scholarly journals Rathke’s Cyst and Adrenal Insufficiency: A Rare Case of Hyponatremia

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A606-A606
Author(s):  
Ranjoy Sen ◽  
Kalaichelvi Geerthan ◽  
Ashutosh Kapoor
Keyword(s):  
Adrenal Insufficiency ◽  
Free Water ◽  
Urine Osmolality ◽  
Serum Testosterone ◽  
Serum Prolactin ◽  
Adrenal Crisis ◽  
Free T4 ◽  
Pituitary Fossa ◽  
Optic Chiasma ◽  
Cortisol Deficiency

Abstract Background: Hyponatremia is the most common electrolyte abnormality encountered in clinical practice, the diagnosis of which can be challenging. A holistic approach with appropriate investigations is imperative to its diagnosis and management. We report this peculiar case of a patient with hypopituitarism secondary to Rathke’s cyst resulting in secondary Adrenal Insufficiency, thus causing Hyponatremia. Case Details: A 32 year male was admitted to hospital with an intractable headache and deterioration in his general wellbeing. His admission parameters revealed a GCS of 15 with normal observations. He had no evidence of meningism and examination of all other systems was unremarkable. He was not on any regular medications and there was no history of trauma. Bloods revealed a Sodium of 122mmol/l, the rest being normal. Investigations including a CT brain, CXR, paired serum & urine osmolality, urinary sodium, Thyroid functions and a 9am cortisol were conducted. Radiological imaging was unremarkable. Subsequently, he was fluid restricted due to a euvolemic fluid status. Serum osmolality was 246 mmol/kg (275-295 mmol/kg), Urine osmolality 847 mmol/kg, urine sodium 85 mmol/l and a 9 am serum cortisol of 29 nmol/L, in keeping with Adrenal Insufficiency. A further decline in his Sodium to 116 mmol/L resulted in Hyponatremic Encephalopathy. In view of impending Adrenal crisis, IV hydrocortisone was commenced in conjunction with hypertonic Saline. This was followed by strict monitoring with cautious correction. An anterior Pituitary profile, serum testosterone and Prolactin were requested. Serum Testosterone levels were 0.4nmol/L (10.0-36nmol/L), FSH- 2.5 IU/L (1.0-11.0 IU/L) and LH- 1.9 IU/L (1.5-9.3 IU/L). Serum prolactin was 85mU/L (45-375 mU/L), TSH- 0.59 mU/L (0.30-6.00 mU/L), Free T4- 13.0 pmol/L (10.4-24.5 pmol/L), IGF1-135 ug/L (60-197 ug/L). This was suggestive of partial hypopituitarism. An MRI Pituitary revealed appearances in keeping with a Rathke’s cyst occupying the pituitary fossa without compromise of the Optic Chiasma. Once stable, he was safely discharged with follow-up appointments planned with the Endocrine and Neurosurgical teams. Discussion: Rathke cleft cysts are non-neoplastic cysts arising from the embryological remnants of Rathke’s pouch in the pituitary gland. Hormonal and visual manifestations can occur if these cysts enlarge and interfere with the Pituitary production and optic chiasma. A proposed mechanism causing Hyponatremia in the context of Cortisol deficiency is increased hypothalamic secretion of Corticotropin releasing hormone (CRH), a Vasopressin secretagogue. Cortisol feeds back negatively on CRH, which is removed with adrenal insufficiency. Hyponatremia is thus often seen in patients with adrenal insufficiency, caused by an inappropriate increase in vasopressin due to cortisol deficiency and inability to excrete free water.

scholarly journals Adrenal Insufficiency Masquerading as Primary Hypothyroidism Following Immune Checkpoint Inhibitors Treatment

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A110-A111
Author(s):  
Michael Salim ◽  
Wafa Dawahir ◽  
Janice L Gilden ◽  
Andriy Havrylyan
Keyword(s):  
Adrenal Insufficiency ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Cytotoxic T Lymphocyte ◽  
Checkpoint Inhibitors ◽  
Primary Hypothyroidism ◽  
Adrenal Crisis ◽  
Thyroid Peroxidase ◽  
Endocrine Disorders ◽  
Free T4

