National German Audit of Diagnosis, Treatment, and Teaching in Secondary Adrenal Insufficiency

2017 ◽  
Vol 49 (08) ◽  
pp. 580-588 ◽  
Author(s):  
Stephan Petersenn ◽  
Jürgen Honegger ◽  
Marcus Quinkler
Keyword(s):  
Clinical Practice ◽  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Diagnostic Testing ◽  
Treatment Strategies ◽  
Serum Cortisol ◽  
National Audit ◽  
Secondary Adrenal Insufficiency ◽  
Endocrine Society ◽  
Great Heterogeneity

AbstractGreat heterogeneity seems to exist regarding diagnosis, therapy, and teaching of patients with secondary adrenal insufficiency (SAI) across Germany resulting in different diagnosis and treatment strategies. The aim of the work was to present the first national audit on diagnosis, treatment, and patient teaching of SAI reflecting common clinical practice in Germany. A self-designed questionnaire was sent via e-mail to all members of the German Endocrine Society (approx. 120 centers). Returned questionnaires (response rate 38.3%) were checked for duplicity of institutions and analyzed. Diagnostic testing focuses on those patients with relevant risk for adrenal insufficiency. Basal serum cortisol is mostly used as screening test. Short synacthen and CRH tests are the preferred confirmatory tests, however, cut-off values vary due to different assays used. Patients with radiation, second surgery, progressive disease or new symptoms are followed by serial re-testing. Perioperative management and frequency of postoperative re-evaluations differ among centers. Hydrocortisone is the preferred glucocorticoid for replacement therapy, but daily doses vary considerably (10–30 mg/day). Some centers perform hormone measurements for dose adjustment of glucocorticoid replacement therapy whereas others rely on clinical judgement. Patients’ teaching is done in 84% of centers, but only half of the centers include patients’ relatives. Homogeneity exists in patients’ teaching regarding intercurrent illnesses (fever, diarrhoea). Recommendations regarding dose adaptations in situations such as sport-activities, dental-procedures, or coughing are highly variable. This first national audit reveals great heterogeneity among German centers and could improve patients’ care in SAI, for example, by initiating new trials and developing clinical practice guidelines.

scholarly journals Reduced epinephrine reserve in response to insulin-induced hypoglycemia in patients with pituitary adenoma

2007 ◽  
Vol 157 (3) ◽  
pp. 265-270 ◽  
Author(s):  
Shinya Morita ◽  
Michio Otsuki ◽  
Maki Izumi ◽  
Nobuyuki Asanuma ◽  
Shuichi Izumoto ◽  
...  
Keyword(s):  
Pituitary Adenoma ◽  
Adrenal Insufficiency ◽  
Serum Cortisol ◽  
Tolerance Test ◽  
Secondary Adrenal Insufficiency ◽  
Counterregulatory Hormones ◽  
Insulin Tolerance ◽  
Secondary Hypothyroidism ◽  
Severe Impairment ◽  
Plasma Gh

Objective: Hypoglycemia induces rapid secretion of counterregulatory hormones such as catecholamine, glucagon, cortisol, and GH. Insulin-induced hypoglycemia is used for evaluating GH–IGF-I and ACTH–adrenal axes in patients with pituitary disorders. The aim of this study was to determine whether the response of catecholamine secretion to hypoglycemia is disrupted in patients with pituitary adenoma. Methods: The study population comprised 23 patients with pituitary adenoma (non-functioning adenoma or prolactinoma). An insulin tolerance test was performed and serum catecholamines as well as plasma GH and serum cortisol were measured. Results: The study patients showed diminished response of plasma epinephrine to insulin-induced hypoglycemia. With the cutoff level of peak epinephrine for defining severe impairment set at 400 pg/ml, more patients with secondary adrenal insufficiency showed severe impairment of the epinephrine response than did those without it. Peak epinephrine levels to insulin-induced hypoglycemia were significantly correlated with peak cortisol levels. In patients with secondary hypothyroidism, secondary hypogonadism, GH deficiency, or diabetes insipidus, the prevalence of severe impairment of the epinephrine response was similar to that in patients without these deficiencies. Conclusions: Impaired epinephrine secretion in response to insulin-induced hypoglycemia was frequently observed in patients with pituitary adenoma. This disorder was especially severe in patients with secondary adrenal insufficiency.

scholarly journals Glycometabolic Alterations in Secondary Adrenal Insufficiency: Does Replacement Therapy Play a Role?

