Inadequate stress response to anaesthesia and surgery due to suspected glucocorticoid deficiency in a dog undergoing exploratory laparotomy with known Addison's disease

2012 ◽  
Vol 39 (3) ◽  
pp. 315-316
Author(s):  
Maja Rysnik ◽  
Alex Dugdale
Keyword(s):  
Stress Response ◽  
Addison’S Disease ◽  
Exploratory Laparotomy ◽  
Addison's Disease ◽  
Glucocorticoid Deficiency

Mineralocorticoid Before Glucocorticoid Deficiency in a Dog with Primary Hypoadrenocorticism and Hypothyroidism

2013 ◽  
Vol 49 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Kathryn M. McGonigle ◽  
John F. Randolph ◽  
Sharon A. Center ◽  
Richard E. Goldstein
Keyword(s):  
Clinical Signs ◽  
Addison’S Disease ◽  
Serum Cortisol ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Acth Stimulation Test ◽  
Acth Stimulation ◽  
Clinical Illness ◽  
Glucocorticoid Deficiency ◽  
Electrolyte Abnormalities

A dog with an unexpected presentation of primary hypoadrenocorticism was evaluated for clinical signs and electrolyte abnormalities characteristic of Addison’s disease. Although the initial adrenocorticotropic hormone (ACTH) stimulation test documented serum cortisol concentrations within the reference range, subsequent assessments confirmed hypoaldosteronism. Mineralocorticoid replacement promptly normalized electrolytes and transiently improved clinical illness. Six weeks after initial ACTH stimulation testing, the dog became glucocorticoid deficient. Concurrent primary hypothyroidism was also documented. Hypoaldosteronism preceding hypocortisolemia is a unique presentation of canine Addison’s disease.

Familial glucocorticoid deficiency

2011 ◽  
pp. 860-864
Author(s):  
Claire Hughes ◽  
Louise Metherell ◽  
Adrian J.L. Clark
Keyword(s):  
Genetic Disorder ◽  
Recurrent Infection ◽  
Failure To Thrive ◽  
Addison’S Disease ◽  
Autosomal Recessive Disorder ◽  
Early Response ◽  
Addison's Disease ◽  
Number Of Patients ◽  
Genes Encoding ◽  
Glucocorticoid Deficiency

Familial glucocorticoid deficiency (FGD), also known as isolated glucocorticoid deficiency or hereditary unresponsiveness to ACTH, is a rare, genetically heterogeneous autosomal recessive disorder. It is characterized by resistance of the adrenal cortex to ACTH, resulting in adrenal failure with isolated glucocorticoid deficiency. Mineralocorticoid production by the adrenal gland remains near normal. Patients with FGD usually present in early childhood with symptoms relating to cortisol deficiency, including hypoglycaemia, jaundice, recurrent infection, and failure to thrive. Patients are hyperpigmented due to grossly elevated ACTH levels. FGD was first described in 1959 by Shepard et al. who reported two sisters as having Addison’s disease without hypoaldosteronism (1). Subsequently, a number of patients were reported with an inherited form of adrenal insufficiency also without hypoaldosteronism (2–5). In contrast to Addison’s disease (see Chapter 5.9), FGD is a genetic disorder resulting from mutations in genes encoding essential proteins involved in the early response to ACTH.

scholarly journals Isolated Addison's disease is unlikely to be caused by mutations in MC2R, MRAP or STAR, three genes responsible for familial glucocorticoid deficiency

2010 ◽  
Vol 162 (2) ◽  
pp. 357-359 ◽  
Author(s):  
R P Dias ◽  
L F Chan ◽  
L A Metherell ◽  
S H S Pearce ◽  
A J L Clark
Keyword(s):  
Autosomal Recessive ◽  
Regulatory Protein ◽  
Addison’S Disease ◽  
Promoter Polymorphism ◽  
Addison's Disease ◽  
Acth Receptor ◽  
Glucocorticoid Deficiency ◽  
Steroidogenic Acute Regulatory ◽  
Rare Autosomal Recessive Disease ◽  
Receptor Accessory Protein

BackgroundFamilial glucocorticoid deficiency (FGD) is a rare autosomal recessive disease caused by ACTH resistance and leads to isolated glucocorticoid deficiency. Although FGD patients typically have normal mineralocorticoid secretion, subtle alterations in the renin–angiotensin–aldosterone axis have been reported in a subset of patients at presentation. Anecdotally, some patients with FGD have been initially diagnosed as having Addison's disease (AD), with implications for treatment and genetic counselling. Currently, mutations in three genes: the ACTH receptor (MC2R); the melanocortin 2 receptor accessory protein (MRAP); and the steroidogenic acute regulatory protein (STAR) are known to give rise to FGD types 1–3. We investigated a cohort of autoantibody-negative AD patients for mutations in these genes.MethodsForty patients with known AD without evidence of autoimmune disease were screened for mutations in MC2R, MRAP and STAR. In addition, patients were genotyped for the MC2R promoter polymorphism previously associated with reduced responsiveness to ACTH.ResultsNo mutations in MC2R, MRAP or STAR were identified in any patient. The frequencies of the MC2R promoter polymorphism were similar to those reported in healthy controls.ConclusionsFGD does not appear to be underdiagnosed in the AD population. However, in ∼50% of patients with FGD, no genetic cause has yet been identified and it is possible that the other, as yet unidentified, genes giving rise to FGD may be implicated in AD.

scholarly journals Prolonged Dyspnea after Interscalene Block: Attributed to Undiagnosed Addison's Disease and Myasthenia Gravis

