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Steroids in Septic Shock
Published in Stephen M. Cohn, Alan Lisbon, Stephen Heard, 50 Landmark Papers, 2021
Despite the stated intention to study all patients regardless of corticotropin response, the CORTICUS trial was powered to detect a mortality difference among non-responders [6]. There was no difference in 28-day mortality in the hydrocortisone group among non-responders or responders, but median time to shock reversal was shorter by 2.5 days in all patients with steroids. Of note, this trial was underpowered because actual mortality was lower than estimated, and enrollment did not achieve the initial target recruitment of 800 participants.
The Hypothalamic-Pituitary-Adrenal Axis in Functional Somatic Illness
Published in Peter Manu, The Psychopathology of Functional Somatic Syndromes, 2020
The patients were randomly assigned to receive an intravenous infusion of either desmopressin (10 μg) or ovine corticotropin-releasing hormone (100 μg) or the combination of the two hormones. The subjects who received the combination were first given desmopressin as an intravenous bolus followed two minutes later by the infusion of corticotropin-releasing hormone. Blood samples were drawn at baseline and six times during the two-hour interval following the hormone administration and assayed for cortisol and adrenocorticotropin hormone levels. Statistical analyses processed the baseline levels and the maximum increase from baseline in the concentration of these hormones.
The Chemical Environment
Published in Vilma R. Hunt, Kathleen Lucas-Wallace, Jeanne M. Manson, Work and the Health of Women, 2020
Vilma R. Hunt, Kathleen Lucas-Wallace, Jeanne M. Manson
The detailed clinical course of a woman chemical worker exposed to beryllium, has been described by McCallum et al.158 In their summary they state that pregnancy was associated with relief of symptoms which persisted for some months after a normal birth. The detailed paper, however, reports that at about 4 months gestation, she experienced spontaneous pneumothorax, delivered at 8 months gestation, and died 7 months later of acute right heart failure. The onset of symptoms 2 years before pregnancy (parity not noted) was 2 years after termination of high exposure in an English laboratory with measured levels of beryllium of 2.7 μg/m3 and other rooms with levels of over 30 μg/m3. The present federal standard for beryllium is 2 μg/m3 as an 8-hr time-weighted average with an acceptable ceiling concentration of 5 μg/m3. The acceptable maximum peak is 25 μg/m3 for a maximum of 30 minutes.159 Severe lassitude, loss of weight, breathlessness, and radiological lung changes indicated the chronicity of the beryllium poisoning. Pregnancy itself provided some improvement of symptoms, sufficient to allow suspension of corticotropin therapy. It would be of considerable interest to compare the course of pregnancy in the women in the U.S. Beryllium Registry in detail.
Effect of dexamethasone on labour induction and cervical ripening in term pregnancies: a systematic review and meta-analysis
Published in Journal of Obstetrics and Gynaecology, 2022
Shahla Hemmatzadeh, Parivash Ahmadpoor, Sevda Kamrani, Mojgan Mirghafourvand
The role of corticosteroid hormones in the mechanisms responsible for parturition in mammalian species has been a subject of intensive investigation. There is evidence supporting the role of glucocorticosteroid receptors in the foetal membranes at the beginning of the labour process. In pregnant sheep the sequence of events leading to parturition includes activation of the foetal hypothalamic-pituitary adrenal axis with the production of corticotropin-releasing hormone, adrenocorticotropic hormone, and cortisol. Cortisol, produced by the foetal adrenal gland, is presumed to induce the expression of P-450 17-20 lyase by the placenta. This enzyme catalyses the transformation of pregnenolone to 17a-hydroxypregnenolone, which is a source of androgens (dehydroepiandrosterone, androstenedione) that are subsequently aromatised to oestrogens. The net effect of the activity of P450 17-20 lyase is to decrease the production of progesterone (‘progesterone withdrawal’) and to increase the bioavailability of oestrogens (Campbell et al. 1987; Meyer et al. 2016). Maternal cortisol acts on the developing foetus either directly by passing through the placenta, or indirectly via its effects on placental production of corticotrophin-releasing hormone (CRH) (Mastorakos and Ilias 2003; Entringer et al. 2011).
The pharmacotherapeutics of sarcoidosis
Published in Expert Review of Clinical Pharmacology, 2022
Patrick Mangialardi, Richart Harper, Timothy E Albertson
Cortisone and adrenal corticotropin hormone (ACTH) were introduced as therapeutics in the 1940s after Hench and Kendall observed anti-inflammatory effects of high circulating cortisol in Cushing’s Syndrome patients with rheumatoid arthritis (RA) [4,5]. Prednisone and prednisolone were developed in the early 1950s as alternatives to cortisone in an attempt to limit the salt-retaining effects of cortisone and ACTH at therapeutic doses. Nobile and colleagues first produced prednisone from cortisone using Corynebacterium simplex to catalyze the reaction. They observed it to be three to five times as active as the parent compound, but with less salt-retaining properties [4]. Prednisone received United States (US) Food and Drug Administration (FDA) approval in 1955 and has since been approved for a multitude of inflammatory, neoplastic, endocrine, autoimmune, neurologic, and other conditions. The earliest use of GCs to treat sarcoidosis came in 1951 with simultaneous case reports of using intramuscular cortisone to successfully treat pulmonary, ocular, and cutaneous sarcoidosis, with one report of severe post-treatment psychosis requiring emergent electroshock therapy [6,7].
Acute severe Cushing’s disease presenting as a hypercoagulable state
Published in Baylor University Medical Center Proceedings, 2021
Maria Mohammed Fariduddin, Wajihuddin Syed, Vidita Divan, Prashant Nadkarni, Ruban Dhaliwal
The refractory and profound hypokalemia, wide excursions in blood glucose, and vertebral compression fractures in the setting of a hypercoagulable state raised suspicion of hypercortisolism. Laboratory testing revealed elevated random cortisol, loss of circadian rhythm with elevated midnight cortisol, and failure of a low-dose dexamethasone suppression test (DST) (Table 1). A high-dose DST showed a response with relative decline of cortisol and ACTH. No masses were seen on CT imaging of the chest, abdomen, and pelvis. No pituitary enlargement or intracranial masses were seen on magnetic resonance imaging (MRI). A corticotropin-releasing hormone stimulation test showed an immediate rise in ACTH and cortisol. Subsequently, inferior petrosal venous sinus sampling showed lateralization to the right, confirming a pituitary microadenoma as the source of excessive ACTH. A transsphenoidal hypophysectomy was planned. In the midst of investigations, the patient developed another pulmonary embolism complicated by bacterial pneumonia, resulting in significant deterioration of her clinical status, and she unfortunately succumbed to the disease.