desired goal. Presentation: Friday, June 16, 2023

Evaluating renin and aldosterone levels in children with organic acidemia-therapeutic experience with fludrocortisone.

Hyporeninemic hypoaldosteronism has been reported in only a few cases with methylmalonic acidemia (MMA) and has been attributed to the renal involvement. This study aims to investigate renin-aldosterone levels along with the renal functions of the patients with organic acidemia.This is a cross-sectional study conducted in patients with MMA, propionic acidemia (PA), and isovaleric acidemia (IVA). Serum renin, aldosterone, sodium, and potassium levels were measured, and glomerular filtration rates (GFR) were calculated. Comparisons were made between the MMA and non-MMA (PA+IVA) groups.Thirty-two patients (MMA:PA:IVA = 14:13:5) were included. The median GFR was significantly lower in the MMA group than in the non-MMA group (p < 0.001). MMA patients had the highest incidence of kidney damage (71.4%), followed by PA patients (23%), while none of the IVA patients had reduced GFR. GFR positively correlated with renin levels (p = 0.015, r = 0.433). Although renin levels were significantly lower in the MMA group than the non-MMA group (p = 0.026), no significant difference in aldosterone levels was found between the two groups. Hyporeninemic hypoaldosteronism was found in 3 patients with MMA who had different stages of kidney damage, and fludrocortisone was initiated, which normalized serum sodium and potassium levels. Conclusions: This study, which has the largest number of patients among the studies investigating the renin-angiotensin system in organic acidemias to date, has demonstrated that hyporeninemic hypoaldosteronism is not a rare entity in the etiology of hyperkalemia in patients with MMA, and the use of fludrocortisone is an effective treatment of choice in selected cases. What is Known: • Hyperkalemia may be observed in cases of methylmalonic acidemia due to renal involvement and can be particularly prominent during metabolic decompensation. • Hyporeninemic hypoaldosteronism has been reported to be associated with hyperkalemia in only a few cases of methylmalonic acidemia. What is New: • Hyporeninemic hypoaldosteronism was found in one-fifth of cases with methylmalonic acidemia. • Fludrocortisone therapy leads to the normalization of serum sodium and potassium levels.

Pivalato de desoxicorticosterona no controle do hipoadrenocorticismo canino – relato de casos

Primary hypoadrenocorticism or Addison’s disease is an endocrinopathy involving glucocorticoid deficiency, commonly associated with mineralocorticoid deficiency. The most commonly used treatment for hormone replacement involves the combination of fludrocortisone and prednisone. Deoxycorticosterone pivalate (DOCP) has been shown in the literature to be superior in electrolyte control in patients with hypoadrenocorticism, and should always be associated with prednisone/prednisolona. In this study, we report the benefit of DOCP and the two-stage dose adjustment protocol for this drug in 2 different cases. There was superior efficacy in electrolyte control and reduction of side effects with the DOCP and prednisolone protocol compared to the use of fludrocortisone in both patients.

Successful Use of Fludrocortisone in a Child with Refractory Cerebral Salt Wasting Syndrome: A Case Report and Review of Literature

Hyponatremia post-neurosurgical intervention can be dangerous and potentially life-threatening. Two of its most common causes are cerebral salt wasting (CSW) and syndrome of inappropriate anti-diuretic hormone release (SIADH). CSW is proposed to be secondary not only to the elevated levels of circulating atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) but inhibition of steroidogenesis in the zona glomerulosa of the adrenal cortex, thus resulting in mineralocorticoid deficiency. We present a two-year-old male who had developed acute hyponatremia secondary to CSW on post-operative day two after a sub-total resection of a low-grade juvenile pilocytic astrocytoma (WHO grade I). Fludrocortisone was successfully used to manage the refractory hyponatremia and alleviated the need to use very large amounts of oral sodium supplementation.

Use of fludrocortisone for intradialytic hypotension.

