Adrenal Insufficiency: Hidden Mimicker With Other Autoimmune Disease Potentials

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.

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Adrenal Insufficiency Masquerading as Primary Hypothyroidism Following Immune Checkpoint Inhibitors Treatment

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.222 ◽

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.

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Steroid-Induced Iatrogenic Adrenal Insufficiency in Children: A Literature Review

Endocrines ◽

10.3390/endocrines1020012 ◽

2020 ◽

Vol 1 (2) ◽

pp. 125-137

Author(s):

Shogo Akahoshi ◽

Yukihiro Hasegawa

Keyword(s):

Adrenal Insufficiency ◽

Serum Cortisol ◽

Early Morning ◽

Serum Cortisol Level ◽

Adrenal Crisis ◽

Acth Stimulation ◽

Morning Serum Cortisol ◽

High Doses ◽

Loss Of Appetite ◽

Cortisol Suppression

The present review focuses on steroid-induced adrenal insufficiency (SIAI) in children and discusses the latest findings by surveying recent studies. SIAI is a condition involving adrenocorticotropic hormone (ACTH) and cortisol suppression due to high doses or prolonged administration of glucocorticoids. While its chronic symptoms, such as fatigue and loss of appetite, are nonspecific, exposure to physical stressors, such as infection and surgery, increases the risk of adrenal crisis development accompanied by hypoglycemia, hypotension, or shock. The low-dose ACTH stimulation test is generally used for diagnosis, and the early morning serum cortisol level has also been shown to be useful in screening for the condition. Medical management includes gradually reducing the amount of steroid treatment, continuing administration of hydrocortisone corresponding to the physiological range, and increasing the dosage when physical stressors are present.

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Bilateral adrenal masses due to tuberculosis: how to diagnose without extra-adrenal tuberculosis

Endocrinology Diabetes and Metabolism Case Reports ◽

10.1530/edm-21-0093 ◽

2021 ◽

Vol 2021 ◽

Author(s):

Nam Quang Tran ◽

Chien Cong Phan ◽

Thao Thi Phuong Doan ◽

Thang Viet Tran

Keyword(s):

Adrenal Insufficiency ◽

Plasma Cortisol ◽

Histopathological Examination ◽

Epigastric Pain ◽

High Plasma ◽

Diagnostic Process ◽

Adrenal Crisis ◽

List Type ◽

Primary Adrenal Insufficiency ◽

Adrenal Masses

Summary Primary adrenal insufficiency is a rare disease and can masquerade as other conditions; therefore, it is sometimes incorrectly diagnosed. Herein, we reported the case of a 39-year-old Vietnamese male with primary adrenal insufficiency due to bilateral adrenal tuberculosis. The patient presented to the emergency room with acute adrenal crisis and a 3-day history of nausea, vomiting, epigastric pain, and diarrhoea with a background of 6 months of fatigue, weight loss, and anorexia. Abdominal CT revealed bilateral adrenal masses. Biochemically, unequivocal low morning plasma cortisol (<83 nmol/L) and high plasma adrenocorticotropic hormone levels were consistent with primary adrenal insufficiency. There was no evidence of malignancy or lymphoma. As the patient was from a tuberculosis-endemic area, extra-adrenal tuberculosis was excluded during the work up. A retroperitoneal laparoscopic left adrenalectomy was performed, and tuberculous adrenalitis was confirmed by the histopathological results. The patient was started on antituberculous therapy, in addition to glucocorticoid replacement. In conclusion, even without evidence of extra-adrenal tuberculosis, a diagnosis of bilateral adrenal tuberculosis is required. A histopathological examination has a significant role along with clinical judgement and hormonal workup in establishing a definitive diagnosis of adrenal tuberculosis without evidence of active extra-adrenal involvement. Learning points Primary adrenal insufficiency can be misdiagnosed as other mimicking diseases, such as gastrointestinal illness, leading to diagnostic pitfalls. Adrenal insufficiency can be confirmed with significantly low morning plasma cortisol levels of <83 nmol/L without a dynamic short cosyntropin stimulation test. Tuberculous adrenalitis is an uncommon treatable condition; however, it remains an important cause of primary adrenal insufficiency, especially in developing countries. In the absence of extra-adrenal involvement, adrenal biopsy plays a key role in the diagnostic process. Alternatively, adrenalectomy for histopathological purposes should be considered if CT scan-guided fine needle aspiration is infeasible in cases of small adrenal masses.

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

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.1235 ◽

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.

