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.

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 Severe hyponatremia due to hypopituitarism with adrenal insufficiency: report on 28 cases

2003 ◽  
pp. 609-617 ◽  
Author(s):  
S Diederich ◽  
NF Franzen ◽  
V Bahr ◽  
W Oelkers
Keyword(s):  
Adrenal Insufficiency ◽  
Antidiuretic Hormone ◽  
Hospital Admissions ◽  
Clinical Signs ◽  
University Hospital ◽  
Pituitary Hormone ◽  
Stressful Situation ◽  
Secondary Adrenal Insufficiency ◽  
Severe Hyponatremia ◽  
Underlying Disorder

OBJECTIVE: Severe hyponatremia due to hypopituitarism and adrenal insufficiency can be life-threatening, and treatment with glucocorticoids is very effective once the diagnosis of the underlying disorder has been made. In our experience, the diagnosis of hypopituitarism in hyponatremic patients is often overlooked. METHODS: In a retrospective study we screened the files of 185 patients with severe hyponatremia (<130 mmol/l) that had been seen in one endocrinological unit of a university hospital between 1981 and 2001 in order to describe the clinical spectrum of patients with hyponatremia and hypopituitarism including secondary adrenal insufficiency. RESULTS: In 139 cases it was possible to clearly ascribe the patients to the pathophysiological groups of (i) primary sodium deficiency, (ii) edematous disorders, and (iii) normovolemic disorders including the "syndrome of inappropriate secretion of antidiuretic hormone" (SIADH). Twenty-eight patients with severe "normovolemic hyponatremia" (serum sodium: 116+/-7 mmol/l, mean+/-s.d.) had hypopituitarism and secondary adrenal insufficiency as shown by basal cortisol measurements and dynamic tests of adrenal function. In 25 cases of this group hypopituitarism (mostly due to empty sella, Sheehan's syndrome and pituitary tumors) had not been recognized previously, and in 12 cases recurrent hyponatremia during previous hospital admissions (up to four times) could be documented. The mean age of these patients (21 women, seven men) was 68 Years. The most frequently occurring clinical signs were missing or scanty pubic and axillary hair, pale and doughy skin, and small testicles in the men. Frequent symptoms like nausea and vomiting, confusion, disorientation, somnolence or coma were similar to those in 91 patients with SIADH. Basal serum cortisol levels in the acutely ill state ranged from 20 to 439 nmol/l (mean+/-s.d.: 157+/-123), while in 30 other severely hyponatremic patients it ranged from 274 to 1732 nmol/l (732+/-351 nmol/l). In most patients with hyponatremic hypopituitarism, plasma antidiuretic hormone levels were inappropriately high, probably due to a failure of endogenous cortisol to suppress the hormone in a stressful situation. All patients recovered after low-dose hydrocortisone substitution. Most patients had other pituitary hormone deficiencies and were appropriately substituted subsequently. CONCLUSIONS: Hypopituitarism including secondary adrenal insufficiency seems to be a frequently overlooked cause of severe hyponatremia. A high level of suspicion is the best way to recognize the underlying disorder. Treatment with hydrocortisone is very effective.

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 SUN-276 Pembrolizumab-Induced Secondary Adrenal Insufficiency Presenting as Severe Hyponatremia in an 80-Year-Old Male

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Leslie Daphne R Kawaji ◽  
Mary Grace M Villanueva ◽  
Michael L Villa
Keyword(s):  
Adverse Events ◽  
Adrenal Insufficiency ◽  
Endocrine System ◽  
Stage Iv ◽  
Blood Chemistry ◽  
Oral Feeding ◽  
Low Grade ◽  
Thyroid Function Tests ◽  
Secondary Adrenal Insufficiency ◽  
Severe Hyponatremia

Abstract Background Pembrolizumab is an anti-programmed death 1 (PD-1) antibody designed to incite an immune response against malignant cells. By virtue of this mechanism of action, its use has given rise to immune-related adverse events including those affecting the endocrine system. Adrenal insufficiency can occur rarely with anti-PD-1 therapy, and symptoms are usually non-specific. Clinical Case An 80-year-old male, known case of non-small cell lung cancer stage IV presented with a 2-week history of progressive body weakness with anorexia, shortness of breath and low-grade fever. He had just received the 4th cycle of pembrolizumab prior to the onset of symptoms. Past medical history was significant for hypertension and type 2 diabetes mellitus which were both controlled, and pulmonary tuberculosis with completed treatment. On physical examination, he was drowsy but oriented. He was normotensive (110/70 mmHg) and tachypneic (28 cpm) with rales on both lung fields. Baseline capillary glucose level was 107 mg/dL. Chest radiograph showed hazy opacities in the right upper to middle region. Blood chemistry revealed severe hyponatremia (114 mmol/L, NV 135-145 mmol/L) and low serum osmolality (247 mOsm/kg, NV 280-300 mOsm/kg). Random (taken 1230H) ACTH and cortisol were &lt;5.00 pg/mL (NV &lt;46 pg/mL) and 2.00 μg/dL (NV 4.30-22.40 μg/dL), respectively. Such levels were judged to be low in the background of an acute illness. Thyroid function tests were normal – TSH 0.993 μIU/mL (NV 0.55-4.78 uIU/mL), FT3 3.890 pg/mL (2.30-4.20 pg/mL), FT4 1.450 ng/dL (0.89-1.76 ng/dL). Magnetic resonance imaging of the pituitary gland did not show abnormal parenchymal enhancement or enlargement. Pembrolizumab-induced secondary adrenal insufficiency was the most probable cause of the hyponatremia. He was started on IV hydrocortisone, as well as piperacillin-tazobactam for pneumonia. Oxygen support via nasal cannula was given. Feeding via nasogastric tube was decided to ensure nutrition and prevent aspiration. He was transferred to the intensive care unit for careful monitoring. Serum sodium level was corrected gradually, with marked clinical improvement thereafter. Within 48 hours, he was transferred to regular room and oral feeding commenced. Hydrocortisone was shifted to prednisone on discharge, with steroid tapering schedule and close follow-up with endocrinologist advised. Conclusion We presented a case of secondary adrenal insufficiency which likely resulted from hypophysitis induced by pembrolizumab. Hypophysitis following anti-PD1 treatment occurs in &lt;1% of patients on immunotherapy. In such cases, ACTH deficiency is usually isolated and pituitary imaging is frequently normal. Since more patients are being placed on immune-checkpoint inhibition, clinicians should be vigilant for these adverse events, particularly the endocrinopathies which may have non-specific symptoms and may be irreversible.

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 &gt;300 nmol/L. Results: Of 23 patients who failed the ITT (peak cortisol &lt;500 nmol/L), 20 also had a day 5, 9 AM serum cortisol &lt;300 nmol/L. Nine of 13 patients who passed the ITT had a day 5, 9 AM cortisol &gt;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 &lt;111 nmol/L reliably detects secondary adrenal insufficiency, and concentrations &gt;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 hyponatremia caused by secondary adrenal insufficiency in a patient with giant pituitary prolactinoma

2013 ◽  
Vol 2 (2) ◽  
pp. 184-189 ◽  
Author(s):  
Akimitsu Kobayashi ◽  
Yasushi Otsuka ◽  
Takeo Yoshizawa ◽  
Masuomi Tomita ◽  
Hideo Asada ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Secondary Adrenal Insufficiency ◽  
Severe Hyponatremia
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