2018 ◽  
Vol 9 ◽  
Author(s):  
Chiara Graziadio ◽  
Valeria Hasenmajer ◽  
Mary A. Venneri ◽  
Daniele Gianfrilli ◽  
Andrea M. Isidori ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Secondary Adrenal Insufficiency

scholarly journals Mifepristone Accelerates HPA Axis Recovery in Secondary Adrenal Insufficiency

2016 ◽  
Vol 2016 ◽  
pp. 1-4 ◽  
Author(s):  
Pejman Cohan
Keyword(s):  
Adrenal Insufficiency ◽  
Hpa Axis ◽  
Adrenal Adenoma ◽  
Serum Cortisol ◽  
Pharmacological Therapy ◽  
Secondary Adrenal Insufficiency ◽  
Unilateral Adrenalectomy ◽  
Undetectable Serum ◽  
Biochemical Testing ◽  
Acth Secreting

Context. Transient secondary adrenal insufficiency (SAI) is an expected complication following successful adenomectomy of ACTH-secreting pituitary adenomas or unilateral adrenalectomy for cortisol-secreting adrenal adenomas. To date, no pharmacological therapy has been shown to hasten recovery of the hypothalamic-pituitary-adrenal (HPA) axis in this clinical scenario.Case Description. A 33-year-old woman underwent uncomplicated unilateral adrenalectomy for a 3.7 cm cortisol-secreting adrenal adenoma. Postoperatively, she developed SAI and was placed on hydrocortisone 15 mg/day, given in divided doses. In the ensuing six years, the patient’s HPA axis failed to recover and she remained corticosteroid-dependent. Quarterly biochemical testing (after withholding hydrocortisone for 18 hours) consistently yielded undetectable serum cortisol and subnormal plasma ACTH levels. While she was on hydrocortisone 15 mg/day, mifepristone was initiated and gradually titrated to a maintenance dose of 600 mg/day after 5 months. Rapid recovery of the HPA axis was subsequently noted with ACTH rising into the supranormal range at 4 months followed by a subsequent rise in cortisol levels into the normal range. After 6 months, the dose of hydrocortisone and mifepristone was lowered and both were ultimately stopped after 8 months. The HPA axis remains normal after an additional 16 months of follow-up.Conclusion. Mifepristone successfully restored the HPA axis in a woman with prolonged secondary adrenal insufficiency (SAI) after adrenalectomy for Cushing’s syndrome (CS).

scholarly journals Diagnosis and treatment of adrenal insufficiency including adrenal crisis: a Japan Endocrine Society clinical practice guideline [Opinion]

2016 ◽  
Vol 63 (9) ◽  
pp. 765-784 ◽  
Author(s):  
Toshihiko Yanase ◽  
Toshihiro Tajima ◽  
Takuyuki Katabami ◽  
Yasumasa Iwasaki ◽  
Yusuke Tanahashi ◽  
...  
Keyword(s):  
Clinical Practice ◽  
Adrenal Insufficiency ◽  
Clinical Practice Guideline ◽  
Practice Guideline ◽  
Diagnosis And Treatment ◽  
Adrenal Crisis ◽  
Endocrine Society

scholarly journals MON-174 Circadian Misalignment of the 24-H Profiles of Melatonin and Cortisol in Adrenal Insufficiency

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Monika Darji ◽  
Silvana Pannain ◽  
Susan Sam ◽  
Eve Van Cauter ◽  
Erin C Hanlon
Keyword(s):  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Dose Range ◽  
Serum Cortisol ◽  
Peripheral Oscillators ◽  
Metabolic Outcomes ◽  
Peripheral Clocks ◽  
Low Levels ◽  
Cycle Dependent ◽  
Cortisol Release

Abstract Patients with adrenal insufficiency (AI), in whom cortisol release is absent, need to be on lifelong replacement therapy. Depending on the modality of glucocorticoid replacement, the resulting 24-h profile of circulating cortisol levels maybe dampened, enhanced, abnormally timed or inconsistent. The 24-h cortisol profile is a major internal synchronizing signal between central and peripheral circadian clocks. Misalignment between central and peripheral clocks has a host of adverse effects, particularly on metabolism and cardiovascular function. Melatonin, normally secreted by the pineal gland exclusively at night and considered a robust marker of central circadian timing, also plays a role as an internal synchronizing signal. Conditions like AI, where the 24-h profile of glucocorticoid levels deviates from normality, could produce misalignment between central and peripheral oscillators. We examined whether AI patients are at higher risk of disturbances of the circadian system. Participants were 13 AI patients (11 females, 2 men; mean age 45.8 yrs old; mean BMI 25.5) and 13 controls (11 females, 2 males; mean age 48.5 yrs old, mean BMI 26.4) matched for age, sex, and BMI. 10 of the AI patients were on hydrocortisone treatment (total dose range: 20 to 40mg/day, number of doses: 1-5 doses/day) and 3 of the AI patients were on prednisone treatment. Cortisol and melatonin were measured over a 24-h period every 30-60 minutes in all patients and controls. The 24-h profile of cortisol was quite variable across patients, dependent on replacement therapy. Those on prednisone had very little detectable cortisol with small peaks that occurred around dosing. Those on hydrocortisone, had multiple peaks across the 24-h cycle dependent on medication regime and dosing. As expected, control subjects had a quiescent period of cortisol release from early evening to mid-sleep (18:00 to 02:00) and a mid-sleep rise in serum cortisol that peaks in the morning and subsequently dissipates across the day. In contrast, AI patients have low levels of cortisol across the entire sleep period, with a sharp morning rise, delayed compared to controls. Unexpectedly, we observed a marked difference in the melatonin profile in AI subjects compared to controls. Indeed, a significant daytime phase of elevated melatonin levels was detected in 7 of the 13 AI patients. The nocturnal elevation in the patients was similar to that observed in controls albeit advanced. In conclusion, the abnormalities of the circadian profile of glucocorticoid levels in AI are associated with an abnormal 24-hr profile of melatonin release, a marker of central circadian function, suggesting that the disruption of the glucocorticoid rhythm may affect central circadian function. It is possible that this circadian dysfunction contributes to the well-known adverse cardio-metabolic outcomes in AI.