Intradialytic hypotension during dialysis adversely affects a patient’s prognosis and increases mortality. We report a case in which intradialytic hypotension that persisted after the administration of midodrine was relieved after the use of fludrocortisone. Administration of 0.2 mg of fludrocortisone occurred 30 minutes before dialysis. We compared 45 sessions of dialysis without fludrocortisone administration and 45 sessions of dialysis with fludrocortisone administration in one patient. The number of times in which systolic blood pressure became lower than 80 mmHg and the number of early terminations of dialysis due to a decrease in systolic blood pressure were higher in the sessions without fludrocortisone administration than in the sessions with fludrocortisone administration (P < 0.05). Fludrocortisone may be helpful for the treatment of intradialytic hypotension that does not respond to midodrine administration.

Fludrocortisone

Fludrocortisone

Histoplasmosis associated with Addison's disease

A 60-year-old female farmer and resident of the hinterlands of Rio Grande do Sul (southern Brazil) had a history of treatment for depression (sertraline, 50mg daily) and widespread pain. Clinical and laboratory examinations revealed mild gastritis, gastric mucosal atrophy, and osteoporosis. She reported continued use of fludrocortisone and prednisone for the treatment of Addison’s disease, which had been diagnosed previously. A total abdominal ultrasound revealed the presence of two solid nodular lesions: one measuring 5cm in diameter, located in the region of the right adrenal gland, and the other measuring 5.7cm at its greatest diameter and located in the region of the left adrenal gland. Histological analysis of hepatic fragments revealed steatosis affecting approximately 20% of hepatocytes and fibrous portal expansion with rare septa formation. Iron overload was not observed (Figure A). Extensive areas of necrosis and peripheral fibrosis were observed in the suprarenal fragments (Figure B). The pericystic lymph node showed granulomatous lymphadenitis. Grocott’s methenamine silver staining revealed the presence of fungal elements characteristic of Histoplasma capsulatum in the suprarenal fragments (Figure C), lymph nodes, and liver histological sections, which confirmed the diagnosis of histoplasmosis. The patient was treated with 100 mg of itraconazole twice a day for a year, during which time she presented a good clinical condition. This case illustrates the fact that infection of the adrenal glands caused by H. capsulatum, particularly in endemic areas, should be considered and included in the differential diagnosis of diseases of the adrenal glands.

Use of Milnacipran in a Patient with Hyponatremia under the Cover of Fludrocortisones

Introduction: Hyponatremia is a known side effect of antidepressant medications.Usually management of hyponatremia in patients receiving antidepressants involves stopping of antidepressant and restriction of fluid intake. However, information is not clear with respect to use of antidepressant in patients with persistent hyponatremia. Objective: To describe a patient detected to have hyponatremia prior to starting of antidepressant. The hyponatremia was corrected with the use of fludrocortisone, but introduction of sertraline led to reemergence of hyponatremia. Later patient tolerated milnacipran along with fludrocortisone, without recurrence of hyponatremia. Conclusion: Fludrocortisone can be used for prevention and management of hyponatremia in patients at high risk of developing the same. Further, milnacipran may be considered as a viable option in patients who develop hyponatremia with SSRIs

Assessment of the hypothalamic-pituitary-adrenal axis activity: glucocorticoid receptor and mineralocorticoid receptor function in depression with early life stress - a systematic review.

The mechanisms involved in the dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, especially in the functioning of glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) in depressed patients, are not well elucidated. The objective of this study was to conduct a systematic review of articles that assess the HPA axis activity from GR and MR in depressed patients and healthy controls with or without early life stress. We conducted a systematic review of articles in PubMed, SCOPUS and SciELO published between 2000 and 2011, using the following search terms: child abuse, depression, HPA axis, dexamethasone, prednisolone, fludrocortisone and spironolactone. Thirty-four papers were selected for this review. Most studies identified in this review used the dexamethasone/corticotropin-releasing hormone test and dexamethasone suppression test. In these studies, hypercortisolaemia was associated with depression. We identified three studies with the Prednisolone suppression test, only one study with the use of fludrocortisone and one with spironolactone. This review found nine studies that evaluated the HPA axis in individuals with early life stress. The majority of the studies assessed in this review show that early life stress leads to permanent changes in the HPA axis and may lead to development of depression in adults. The most consistent findings in the literature show increased activity of the HPA axis in depression associated with hypercortisolaemia and reduced inhibitory feedback. These findings suggest that this dysregulation of the HPA axis is partially attributable to an imbalance between GR and MR. Evidences have consistently showed that GR function is impaired in major depression, but few studies have assessed the activity of MR in depression and early life stress.