Abstract Background: Immune checkpoint inhibitors (ICIs) are novel immunotherapy agents that have been used to treat multiple advanced cancer. Even though they confer potential clinical advantages by regulating immune reactions, they have been linked with serious immune-mediated adverse events. Here we present a case of a patient who was treated with ICIs, Nivolumab (programmed death-1 inhibitor) and Ipilimumab (cytotoxic T lymphocyte antigen-4 inhibitor), and subsequently developed two concurrent immune-related endocrine disorders. Clinical Case: An 83-year-old man with advanced renal cell carcinoma presented with generalized weakness. He had finished four cycles of immunotherapy with Nivolumab and Ipilimumab, and Ipilimumab was discontinued afterward. Two days after the fifth cycle of immunotherapy with Nivolumab, he developed worsening fatigue, nausea, and anorexia. He appeared mildly volume depleted with borderline hypotensive (104/63 mmHg). The rest of the physical exam was unremarkable. Initial tests showed elevated levels of TSH (13.15 uIU/mL, ref 0.45–5.33 uIU/L), reduced levels of free T4 (<0.25 ng/dL, ref 0.58–1.64 ng/dL), free T3 (1.72 pg/mL, ref 2.5–3.9 pg/mL), negative thyroglobulin antibody, and elevated levels of thyroid peroxidase antibody (429 IU/mL, ref <9 IU/mL), thus suggesting primary hypothyroidism. Serum levels of sodium and potassium were unremarkable (136 meQ/L, ref 136–145 mEq/L; 3.6 meQ/L, ref 3.5–5.1 meQ/L respectively). His baseline TSH was normal three months prior to arrival (1.31 uIU/mL) and suppressed one month prior to arrival (0.01 uIU/mL). Immune-related thyroiditis with immune checkpoint inhibitors was suspected. He was given levothyroxine and observed in the hospital. After two days of hospitalization, weakness had slightly improved. However, he still had persistent nausea. He also developed low blood pressure (90/47 mmHg) and mild hyponatremia (133 mEq/L) with a normal potassium level. Further investigation showed low cortisol (1.0 ug/dL, ref 5.0–21.0), low ACTH (13 pg/mL, ref 6–50 pg/mL), cortisol level at 30 and 60 minutes post-cosyntropin stimulation test of 10.8 ug/dL (ref 13.0–30.0 ug/dL) and 14.8 ug/dL (ref 14.0–36.0 ug/dL) respectively, and negative adrenal antibodies, suggesting of secondary adrenal insufficiency due to hypophysitis. The patient was started on hydrocortisone, and his symptoms improved afterward. Conclusion: This case report highlights the common pitfall of managing immune-related endocrine disorders of ICIs. Adrenal insufficiency may present with a broad range of nonspecific symptoms, which could be attributed to hypothyroidism, underlying illness, or medications. Although a rare adverse effect, it is prudent to recognize adrenal insufficiency superimposed on primary hypothyroidism. Introducing thyroxine before replacing glucocorticoids can lead to an adrenal crisis.

scholarly journals Adrenal Insufficiency: Hidden Mimicker With Other Autoimmune Disease Potentials

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A111-A112
Author(s):  
Rabin Banjade ◽  
Binayak Upadhyay ◽  
Bidhisa Kharel
Keyword(s):  
Autoimmune Diseases ◽  
Adrenal Insufficiency ◽  
Epigastric Pain ◽  
Tissue Transglutaminase ◽  
Adrenal Crisis ◽  
Acth Stimulation ◽  
Free T4 ◽  
High Potassium ◽  
Tissue Transglutaminase Antibodies ◽  
Empirical Antibiotics