scholarly journals Glucocorticoid Replacement Affects Serum Adiponectin Levels and HDL-C in Patients With Secondary Adrenal Insufficiency

2019 ◽  
Vol 104 (12) ◽  
pp. 5814-5822
Author(s):  
Reiko Hayashi ◽  
Daisuke Tamada ◽  
Masahiko Murata ◽  
Tetsuhiro Kitamura ◽  
Kosuke Mukai ◽  
...  
Keyword(s):  
Lipid Profile ◽  
Adrenal Insufficiency ◽  
Replacement Therapy ◽  
Serum Levels ◽  
Adrenal Function ◽  
Serum Adiponectin ◽  
Secondary Adrenal Insufficiency ◽  
Glucocorticoid Replacement Therapy ◽  
Cortisol Levels ◽  
The Relationship

Abstract Context Low serum adiponectin and high-density lipoprotein–cholesterol (HDL-C) levels are risk factors for cardiovascular disease. Patients with primary adrenal insufficiency are at higher risk of cardiovascular complications compared with healthy subjects. However, there is no information on the relationship between adiponectin and glucocorticoid replacement therapy in patients with secondary adrenal insufficiency (SAI). Objective To determine the effects of intrinsic adrenal function and glucocorticoid replacement therapy on serum adiponectin levels and lipid profile in patients with SAI. Design Part 1: a cross-sectional study. Part 2: a randomized, double-blind, crossover study. Setting Osaka University Hospital, Osaka, Japan. Patients Part 1: 58 patients diagnosed with nonfunctioning pituitary adenoma who underwent insulin tolerance test (ITT) for assessment of adrenal function. Part 2: 12 SAI patients randomly received hydrocortisone replacement therapy at a dose of 10, 20, or 30 mg/d for 4 weeks per term for three terms. Outcome Measurements Part 1: we analyzed the relationship between serum cortisol levels during ITT and serum adiponectin levels and the lipid profile. Part 2: serum adiponectin levels and lipid profile were measured every 4 weeks. Results Serum levels of adiponectin and HDL-C correlated significantly with peak cortisol levels after ITT. Serum adiponectin and HDL-C levels were significantly lower in patients with SAI than non-SAI. Serum levels of adiponectin and HDL-C increased in a hydrocortisone dose-dependent manner. Conclusions Glucocorticoid replacement therapy increased serum levels of adiponectin, an adipose-derived anti-atherogenic factor, and HDL-C in patients with SAI.

scholarly journals Day 5 Morning Serum Cortisol Predicts Hypothalamic-Pituitary-Adrenal Function after Transsphenoidal Surgery for Pituitary Tumors

2009 ◽  
Vol 55 (5) ◽  
pp. 972-977 ◽  
Author(s):  
Channa N Jayasena ◽  
Kunal A Gadhvi ◽  
Bhavini Gohel ◽  
Niamh M Martin ◽  
Nigel Mendoza ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Transsphenoidal Surgery ◽  
Pituitary Tumors ◽  
Serum Cortisol ◽  
Tolerance Test ◽  
Cortisol Concentration ◽  
Correct Identification ◽  
Secondary Adrenal Insufficiency ◽  
Hypothalamic Pituitary Adrenal ◽  
Hpa Function

