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Drugs and Therapeutics
Published in James Sherifi, General Practice Under the NHS, 2023
They vary in potency from cortisone to dexamethasone. There is a sense that more recent generations of GPs are less familiar and confident regarding the relative potency and potential side effects, both short and long term, of this invaluable class of compounds and are thus misguidedly limiting their use. Fludrocortisone—1953Addison’s Disease, Nocturnal Enuresis Fludrocortisone, the first of the synthetic corticosteroids, was used as a hormone replacement for Addison’s disease. Since its actions mimicked naturally occurring aldosterone, it could cause electrolyte imbalance and fluid retention resulting in oedema, cardiac failure, and cardiac arrhythmia. Urea and electrolytes required regular monitoring.
Metabolic Diseases
Published in Stephan Strobel, Lewis Spitz, Stephen D. Marks, Great Ormond Street Handbook of Paediatrics, 2019
Stephanie Grünewald, Alex Broomfield, Callum Wilson
Cortisol and very occasionally fludrocortisone are used to manage the adrenal insufficiency. Lorenzo’s oil, a 4:1 mixture of the monounsaturated fatty acids mixture of triolein and trierucin, inhibits the elongation of docosanoic acid (22:0) to 26:0 and improves/normalises the plasma VLCFA level in many patients. However, it can lead to thrombocytopenia and its impact on the neurological outcome is uncertain. Activation of peroxisomal B oxidation using peroxisome proliferator activated receptor (PPAR) alpha agonists such as fibrates has been unsuccessful, though the use of conjugated linoleic acid shows some promise. Bone marrow transplant (BMT) if performed in the early stages of COCALD does prevent the progression of the neurological disease but needs to be performed before there is significant neurological impairment and carries significant risks. Thus asymptomatic patients are monitored with regular cerebral imaging. Initial gene therapy work shown it to be effective; long-term treatment clinical trials are ongoing.
Peripheral Autonomic Neuropathies
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Fludrocortisone is commonly used; it has many pharmacologic effects. The initial dose is 0.1 mg per day. The drug increases effective vasoconstriction because it augments the action of noradrenaline release by normal sympathetic efferent activity; it does not usually aggravate recumbent hypertension. Fludrocortisone increases the sensitivity of vascular receptors to pressors and it may increase fluid content of blood vessel walls, therefore decreasing their distensibility. Because patients with postural hypotension are sensitive to sodium intake it is necessary to support all methods of treatment with a high sodium intake provided this is not contraindicated for other reasons.
Routinely accessible parameters of mineralocorticoid receptor function, depression subtypes and response prediction: a post-hoc analysis from the early medication change trial in major depressive disorder
Published in The World Journal of Biological Psychiatry, 2022
Jan Engelmann, Harald Murck, Stefanie Wagner, Lea Zillich, Fabian Streit, David P. Herzog, Dieter F. Braus, Andre Tadic, Klaus Lieb, Marianne B. Műller
Interestingly, a few studies (predominantly case reports) describe the effects of RAAS modifying compounds in patients with depression, including ACE inhibition, while systematic studies and controlled trials are still lacking (Zubenko and Nixon 1984; Hertzman et al. 2005). The authors of an epidemiological study observed a reduced risk of subjects developing depression when treated with ACE-inhibitor or angiotensin receptor antagonists vs no such treatment (Nasr et al. 2011). A placebo-controlled study (Otte et al. 2010) in patients with depression compared the effect of the centrally active MR antagonist spironolactone vs the mainly peripherally acting MR agonist fludrocortisone, a compound that is used for postural tachycardia syndrome. Only fludrocortisone had a clinical effect, i.e. it reduced the time to response in those patients, who responded. At the same time, it reduced plasma aldosterone, whereas spironolactone increased it. This may point to the importance of reducing peripheral aldosterone signalling to support treatment response. A recent open-label study with a compound inhibiting the enzyme 11beta hydroxysteroid-dehydrogenase type 2 (11betaHSD2), confirms these observations: inhibition of 11betaHSD2 leads to an activation of MR by cortisol (which is otherwise prevented from doing this) in the periphery. This peripheral activation of MR leads to a slight increase in blood pressure and a significant clinical improvement of depression symptoms after two weeks of treatment versus a treatment as usual group (Murck et al. 2020b).
Transient Visual Loss in Young Females with Crowded Optic Discs: A Proposed Aetiology
Published in Neuro-Ophthalmology, 2021
I have to explain the mechanism by which fludrocortisone reduced the frequency of the TVL episodes in Patients 1 and 3. If optic nerve head autoregulation is fully functional then both the pre- and post-treatment BPs of Patient 1 should maintain OPPs within the normal autoregulatory plateau. The effect of fludrocortisone can therefore not be explained by an iatrogenic increase in BP alone if associated with normal autoregulation. I note again studies demonstrating impaired autoregulation in a subgroup of healthy individuals,13,22 specifically a linear relationship between increasing OPP and tissue blood flow.13 This effectively suggests zero functioning of optic nerve head autoregulation in some subjects. If Patient 1 had autoregulatory dysfunction to this degree then a small increase in OPP could manifest as an augmented improvement in optic nerve head perfusion, explaining the benefit of fludrocortisone. The improvement in symptomatology with fludrocortisone could therefore also be considered evidence for autoregulatory dysfunction.
Pharmacological management of sepsis in adults with a focus on the current gold standard treatments and promising adjunctive strategies: evidence from the last five years
Published in Expert Opinion on Pharmacotherapy, 2019
Evdoxia Kyriazopoulou, Evangelos J. Giamarellos-Bourboulis
Two RCTs have recently been published shedding more light to this controversy; the ADRENAL trial [52] and the APROCCHSS trial [53]. ADRENAL is a pragmatic large-scale trial in five countries allocating patients at septic shock to treatment with placebo (n = 1,860) or hydrocortisone (n = 1,853). The primary outcome, 90-day mortality, did not differ between the two groups (27.9% versus 28.8%, p: 0.50). However, patients who had been assigned to hydrocortisone had faster resolution of shock than those assigned to placebo (median duration 3 versus 4 days, p < 0.001); less days on initial mechanical ventilation (median 6 versus 7 days, p < 0.001) and required fewer blood transfusions (37% vs 41.7%, p: 0.004) [54]. In the APROCCHSS trial conducted in France, patients at septic shock were randomly assigned to placebo or hydrocortisone for seven days [53]. The hydrocortisone group was also administered 50μg fludrocortisone daily. Intervention was accompanied by a substantial decrease of all-cause 90-mortality (43% versus 49.1% of the placebo group) and this was accompanied by a decrease of vasopressor-free days (median 19 versus 23 days in the placebo group, p < 0.001). The time to weaning from vasopressors, the time to weaning from mechanical ventilation and the time to reaching a SOFA score less than 6 was shorter in the intervention group than the placebo group. The parallel administration of fludrocortisone is a possible explanation for the survival benefit observed in this trial compared to others.