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Endocrinopathies Associated With High Dose Methadone

Journal of the Endocrine Society ◽

10.1210/jendso/bvab048.262 ◽

2021 ◽

Vol 5 (Supplement_1) ◽

pp. A130-A130

Author(s):

Charles C Farmer ◽

Monica Agarwal

Keyword(s):

Adrenal Insufficiency ◽

Chronic Back Pain ◽

Antibody Test ◽

Insulin Level ◽

Inhibitory Effect ◽

Adrenal Crisis ◽

High Dose ◽

Micronutrient Deficiencies ◽

Acth Stimulation ◽

Health Crisis

Abstract Introduction: The opioid epidemic is a public health crisis and clinicians should be aware of the many under-recognized endocrinopathies associated with opioids. Herein, we present a case that exemplifies the endocrine-related adverse effects of methadone therapy. Clinical Case: A 43-year-old Caucasian female with chronic back pain with opioid dependence, high dose methadone use (195 mg daily), and diabetes presented with refractory hypoglycemia. She was diagnosed with ketone prone diabetes eight months prior. She had since been weaned off insulin and her most recent HbA1c was 4.2%. During this time, she had an intentional weight loss of 60 pounds. On examination, she had bilateral lower extremity pitting edema with scaly plaques on the extremities. Laboratory tests showed C-peptide of 0.8 (0.9–7.1 ng/mL), insulin level of < 2 (3–25 mcIntUnits/mL), proinsulin of 4.6 (<18.8 pMol/L) with concurrent glucose of 48 mg/dl. She failed the ACTH stimulation test with 60 minute cortisol of 16.8 mcg/dL and was started on prednisone for adrenal insufficiency (AI). The pituitary and adrenal were normal on imaging. Her albumin was 1.5 (3.7–5.5 gm/dL) and she had vitamin and micronutrient deficiencies including copper, zinc, thiamine, selenium, and vitamin A. The insulin antibody test, paraneoplastic panel, celiac panel, A1 antitrypsin test, EGD, and colonoscopy were all non-revealing. A liver biopsy showed glycogenic hepatopathy. She improved clinically after prednisone initiation and treatment of malnutrition. The hypoglycemia improved but did not resolve as she refused to reduce methadone dose. Discussion: The proposed mechanism of opioid-induced AI is the inhibitory effect on the hypothalamic-pituitary-adrenal axis, similar to the effect on the gonadal axis which causes hypogonadism. The risk for hypoglycemia is increased in patients taking more than 40 mg of oral methadone per day, and although the mechanism remains unclear, it is independent of adrenal function. Our patient had adrenal insufficiency and hypoglycemia related to methadone, which was further complicated by malnutrition. The glycogenic hepatopathy is a benign reversible condition that is believed to be a consequence of fluctuation in glucose levels. Conclusion: Given the life-threatening nature of adrenal crisis and the overlap in symptomatology with opiate overdose, clinicians should be prompt in evaluating for endocrinopathies in patients on chronic high dose opiates, and patients should be appropriately counseled on the potential consequences of methadone use. References: 1.Flory, J. H., et al. (2016). Methadone use and the risk of hypoglycemia for inpatients with cancer pain. JPSM, 51(1), 79–87.2.Li, T. et al. (2020). Prevalence of Opioid-Induced Adrenal Insufficiency in Patients Taking Chronic Opioids. JCEM, 105(10), dgaa499.

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SUN-183 Adrenalitis Induced by Nivolumab

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.041 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Muhammad Atique Alam Khan ◽

Iqra Iqbal ◽

Puneet Dhillon ◽

Waqas Ullah

Keyword(s):