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
John G. Skedros ◽  
Casey J. Kiser ◽  
Shaun D. Mendenhall
Keyword(s):  
Stress Response ◽  
Myasthenia Gravis ◽  
Carotid Body ◽  
Addison’S Disease ◽  
Interscalene Block ◽  
Addison's Disease ◽  
Respiratory Compromise ◽  
Preoperative Testing ◽  
Nerve Blocks ◽  
Prolonged Duration

This report describes a patient who had a series of daily interscalene nerve blocks to treat pain following a shoulder manipulation for postsurgical stiffness. She experienced acute respiratory compromise that persisted for many weeks. All typical and unusual causes of these symptoms were ruled out. Her treating pulmonologist theorized that the ipsilateral carotid body had been injured. However, it was subsequently determined that the constellation of symptoms and their prolonged duration were best explained by a poor stress response from Addison's disease coupled with exacerbation of early onset myasthenia gravis. This patient's case is not a typical reaction to interscalene nerve blocks, and thus preoperative testing would not be recommended for myasthenia gravis or Addison's disease without underlying suspicion. We describe this report to inform physicians to consider a workup for these diagnoses if a typical workup rules out all usual causes of complications from an interscalene block.

scholarly journals GDF15 Is Elevated in Conditions of Glucocorticoid Deficiency and Is Modulated by Glucocorticoid Replacement

2019 ◽  
Vol 105 (5) ◽  
pp. 1427-1434
Author(s):  
Audrey Melvin ◽  
Dimitrios Chantzichristos ◽  
Catriona J Kyle ◽  
Scott D Mackenzie ◽  
Brian R Walker ◽  
...  
Keyword(s):  
Healthy Volunteers ◽  
Addison’S Disease ◽  
Neural Circuitry ◽  
Addison's Disease ◽  
Primary Adrenal Insufficiency ◽  
Site Of Action ◽  
Glucocorticoid Deficiency ◽  
The Impact ◽  
Dose Dependent ◽  
Cortisol Deficiency

Abstract Context GDF15 is a stress-induced hormone acting in the hindbrain that activates neural circuitry involved in establishing aversive responses and reducing food intake and body weight in animal models. Anorexia, weight loss, nausea and vomiting are common manifestations of glucocorticoid deficiency, and we hypothesized that glucocorticoid deficiency may be associated with elevated levels of GDF15. Objective To determine the impact of primary adrenal insufficiency (PAI) and glucocorticoid replacement on circulating GDF15 levels. Methods and Results We measured circulating concentrations of GDF15 in a cohort of healthy volunteers and Addison’s disease patients following steroid withdrawal. Significantly higher GDF15 (mean ± standard deviation [SD]) was observed in the Addison’s cohort, 739.1 ± 225.8 pg/mL compared to healthy controls, 497.9 ± 167.7 pg/mL (P = 0.01). The effect of hydrocortisone replacement on GDF15 was assessed in 3 independent PAI cohorts with classical congenital adrenal hyperplasia or Addison’s disease; intravenous hydrocortisone replacement reduced GDF15 in all groups. We examined the response of GDF15 to increasing doses of glucocorticoid replacement in healthy volunteers with pharmacologically mediated cortisol deficiency. A dose-dependent difference in GDF15 (mean ± SD) was observed between the groups with values of 491.0 ± 157.7 pg/mL, 427.0 ± 152.1 pg/mL and 360 ± 143.1 pg/mL, in the low, medium and high glucocorticoid replacement groups, respectively, P < .0001. Conclusions GDF15 is increased in states of glucocorticoid deficiency and restored by glucocorticoid replacement. Given the site of action of GDF15 in the hindbrain and its effects on appetite, further study is required to determine the effect of GDF15 in mediating the anorexia and nausea that is a common feature of glucocorticoid deficiency.

Addison's disease as a rare cause of chronically elevated transaminases

2004 ◽  
Vol 42 (05) ◽  
Author(s):  
GC Gurakuqi ◽  
V Stadlbauer ◽  
H Warnkross ◽  
M Trauner
Keyword(s):  
Addison’S Disease ◽  
Addison's Disease ◽  
Elevated Transaminases

"STEROID-CELL" ANTIBODY IN ENDOCRINE DISEASES

1974 ◽  
Vol 76 (4) ◽  
pp. 729-740 ◽  
Author(s):  
Peter Kamp ◽  
Per Platz ◽  
Jørn Nerup
Keyword(s):  
Leydig Cells ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Hormone Production ◽  
Cortical Cells ◽  
Endocrine Diseases ◽  
Cell Antibody ◽  
Indirect Immunofluorescence Technique ◽  
Males And Females ◽  
Adrenal Cortical Cells

ABSTRACT By means of an indirect immunofluorescence technique, sera from 116 patients with Addison's disease, an equal number of age and sex matched controls and 97 patients with other endocrine diseases were examined for the occurrence of antibody to steroid-producing cells in ovary, testis and adrenal cortex. Fluorescent staining was observed in the theca cells of growing follicles, the theca lutein cells, testicular Leydig cells and adrenal cortical cells, i. e. cells which contain enzyme systems used in steroid hormone production. The "steroid-cell" antibody was present in 24 % of the patients with idiopathic Addison's disease, equally frequent in males and females, and in 17 % of the patients with tuberculous Addison's disease, but was rarely found in controls, including patients with other endocrine diseases. Female hypergonadotrophic hypogonadism made an exception, since the "steroid-cell" antibody was found in about half the cases with this condition.

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