Abstract Background: Adrenal insufficiency is a complication of transsphenoidal surgery (TSS) for pituitary adenoma, and correct identification of patients requiring glucocorticoid replacement is important. Controversy exists over which early postoperative 9 AM cortisol concentration reliably predicts hypothalamic-pituitary-adrenal (HPA) axis reserve, as defined by the insulin tolerance test (ITT). Methods: Data were reviewed for 36 patients undergoing TSS followed by day 5 postoperative 9 AM cortisol measurement and ITT 6 weeks postsurgery. All patients received postoperative glucocorticoid replacement, which was discontinued if the 9 AM serum cortisol was >300 nmol/L. Results: Of 23 patients who failed the ITT (peak cortisol <500 nmol/L), 20 also had a day 5, 9 AM serum cortisol <300 nmol/L. Nine of 13 patients who passed the ITT had a day 5, 9 AM cortisol >300 nmol/L. The cutoff cortisol concentration of 300 nmol/L had 86.9% (66.4%–97.2%) diagnostic sensitivity, 69.2% (38.6%–90.9%) diagnostic specificity, and 83.3% (61.8%–94.5%) positive predictive value (PPV) for detecting secondary adrenal insufficiency. Increasing the cutoff to 392 nmol/L resulted in 100% (85.2%–100%) sensitivity, 46.1% (19.2%–74.9%) specificity, and 76.6% (57.3%–89.4%) PPV. Decreasing the cutoff to 111 nmol/L resulted in 100% (75.3%–100%) specificity and 100% (67.9%–100%) PPV, although sensitivity was 47.8% (26.8%–69.4%). Conclusions: A day 5 post-TSS 9 AM serum cortisol <111 nmol/L reliably detects secondary adrenal insufficiency, and concentrations >392 nmol/L support intact HPA function. Because concentrations of 111–392 nmol/L are poorly predictive of HPA function, glucocorticoid replacement should continue in such cases until definitive testing is performed using an ITT.

scholarly journals Severe Symptomatic SIADH as a Sign of Unknow Hypopituitarism: A Case Report

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A609-A610
Author(s):  
Juliana Marques-Sá ◽  
Catarina Silva Araújo ◽  
Maria Joana Santos
Keyword(s):  
Adrenal Insufficiency ◽  
Rare Condition ◽  
Urine Osmolality ◽  
Serum Cortisol ◽  
Empty Sella ◽  
Secondary Adrenal Insufficiency ◽  
Severe Hyponatremia ◽  
Long Time ◽  
Remarkable Recovery ◽  
High Level

Abstract Background: SIADH due to secondary adrenal insufficiency is a rare condition that can be life-threatening. Treatment with glucocorticoids is highly effective, but, as symptomatology of hypopituitarism can be mild and unspecific, a high level of clinical suspicion is necessary. Clinical Case: A 64-year-old postmenopausal woman, with a previously diagnosed and treated hypothyroidism and depressive syndrome, presented at the emergency room with nausea, vomits, asthenia and recurrent syncopes over the past three weeks and weight loss in the last months. One week before, she had been admitted at other hospital due to the same complaints and a serum Na+ of 112mmol/L (N 135-145 mmol/L) was detected. One year earlier, she had reported the same symptomology and hyponatremia had also been found, but no etiologic study was performed. At admission, she was conscient, hydrated, pale, hemodynamically stable, with unremarkable cardiopulmonary auscultation. A severe hyponatremia was found (Na+ 111mmol/L), with low serum osmolarity (241mOsm/Kg, N 280-301mOsm/Kg), low urine osmolality (125mOsm/kg N 300-900 mOsm/Kg) and low urinary sodium (33mmol/24h, N 40-220mmol/24h). Treatment with saline fluids was initiated and the patient was admitted for etiological investigation, which showed a low morning serum cortisol (3.7 µg/dl)) with inappropriately low-normal ACTH level (12.2 pg/mL), low FSH (15.07 mUI/mL, N 23.0-116.3 mUI/mL) and LH (4.28 mUI/mL, N 15.9-54 mUI/mL), estradiol of 78.81 pmol/L (N <118.2 pmol/L), undetectable IGF-1 (<25 ng/mL, N 36-244 ng/mL) and PRL of 21.98 ng/mL (N 1.8-20.3 ng/mL). Under 50µg of levothyroxine, TSH was 2.5 µUI/mL (N 0.358-3.74 µUI/ml), and FT4 was 1.1 ng/dL (N 0.76-1.46 ng/dL). Anti-thyroglobulin and anti-TPO antibodies were negative. A pituitary MRI revealed an empty sella with arachnoidocele. Other differential diagnosis of SIADH were excluded. The patient was started on oral hydrocortisone 30 mg/day, with a remarkable recovery, with better mood, more energy and appetite, resolution of all symptoms and normalization of the natremia. Conclusion: Hypopituitarism due to an empty sella is a relative rare disorder, whose etiology may be difficult to prove. It usually develops insidiously, with unspecific symptoms, which often delays the diagnosis. In our patient, this severe hyponatremia likely developed over a long time, allowing adaptation to such low levels of Na+. Moreover, the presence of a previously diagnosed hypothyroidism raises the suspicion if this wasn’t the first manifestation of the pituitary disease and if treatment of levothyroxine did not worsen an undetected secondary adrenal insufficiency.

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