Abstract Background: Adrenal insufficiency has various nonspecific symptoms, which are often overlooked until the patient presents with a life-threatening adrenal crisis. Our patient presented during the COVID19 pandemic, which further blurred our diagnostic sense. Clinical Case: A 26-year-old female presented with sudden intractable non-bloody non-bilious vomiting occurring every 30 minutes along with sharp epigastric pain radiating to her back, dizziness, and extreme fatigue for the last 2 days. She had similar but milder episodes in the past 2–3 years as well and endorsed unintentional weight loss for the same duration. She had been extensively investigated previously but was misdiagnosed as gastroparesis or anxiety and was prescribed medications for the same (pantoprazole, sucralfate, and Lexapro). On presentation this time, she was hypotensive and tachycardic but partially responsive to IV fluids. Her BMI was 15.31 and the abdominal exam was benign. Her basic labs showed Na 125, K 4.9, Calcium 10.5, Cr 1, WBCs 9K, lipase 8, normal LFTs, TSH 6.96, Free T4 1.18. Infectious workup was done and the patient was started on empirical antibiotics. Negative infectious workup, hypotension partially responsive to IV fluid, along with hyponatremia and borderline high potassium level prompted us to check Cortisol. We found Cortisol of 1.3(very low for the degree of her illness). ACTH stimulation test with 250mcg IV cosyntropin showed cortisol of 1.3 at 30 minutes and 1.1 at 60 minutes confirming the diagnosis of adrenal insufficiency. Further workup revealed a positive 21 hydroxylase antibody and ACTH level of 322 (high due to lack of negative feedback to the pituitary). She was comprehensively tested for other autoimmune diseases which showed positive Endomysial IgA and Tissue Transglutaminase antibodies indicating asymptomatic celiac disease. She improved drastically after starting hydrocortisone. TSH was repeated in 3 months which was normal. Conclusion: The onset of chronic adrenal insufficiency is very gradual with vague presentation and it may go undetected unless illness or other stress precipitates acute crisis as in our patient. Since autoimmune adrenalitis is the most common cause of primary adrenal insufficiency (Addison’s disease), patients with a confirmed diagnosis should also undergo workup for other autoimmune diseases.

scholarly journals Frequently Asked Questions in Patients With Adrenal Insufficiency in the Time of COVID-19

2021 ◽  
Vol 12 ◽  
Author(s):  
Chiara Sabbadin ◽  
Corrado Betterle ◽  
Carla Scaroni ◽  
Filippo Ceccato
Keyword(s):  
Adrenal Insufficiency ◽  
Short Review ◽  
Acute Illness ◽  
Self Management ◽  
Vaccine Hesitancy ◽  
Adrenal Crisis ◽  
Risk Of Infection ◽  
Telemedicine Consultation ◽  
Life Threatening ◽  
Cortisol Deficiency

Adrenal insufficiency (AI) is a life-threatening disorder, with increased morbidity and mortality, especially in case of an acute illness that can increase the requirement of cortisol. A novel infectious disease, termed Coronavirus Disease 2019 (COVID-19), appeared in 2020. Therefore, AI patients are experiencing a novel challenge: the risk of infection. In our experience, a prompt contact to the Endocrine center (with a telemedicine consultation) and a full awareness of diseases (cortisol deficiency, COVID-19 and the self-management of an adrenal crisis) are important to motivate patients. Vaccine is an effective treatment to prevent hospitalization and aggressive course of COVID-19. Some patients manifest challenges due to inequitable access and vaccine hesitancy, resulting in a delay in the acceptance of vaccines despite the availability of vaccination services. Therefore, an effort of all physicians must be conducted in order to advise patients with AI. In this short review, we try to answer some frequently asked questions regarding the management of patients with AI.

Adrenal crisis in patients with primary and secondary adrenal insufficiency

2006 ◽  
Vol 114 (S 1) ◽  
Author(s):  
S Hahner ◽  
M Löffler ◽  
D Weismann ◽  
AC Koschker ◽  
M Fassnacht ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Crisis ◽  
Secondary Adrenal Insufficiency

Nonosmotic release of vasopressin and renal aquaporins in impaired urinary dilution in hypothyroidism

2005 ◽  
Vol 289 (4) ◽  
pp. F672-F678 ◽  
Author(s):  
Yung-Chang Chen ◽  
Melissa A. Cadnapaphornchai ◽  
Jianhui Yang ◽  
Sandra N. Summer ◽  
Sandor Falk ◽  
...  
Keyword(s):  
Protein Expression ◽  
Renal Cortex ◽  
Free Water ◽  
Urine Osmolality ◽  
Protein Abundance ◽  
Oral Gavage ◽  
Water Excretion ◽  
Urinary Osmolality ◽  
Water Load ◽  
Fluid Delivery