Clinical effects of adding fludrocortisone to a hydrocortisone-based shock protocol in hypotensive critically ill children

Adult studies evaluating corticosteroids have found varied efficacy. One study showing mortality benefit utilized fludrocortisone (FLU) and hydrocortisone (HC) (Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock. JAMA 288:862-871, 2002). Use of FLU in children has not been described. We developed a protocol using HC for systemic inflammatory response syndrome (SIRS) and shock with optional addition of FLU. Addition of FLU to a HC-based steroid protocol is associated with decreased vasopressor duration without adverse effects in hypotensive children with SIRS. Retrospective review of low-dose HC and FLU supplementation in children with SIRS and fluid refractory shock. Patients receiving FLU in addition to HC were compared with patients receiving HC alone. Ninety-seven children with SIRS and shock received steroids. Sixty of 97 (62%) received FLU in addition to HC. Seventy-three children required dopamine (DA) infusion, and 56 received norepinephrine (NE). Overall mortality was 7/97 (7%), with 5/7 (71%) nonsurvivors receiving HC + FLU. Fifty of 97 (52%) children with SIRS met definition for sepsis. Septic children who received HC + FLU required NE for significantly shorter duration than those receiving HC alone (p = 0.011). Nineteen of 60 HC + FLU patients (32%) developed nonsymptomatic hypokalemia. Hypokalemia was significantly more common in HC + FLU patients compared with those receiving HC alone (p = 0.05). Overall, addition of FLU in children with SIRS was not associated with decreased vasopressor duration or vasopressor score. However, HC + FLU was associated with shorter duration of NE support in the septic subgroup. Hypokalemia was a frequent adverse finding with HC + FLU (p = 0.05). Use of FLU should be considered in further studies evaluating the role of steroids in refractory pediatric septic shock.

Steroids in sepsis, etomidate and Pearl Harbor

Steroids in sepsis, … etomidate, … Pearl Harbor, … what’s the connection? Well, there is one, and it is relevant to the practice of emergency medicine. Steroids have enjoyed mixed...

Fludrocortisone Therapy in Cerebral Salt Wasting

Cerebral salt wasting is an increasingly recognized condition in pediatrics and is characterized by inappropriate natriuresis and volume contraction in the presence of cerebral pathology. Diagnosis can be difficult and therapy challenging. A few single case reports of the successful use of fludrocortisone exist. We report 4 patients with cerebral salt wasting, all of whom presented with hyponatremia in the presence of known intracerebral pathology. All had clinically significant hyponatremia, and 3 had hyponatremic seizures. Two of the patients also satisfied clinical criteria for diabetes insipidus. They all were treated with regimens using increased sodium and fluid administration but experienced ongoing salt wasting. Fludrocortisone was instituted in all 4 patients and in 3 resulted in rapid improvement in net sodium balance, enabling the weaning of hypertonic fluids and stabilization of serum electrolytes. In 3 patients, fludrocortisone treatment was complicated by hypokalemia, and in 1 patient by hypertension, which necessitated a dose reduction or brief cessation of therapy. Duration of therapy was 4 to 125 days. Cerebral salt wasting presents considerable management challenges; however, fludrocortisone therapy can be an effective adjunct to treatment.

