Diseases of the adrenal cortex

Kannan, C. R.

doi:10.1016/0011-5029(88)90023-5

Cited by 37 publications

(3 citation statements)

References 162 publications

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“…Thyroid hormone replacement in undiagnosed Addison’s disease may precipitate adrenal crisis because thyroid hormone increases the hepatic clearance of cortisol. In addition, individuals with newly diagnosed Addison’s disease can have a reversible increase in thyrotropin levels as glucocorticoids inhibit thyrotropin secretion [72]. Replacement of glucocorticoid deficiency can result in the normalization of thyrotropin levels less than 30 μU per milliliter.…”

Section: Therapymentioning

confidence: 99%

Autoimmune polyendocrine syndrome type 1 (APS‐1) as a model for understanding autoimmune polyendocrine syndrome type 2 (APS‐2)

Michels¹,

Eisenbarth

2009

Journal of Internal Medicine

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Abstract. Michels AW, Eisenbarth GS (Barbara Davis Center for Childhood Diabetes, University of Colorado Denver). Autoimmune polyendocrine syndrome type 1 (APS-1) as a model for understanding autoimmune polyendocrine syndrome type 2 (APS-2) (Review). J Intern Med 2009; 265: 530-540.Autoimmune polyendocrine syndromes type 1 and 2 (APS-1 and APS-2) are diverse in regards to their component diseases and immunologic features of pathogenesis. Animal models and human studies highlight the importance of alleles of HLA (human leukocyte antigen)-like molecules determining tissue specific targeting that with the loss of tolerance leads to organ specific autoimmunity. Knowledge of the syndromes and component diseases allows clinicians to recognize and prevent illness prior to morbidity.With the current understanding of the syndromes, a paradigm for diagnosis, screening and treatment can be established. Once genetically susceptible individuals are identified screening for autoantibodies can be performed. Amongst autoantibody positive individuals, monitoring for physiologic decompensation, with a goal of treating prior to morbidity and in some cases mortality, follows. With continued basic and clinical research, therapies aimed at treating the underlying autoimmunity and disease prevention should become possible.

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Section: Therapymentioning

confidence: 99%

Autoimmune polyendocrine syndrome type 1 (APS‐1) as a model for understanding autoimmune polyendocrine syndrome type 2 (APS‐2)

Michels¹,

Eisenbarth

2009

Journal of Internal Medicine

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“…Nowadays patients may present with overweight or obesity, not just because the increase trend describe above, but also because it can represent an earlier stage of the disease. So an underweight patient its not imprescindible to suspected adrenal insufficiency, since the typically wasted, underweight patient reported in the past, may represent a late stage of the disease [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Low-Dose ACTH Stimulation Test in Obesity: A Randomized Dose Assessment

Mancillas-Adame

Sánchez‐García

Rodríguez-Gutiérrez

et al. 2022

International Journal of Endocrinology

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Background. The short cosyntropin test is widely used for adrenal insufficiency screening and diagnosis. Lower cosyntropin doses may have greater sensitivity vs. the standard dose in detecting adrenal dysfunction. Obesity and overweight are increasing, impacting the clinical presentation of some diseases. Currently more than 50% of the subjects diagnosed with autoimmune adrenal insufficiency have a BMI greater than 25, and hence individuals living with overweight and obesity are more frequently requiring evaluation of the adrenal cortical function. Fixed-dose cosyntropin stimulation may not be appropriate for individuals with obesity. Objective. The primary objective was to compare cortisol response to a weight-adapted cosyntropin dose vs. a fixed low dose (1 µg) and a more physiologically fixed dose (10 µg). Methods. Twenty individuals with obesity and 20 age-matched healthy controls underwent in a randomized sequence at least one-week apart, to the The short cosyntropin test with three different doses, 0.2 µg/kg of body weight, 1 or 10 µg fixed dose stimuli. The assessment and data analysis were blinded to the individual and the investigator. Results. Cortisol response was reduced in the group with obesity with the 1 µg fixed dose stimuli at 30 minutes (median, IQR) 649.6 µg, 567.3–738.4 µg for the control group vs. 568.6 µg, 528.4–623.13 µg, p = 0.04 ; there was a lower cortisol peak at 60′ in all the three evaluated doses, with a dose-dependent trend. A weight-adapted cosyntropin dose of 0.2 µg in obesity produces a similar response to the one observed in individuals without obesity. The 1 µg ACTH test falls short on stimulating the cortisol adrenal response in individuals with obesity.

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“…Hypo-and hyper-aldosteronism have been reviewed previously [Kannan, 1988;Torpy et al, 1999]. Primary hyperaldosteronism is a disease of uncontrolled aldosterone release from the adrenal gland.…”

Section: Mineralocorticoids and Hypertensionmentioning

confidence: 99%

Adrenal corticosteroids, their receptors and hypertension

Hu¹,

Bolten²

2006

Drug Development Research

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Mineralocorticoids and glucocorticoids are primarily synthesized in the adrenal cortex, and play key roles in mediating physiological responses under stressful conditions, such as lack of water or nutrients. Both types of corticosteroid elevate blood pressure and elevated levels of these steroids are found in hypertensive patients. The major mineralocorticoid and glucocorticoid in humans are aldosterone and cortisol, respectively. Aldosterone activates the mineralocorticoid receptor (MR) and cortisol the glucocorticoid receptor (GR). In this overview, the clinical and genetic evidence that both MR and GR are involved in blood pressure regulation is reviewed as are the mechanisms by which MR and GR regulate blood pressure in response to agonists. MR antagonists have been used to treat hypertension. However, GR antagonists have not been fully explored in the clinic. Based on the prevalence of abnormal mineralocorticoid and glucocorticoid signaling in hypertension patients, it is proposed that antagonizing these adrenal corticosteroid receptors will provide benefit in treating hypertension. Drug Dev. Res. 67:871-883, 2006.

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Diseases of the adrenal cortex

Cited by 37 publications

References 162 publications

Autoimmune polyendocrine syndrome type 1 (APS‐1) as a model for understanding autoimmune polyendocrine syndrome type 2 (APS‐2)

Autoimmune polyendocrine syndrome type 1 (APS‐1) as a model for understanding autoimmune polyendocrine syndrome type 2 (APS‐2)

Low-Dose ACTH Stimulation Test in Obesity: A Randomized Dose Assessment

Adrenal corticosteroids, their receptors and hypertension

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