The purpose of this study was to examine protein expression of renal aquaporins (AQP) and ion transporters in hypothyroid (HT) rats in response to an oral water load compared with controls (CTL) and HT rats replaced with l-thyroxine (HT+T). Hypothyroidism was induced by aminotriazole administration for 10 wk. Body weight, water intake, urine output, solute and urea excretion, and serum and urine osmolality were comparable among the three groups at the conclusion of the 10-wk treatment period. One hour after oral gavage of water (50 ml/kg body wt), HT rats demonstrated significantly less water excretion, higher minimal urinary osmolality, and decreased serum osmolality compared with CTL and HT+T rats. Despite the hyposmolality, plasma vasopressin concentration was elevated in HT rats. These findings in HT rats were associated with an increase in protein abundance of renal cortex AQP1 and inner medulla AQP2. AQP3, AQP4, and the Na-K-2Cl cotransporter were also increased. Moreover, 1 h following the oral water load, HT rats demonstrated a significant increase in the membrane-to-vesicle fraction of AQP2 by Western blot analysis. The defect in urinary dilution in HT rats was reversed by the V2 vasopressin antagonist OPC-31260. In conclusion, impaired urinary dilution in HT rats is primarily compatible with the nonosmotic release of vasopressin and increased protein expression of renal AQP2. The impairment of maximal solute-free water excretion in HT rats, however, appears also to involve diminished distal fluid delivery.

scholarly journals Epidemiology of adrenal crisis in chronic adrenal insufficiency: the need for new prevention strategies

2010 ◽  
Vol 162 (3) ◽  
pp. 597-602 ◽  
Author(s):  
Stefanie Hahner ◽  
Melanie Loeffler ◽  
Benjamin Bleicken ◽  
Christiane Drechsler ◽  
Danijela Milovanovic ◽  
...  
Keyword(s):  
Risk Factors ◽  
Adrenal Insufficiency ◽  
Educational Status ◽  
Cross Sectional Study ◽  
Sudden Onset ◽  
Stressful Events ◽  
Adrenal Crisis ◽  
Cross Sectional ◽  
Crisis Prevention ◽  
Dhea Treatment

ObjectiveAdrenal crisis (AC) is a life-threatening complication of adrenal insufficiency (AI). Here, we evaluated frequency, causes and risk factors of AC in patients with chronic AI.MethodsIn a cross-sectional study, 883 patients with AI were contacted by mail. Five-hundred and twenty-six patients agreed to participate and received a disease-specific questionnaire.ResultsFour-hundred and forty-four datasets were available for analysis (primary AI (PAI), n=254; secondary AI (SAI), n=190). Forty-two percent (PAI 47% and SAI 35%) reported at least one crisis. Three hundred and eighty-four AC in 6092 patient years were documented (frequency of 6.3 crises/100 patient years). Precipitating causes were mainly gastrointestinal infection and fever (45%) but also other stressful events (e.g. major pain, surgery, psychic distress, heat and pregnancy). Sudden onset of apparently unexplained AC was also reported (PAI 6.6% and SAI 12.7%). Patients with PAI reported more frequent emergency glucocorticoid administration (42.5 vs 28.4%, P=0.003). Crisis incidence was not influenced by educational status, body mass index, glucocorticoid dose, DHEA treatment, age at diagnosis, hypogonadism, hypothyroidism or GH deficiency. In PAI, patients with concomitant non-endocrine disease were at higher risk of crisis (odds ratio (OR)=2.02, 95% confidence interval (CI) 1.05–3.89, P=0.036). In SAI, female sex (OR=2.18, 95% CI 1.06–4.5, P=0.035) and diabetes insipidus (OR=2.71, 95% CI 1.22–5.99, P=0.014) were associated with higher crisis incidence.ConclusionAC occurs in a substantial proportion of patients with chronic AI, mainly triggered by infectious disease. Only a limited number of risk factors suitable for targeting prevention of AC were identified. These findings indicate the need for new concepts of crisis prevention in patients with AI.