Fludrocortisone for the Treatment of Heparin-Induced Hyperkalemia

OBJECTIVE:To report the use of fludrocortisone for heparin-induced hyperkalemia and to briefly review the available literature relating to heparin-induced hyperkalemia.CASE SUMMARY:A 34-year-old African-American man was admitted to the hospital for pneumococcal pneumonia and sepsis. His hospital course was complicated by the development of acute respiratory distress syndrome, severe sepsis, acute renal failure, placement of a tracheostomy, and recurrent nasopharyngeal bleeding. The patient also developed a subclavian vein thrombosis with extension to the cephalic and basilic veins secondary to placement of a pulmonary artery catheter; anticoagulation with heparin was required. On day 9 of heparin therapy, the patient developed symptomatic hyperkalemia refractory to conventional therapies. Oral fludrocortisone 0.1 mg/d was initiated with resolution of the hyperkalemia within 24 hours despite the continued administration of heparin.DATA SOURCES:A MEDLINE (1966–October 1999) search was performed to identify case reports and clinical trials discussing heparin-induced hyperkalemia or the use of fludrocortisone for hyperkalemia.DISCUSSION:Heparin has the potential to induce hyperkalemia by several mechanisms, including decreased aldosterone synthesis, reduction in number and affinity of aldosterone II receptors, and atrophy of the renal zona glomerulosa. Fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules. In this patient, fludrocortisone resulted in a significant and rapid decrease in serum potassium even with continued heparin administration and acute renal failure.CONCLUSIONS:This case suggests that fludrocortisone is a reasonable alternative therapy for patients with hyperkalemia secondary to heparin therapy when the continued administration of heparin is necessary.

Efficacy of midodrine vs placebo in neurogenic orthostatic hypotension. A randomized, double-blind multicenter study. Midodrine Study Group

To evaluate the efficacy of a 10-mg dose of midodrine 3 times per day in improving blood pressure (BP) and ameliorating symptoms of orthostatic hypotension in patients with neurogenic orthostatic hypotension. Midodrine hydrochloride, an alpha-agonist, could improve orthostatic BP by increasing vasomotor and venomotor tone. A total of 171 patients with orthostatic hypotension participated in a multicenter, randomized, placebo-controlled study. They were randomized to a 10-mg dose of midodrine or placebo 3 times per day in a 6-week study, comprising single-blind run-in (at week 1) and washout at weeks 5 and 6, with an intervening double-blind period (weeks 2 to 4). Twenty-five centers, with most patients evaluated in referral centers. The primary end points were improvement in standing systolic BP, symptoms of lightheadedness, and a global symptom relief score (by the investigator and patient separately). Nine patients were not evaluable because of noncompliance or taking concomitant vasoactive medications (3 in the midodrine group, 6 in the placebo group). In the evaluable patients, midodrine resulted in improvements in standing systolic BP at all time points (P<.001 at visits 2, 3, 4, and 5), in reported symptoms by the end of the second week of treatment (P=.001), and in the global symptom relief score rated by both the patient (P=.03) and the investigator (P<.001). There was no effect by center, severity of orthostatic hypotension, use of fludrocortisone or compression garments, or diagnosis. The main adverse effects were those of pilomotor reactions, urinary retention, and supine hypertension. Midodrine is efficacious and safe in the treatment of neurogenic orthostatic hypotension.

Treatment of Postural Hypotension A Review

Many drugs have been used in treating patients with postural hypotension but for a large number the evidence of benefit is small and the potential for adverse effects, particularly supine hypertension, is great. Full clinical assessment is essential at the outset to define the nature and extent of pathophysiological disturbance of autonomic function. Many patients can be treated adequately by sleeping with the head of the bed elevated, and the use of fludrocortisone. Patients without evidence of central neurological deficit may benefit from additional treatment with drugs which alter beta-adrenoceptor tone. Patients who respond poorly to these measures should be admitted to hospital, and treatment with desmopressin initiated. Symptomatic postprandial hypotension should be identified early since the response to these measures alone is often poor, caffeine administered before eating, with abstinence for the rest of the day, may be very helpful.

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.