Adrenal Insufficiency ◽

Checkpoint Inhibitors ◽

Death Receptor ◽

Stimulation Test ◽

Adrenal Crisis ◽

High Dose ◽

Acth Stimulation ◽

Activated T Cells ◽

Programmed Death ◽

Cortisol Levels

Abstract Introduction: Tumor cells often express a programmed death-ligand 1 (PD-L1), which binds to the programmed death receptor-1 (PD-1) on activated T-cells to induce immune tolerance. Among the class of immune checkpoint inhibitors (ICI), Nivolumab is an anti-PD-1 antibody which blocks these tumor cell interactions. Although some endocrinopathies have been reported for other PD-1 inhibitors, the adverse event of adrenalitis with nivolumab has not been reported before. Clinical Case: A 65-year-old female presented to the hospital with complaints of nausea, vomiting, fatigue, and headache for five days. She was recently diagnosed with metastatic lung adenocarcinoma, complicated by cerebellar metastases, and the left cerebellar mass was resected. She was also started on Nivolumab. Her blood pressure was 98/65 mmHg on the presentation. Serum sodium was 122mEq/L (normal 135–145) and potassium was 5mEq/L (3.5–5). TSH, LH, and prolactin were all normal. Aldosterone was low: 23pmol/L (27.7–582.5) and renin was high: 11 ng/ml/h (0.167- 1.38). Morning cortisol levels were low: 2.2 ug/dl (5- 25) and concomitant ACTH was high: 78 pg/ml (7.2- 63.3). Upon standard high dose cosyntropin stimulation test, basal cortisol was 2.0 ug/dl (5- 25). Cortisol level 30 minutes post cosyntropin was 7.1 ug/dl, while Cortisol 60 minutes post cosyntropin was 12.2 ug/dl (normal >18 -20 ug/dl). Considering the low cortisol levels with high ACTH, and an inadequate rise in cortisol after the ACTH stimulation test, adrenal insufficiency was suspected as a result of adrenalitis due to Nivolumab. Hyponatremia along with low aldosterone and high renin levels also reinforced this clinical diagnosis. A computerized tomographic scan of the chest abdomen and pelvis only showed calcified uterine fibroids. She was initially resuscitated with intravenous fluids. Hydrocortisone 100 mg every 8 hours was started and then gradually tapered down to 60mg every 12 hours. Fludrocortisone was also initiated at 0.2mg daily. Symptoms began to improve, and sodium levels normalized to136 mEq/dl. She was discharged on 30mg of hydrocortisone and 0.1 mg of fludrocortisone daily and is stable since then. Conclusion: This is a rare case of Nivolumab-induced adrenalitis. It highlights the importance of checking for adrenal insufficiency in a patient who presents with symptoms of hypotension and hyponatremia while being on ICI drugs, as unidentified adrenal insufficiency and adrenal crisis can be fatal.

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Looking for Celiac Disease in Italian Women with Endometriosis: A Case Control Study

BioMed Research International ◽

10.1155/2014/236821 ◽

2014 ◽

Vol 2014 ◽

pp. 1-5 ◽

Cited By ~ 9

Author(s):

Luca Santoro ◽

Sebastiano Campo ◽

Ferruccio D’Onofrio ◽

Antonella Gallo ◽

Marcello Covino ◽

...

Keyword(s):

Celiac Disease ◽

Autoimmune Diseases ◽

Tissue Transglutaminase ◽

Statistical Significance ◽

Intestinal Biopsy ◽

Control Group ◽

Italian Population ◽

Tissue Transglutaminase Antibodies ◽

History Of ◽

Italian Women

In the last years, a potential link between endometriosis and celiac disease has been hypothesized since these disorders share some similarities, specifically concerning a potential role of oxidative stress, inflammation, and immunological dysfunctions. We investigated the prevalence of celiac disease among Italian women with endometriosis with respect to general population. Consecutive women with a laparoscopic and histological confirmed diagnosis of endometriosis were enrolled; female nurses of our institution, without a known history of endometriosis, were enrolled as controls. IgA endomysial and tissue transglutaminase antibodies measurement and serum total IgA dosage were performed in both groups. An upper digestive endoscopy with an intestinal biopsy was performed in case of antibodies positivity. Presence of infertility, miscarriage, coexistence of other autoimmune diseases, and family history of autoimmune diseases was also investigated in all subjects. Celiac disease was diagnosed in 5 of 223 women with endometriosis and in 2 of 246 controls (2.2% versus 0.8%;P=0.265). Patients with endometriosis showed a largely higher rate of infertility compared to control group (27.4% versus 2.4%;P<0.001). Our results confirm that also in Italian population an increased prevalence of celiac disease among patients with endometriosis is found, although this trend does not reach the statistical significance.

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Adrenal Insufficiency After Unilateral Adrenalectomy in Primary Aldosteronism: Long-Term Outcome and Clinical Impact

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jc.2019-00996 ◽

2019 ◽

Vol 104 (11) ◽

pp. 5658-5664 ◽

Cited By ~ 4

Author(s):

Daniel A Heinrich ◽

Christian Adolf ◽

Finn Holler ◽

Benjamin Lechner ◽

Holger Schneider ◽

...

Keyword(s):

