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PubMed · 11445745

Corticosteroids for septic shock.

D Annane
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Abstract

OBJECTIVE: To gather the data to provide a rationale for using replacement therapy with hydrocortisone in septic shock patients. DATA SOURCES: The Medline and the Cochrane Library databases. STUDY SELECTION: Studies in animals and in humans were considered when significant data were available about the mechanisms of action of corticosteroids or about their use in severe sepsis. DATA SUMMARY: Corticosteroids were the first anti-inflammatory drugs tested in septic patients. Randomized trials clearly showed that a short course of a large dose of anti-inflammatory steroids is ineffective and potentially harmful in patients with severe sepsis. Recent demonstrations of altered hypothalamic-pituitary-adrenal axis response to septic insult have led to a reappraisal of the use of steroids in septic shock. Randomized trials in catecholamine-dependent septic shock patients strongly suggest that replacement therapy with hydrocortisone may alleviate the symptoms of systemic inflammatory response, reduce the duration of shock, and favorably affect survival. CONCLUSIONS: Current evidence that the therapeutic interest of replacement therapy with corticosteroids increases suggests that low doses of hydrocortisone should be offered to patients with catecholamine-dependent septic shock.

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Adrenal InsufficiencyAnimalsAnti-Inflammatory AgentsDisease Models, AnimalDrug Evaluation, PreclinicalHumansHydrocortisoneHypothalamo-Hypophyseal SystemInflammationPituitary-Adrenal SystemShock, SepticSurvival AnalysisTime FactorsTreatment OutcomeJournal ArticleReview

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D Annane. 2001. Corticosteroids for septic shock.. https://doi.org/10.1097/00003246-200107001-00036

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Adrenal Insufficiency↗
PubMed2007

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OBJECTIVE: Familial glucocorticoid deficiency type I (FGD1) is a rare form of primary adrenal insufficiency resulting from recessive mutations in the ACTH receptor (MC2R, MC2R). Individuals with this condition typically present in infancy or childhood with signs and symptoms of cortisol insufficiency, but disturbances in the renin-angiotensin system, aldosterone synthesis or sodium homeostasis are not a well-documented association of FGD1. As ACTH stimulation has been shown to stimulate aldosterone release in normal controls, and other causes of hyponatraemia can occur in children with cortisol deficiency, we investigated whether MC2R changes might be identified in children with primary adrenal failure who were being treated for mineralocorticoid insufficiency. DESIGN: Mutational analysis of MC2R by direct sequencing. PATIENTS: Children (n = 22) who had been diagnosed with salt-losing forms of adrenal hypoplasia (19 isolated cases, 3 familial), and who were negative for mutations in DAX1 (NR0B1) and SF1 (NR5A1). RESULTS: MC2R mutations were found in three individuals or kindred (I: homozygous S74I; II: novel compound heterozygous R146H/560delT; III: novel homozygous 579-581delTGT). These changes represent severely disruptive loss-of-function mutations in this G-protein coupled receptor, including the first reported homozygous frameshift mutation. The apparent disturbances in sodium homeostasis were mild, manifest at times of stress (e.g. infection, salt-restriction, heat), and likely resolved with time. CONCLUSIONS: MC2R mutations should be considered in children who have primary adrenal failure with apparent mild disturbances in renin-sodium homeostasis. These children may have been misdiagnosed as having salt-losing adrenal hypoplasia. Making this diagnosis has important implications for treatment, counselling and long-term prognosis.

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