Effect of sodium fluoride on concentrating and diluting ability in the rat

1977 ◽  
Vol 232 (4) ◽  
pp. F335-F340 ◽  
Author(s):  
J. D. Wallin ◽  
R. A. Kaplan
Keyword(s):  
Cyclic Amp ◽  
Urine Volume ◽  
Free Water ◽  
Urine Osmolality ◽  
Inhibitory Effect ◽  
Sprague Dawley ◽  
Free Water Clearance ◽  
Sprague Dawley Rats ◽  
Direct Inhibitory Effect ◽  
Hereditary Hypothalamic Diabetes Insipidus

Mechanisms for the concentrating defect produced by fluoride were examined in the rat. Free-water clearance at all levels of delivery was normal after 5 days of chronic fluoride administration in the hereditary hypothalamic diabetes insipidus rat. In the Sprague-Dawley rats, during moderate fluoride administration (120 micronmol/kg per day), urine osmolality and cyclic AMP excretion decreased and urine volume increased, but after exogenous vasopressin, volume decreased and osmolality and cyclic AMP increased appropriately. During larger daily doses of fluoride (240 micronmol/kg per day) urinary osmolality and cyclic AMP decreased and volume increased, which was similar to the changes seen during lower fluoride dosages, but these parameters did not change after exogenous vasopressin. These data suggest that ascending limb chloride reabsorption is unaltered by fluoride administration; in the presence of sufficient fluoride, collecting tubular cells apparently do not generate cyclic AMP or increase permeability appropriately in response to vasopressin. The postulated defect is felt to be due to either a decrease in ATP availability or to a direct inhibitory effect of fluoride on the vasopressin-dependent cyclic AMP generating system.

scholarly journals EXTENSIVE EXPERTISE IN ENDOCRINOLOGY: Adrenal crisis

2015 ◽  
Vol 172 (3) ◽  
pp. R115-R124 ◽  
Author(s):  
Bruno Allolio
Keyword(s):  
Patient Education ◽  
Adrenal Insufficiency ◽  
Well Being ◽  
Stressful Events ◽  
Major Surgery ◽  
Adrenal Crisis ◽  
Self Administration ◽  
Necrosis Factor Alpha ◽  
Hydrocortisone Administration ◽  
Glucocorticoid Deficiency

Adrenal crisis is a life-threatening emergency contributing to the excess mortality of patients with adrenal insufficiency. Studies in patients on chronic replacement therapy for adrenal insufficiency have revealed an incidence of 5–10 adrenal crises/100 patient years and suggested a mortality rate from adrenal crisis of 0.5/100 patient years. Patients with adrenal crisis typically present with profoundly impaired well-being, hypotension, nausea and vomiting, and fever responding well to parenteral hydrocortisone administration. Infections are the major precipitating causes of adrenal crisis. Lack of increased cortisol concentrations during infection enhances pro-inflammatory cytokine release and sensitivity to the toxic effects of these cytokines (e.g. tumour necrosis factor alpha). Furthermore, pro-inflammatory cytokines may impair glucocorticoid receptor function aggravating glucocorticoid deficiency. Treatment of adrenal crisis is simple and highly effective consisting of i.v. hydrocortisone (initial bolus of 100 mg followed by 200 mg over 24 h as continuous infusion) and 0.9% saline (1000 ml within the first hour). Prevention of adrenal crisis requires appropriate hydrocortisone dose adjustments to stressful medical procedures (e.g. major surgery) and other stressful events (e.g. infection). Patient education is a key for such dose adjustments but current education concepts are not sufficiently effective. Thus, improved education strategies are needed. Every patient should carry an emergency card and should be provided with an emergency kit for parenteral hydrocortisone self-administration. A hydrocortisone pen would hold a great potential to lower the current barriers to hydrocortisone self-injection. Improved patient education and measures to facilitate parenteral hydrocortisone self-administration in impending crisis are expected to significantly reduce morbidity and mortality from adrenal crisis.

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