Adrenal Insufficiency ◽

Primary Aldosteronism ◽

Serum Cortisol ◽

Adrenal Crisis ◽

Acth Stimulation ◽

Term Outcome ◽

Unilateral Adrenalectomy ◽

Long Term Outcome ◽

Cortisol Levels

Abstract Context Primary aldosteronism (PA) represents a secondary form of arterial hypertension that can be cured by surgery. Evidence of adrenal insufficiency (AI) was recently found in patients with PA who had undergone unilateral adrenalectomy (uADX). Objective To study the incidence and long-term outcome of postoperative AI after uADX for PA. Design Prospective registry study (August 2014 until the end of 2018). Setting Tertiary referral center. Patients One hundred consecutive patients undergoing uADX for PA were included. All patients underwent postoperative ACTH stimulation testing. Intervention Postoperative ACTH stimulation testing to identify patients with AI. Main Outcome Measures Incidence of patients with postoperative AI and definition of long-term outcome. Results Twenty-seven percent of patients developed postoperative AI. Of these, 48% had postoperative ACTH stimulation serum cortisol levels ≤13.5 µg/dL (severe AI); 52% were classified into the group with moderate AI (stimulated serum cortisol levels: 13.5 to 17 µg/dL). Patients with severe AI required significantly longer hydrocortisone replacement therapy than the moderate group (median [25th, 75th percentiles]: 353 [294, 476] days; 95% CI: 284 to 322 days; vs 74 [32, 293] days; 95% CI: 11 to 137 days; P = 0.016). One patient with severe AI was hospitalized for an acute adrenal crisis. With a cumulative follow-up of 14.5 years, this produced an incidence rate of 6.9 adrenal crises per 100 patient-years. Conclusion We suggest performing postoperative ACTH stimulation tests in all patients who undergo uADX for PA.

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SUN-166 Primary Adrenal Insufficiency Caused by Underlying Tuberculosis

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa046.1157 ◽

2020 ◽

Vol 4 (Supplement_1) ◽

Author(s):

Umara Zahir Jamal

Keyword(s):

Adrenal Insufficiency ◽

Opportunistic Infections ◽

Clinical Signs ◽

Lower Lobe ◽

Granulomatous Inflammation ◽

Developed Countries ◽

Adrenal Tumors ◽

Adrenal Crisis ◽

Acth Stimulation ◽

Primary Adrenal Insufficiency

Abstract Introduction Primary adrenal insufficiency (AI) is a rare endocrine disorder affecting 1 in 100,000 people. Primary AI is a gradual destruction of the adrenal cortex. Etiology includes autoimmune, tuberculosis, histoplasmosis, blastomycosis, adrenal metastases, primary adrenal tumors, and opportunistic infections of HIV. Since aggressive treatment of TB, the incidence of TB adrenalitis has significantly declined, now accounting for 20% of reported cases where as autoimmune causes of AI account for 70%. Most common symptoms are non-specific, and diagnosis is often delayed, with patient initially presenting with a life-threatening adrenal crisis. Case Patient is an incarcerated 65 y/o African American male with PMHx of hypothyroidism who was admitted to the hospital for AMS after being found unresponsive in his prison cell. On admission, patient was febrile, hypotensive and tachycardic. He looked disheveled, confused, and lethargic. Other exam findings were negative. Lab results revealed WBC 11.7/μL, serum sodium 116 mmol/L, serum potassium 5.2 mmol/L, serum glucose 68 mg/dL, serum osmolality 237mOsm/kg, TSH 26.3mIU/L, and random cortisol 1.6ug/dL. ACTH stimulation test revealed pre-challenge cortisol levels 5.1ug/dL, 30-minute 4.9ug/dL and 60-minute 4.5ug/dL. ACTH 1271 pg/mL (normal range 7.2-63.3pg/mL). A normal response is a stimulated cortisol level > 18ug/dl. Chest x-ray revealed left lower lobe pneumonia. Clinical signs/symptoms and labs were consistent with primary AI. Adrenal crisis was most likely precipitated by underlying pneumonia. Workup was negative for 21-Hydrolase Antibodies, HIV, CMV, and histoplasmosis. However, QuantiFERON-TB Gold Test was positive. Abdominal CT revealed bilateral enlarged non-enhancing adrenal nodules with coarse calcifications. Biopsy of right adrenal gland revealed necrotizing caseating granulomatous inflammation. Biopsy was negative for isolated aerobic, anerobic, fungal organisms, AFB, and mycobacterium PCR. Due to current findings and high suspicion of TB adrenalitis, patient is currently being treated as culture-negative tuberculosis along with PO hydrocortisone for underlying AI. Discussion Adrenal tuberculosis is a rare cause of primary adrenal insufficiency in developed countries. There should be high suspicion for AI when a patient presents with hypotension, hyponatremia, hyperkalemia and/or hypoglycemia. In this case, although patient did not have a positive AFB culture, he did have a positive QuantiFERON-TB Gold Test along with consistent findings on CT and biopsy. Thus, case was concluded to have high suspicion of primary AI secondary to underlying untreated tuberculosis. Prompt treatment with antituberculosis medication, appropriate steroid therapy, along with monitoring of adrenal function, underlying adrenal insufficiency may be reversible if detected in early stages and decrease mortality.

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Adrenal crisis in patients with primary and secondary adrenal insufficiency

Experimental and Clinical Endocrinology & Diabetes ◽

10.1055/s-2006-932893 ◽

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

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