scholarly journals SUN-166 Primary Adrenal Insufficiency Caused by Underlying Tuberculosis

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.

scholarly journals Adrenal Crisis in Long Term Use of Exogenous Steroid With Inappropriate Tapering off Process

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A108-A109
Author(s):  
Nani Oktavia ◽  
Chici Pratiwi ◽  
Jerry Nasaruddin ◽  
Muhammad Ikhsan Mokoagow ◽  
Marina Epriliawati ◽  
...  
Keyword(s):  
Abdominal Pain ◽  
Blood Glucose ◽  
Adrenal Insufficiency ◽  
Clinical Manifestations ◽  
Adrenal Crisis ◽  
High Dose ◽  
Symptomatic Therapy ◽  
Bowel Sound ◽  
Primary Adrenal Insufficiency

Abstract Background: Adrenal crisis is an emergency condition in endocrinology that commonly found in primary adrenal insufficiency but also occur in chronic adrenal insufficiency triggered by various conditions such as sepsis, infection, trauma, burns, surgery, and myocardial infarction. In chronic adrenal insufficiency, adrenal crisis can be induced by excessive reductions or inadequate discontinuation of steroid treatment. Case Illustration: A 40-year old-man admitted with chief complaint abdominal pain since seven days before admission. He felt pain in the umbilical area and slowly radiated to all the part of abdomen. Other than that, he also felt nausea, had vomitus, fever, and constipation for five days. He was immobilized for four months, with muscles weakness and atrophy. He was diagnosed with Focal Segmented Glomerulosclerosis and had a high dose of methylprednisolone (48 mg) for 6 months, 40 mg for the next 2 months and methylprednisolone 12 mg for the last 2 months. The last two month, he began to have severe general weakness and hypotension. On physical examination we found hypotension, fever (38.1o C), pale conjunctiva, moon face, buffalo hump, slightly distended and tenderness of abdomen, normal bowel sound, and purple striae all over the abdomen and extremities. On laboratory examination, Hb was 8.2 (n 11.7 – 15.5 g/dl), leukocytes 10,400 (5.00 – 10.00 x 103/μL), Na 123 (n 135 – 147 mmol/L), random blood glucose 74 (n 70 – 140 mg/dL). On abdominal X ray, there was prominent faecal material and no signs of ileus. No sign of infection found in urinalysis. He had sodium correction, packed red cell transfusion, symptomatic therapy including laxative, methylprednisolone 12 mg, but no improvement of signs and symptoms beside be able to defecate. The abdominal ultrasound gave a normal result. The morning cortisol level was then examined, with the result 14.4 (n 3.7–19.4). The patient was then diagnosed with adrenal crisis based on the clinical manifestations and had hydrocortisone therapy 100 mg a day for 2 consecutive days. After hydrocortisone administration, the symptoms improved, no fever and abdominal pain, he had normotension, increased sodium level 132 (n 135 – 147 mmol/L) and blood glucose level 118 (n 70 – 140 mg/dL). On the third day the patient discharged with oral hydrocortisone 15 mg in the morning and 10 mg in the afternoon. Conclusion: Adrenal crisis was generally found in primary adrenal insufficiency but could also occur in secondary adrenal insufficiency due to inappropriate tapering off process of long term glucocorticoid use.

scholarly journals Adrenal insufficiency in a woman secondary to standard-dose inhaled fluticasone propionate therapy

2014 ◽  
Vol 2014 ◽  
Author(s):  
Casey M Hay ◽  
Daniel I Spratt
Keyword(s):  
Fluticasone Propionate ◽  
Adrenal Insufficiency ◽  
Cortisol Level ◽  
Standard Dose ◽  
Clinical Signs ◽  
Unknown Origin ◽  
Adrenal Crisis ◽  
List Type ◽  
Morning Cortisol ◽  
Low Serum

Summary A 55-year-old woman with asthma presented with adrenal insufficiency of unknown origin. She was referred to our Division of Reproductive Endocrinology to further evaluate an undetectable morning cortisol level discovered during the evaluation of a low serum DHEA-S level. She was asymptomatic other than having mild fatigue and weight gain. Her medication list included 220 μg of inhaled fluticasone propionate twice daily for asthma, which she was taking as prescribed. On presentation, the undetectable morning cortisol level was confirmed. A urinary measurement of fluticasone propionate 17β-carboxylic acid was markedly elevated. Fluticasone therapy was discontinued and salmeterol therapy initiated with supplemental hydrocortisone. Hydrocortisone therapy was discontinued after 2 months. A repeat urinary fluticasone measurement 4 months after the discontinuation of fluticasone therapy was undetectably low and morning cortisol level was normal at 18.0 μg/dl. Inhaled fluticasone is generally considered to be minimally systemically absorbed. This patient's only clinical evidence suggesting adrenal insufficiency was fatigue accompanying a low serum DHEA-S level. This case demonstrates that adrenal insufficiency can be caused by a routine dose of inhaled fluticasone. Missing this diagnosis could potentially result in adrenal crisis upon discontinuation of fluticasone therapy. Learning points Standard-dose inhaled fluticasone can cause adrenal insufficiency. Adrenal insufficiency should be considered in patients taking, or who have recently discontinued, inhaled fluticasone therapy and present with new onset of nonspecific symptoms such as fatigue, weakness, depression, myalgia, arthralgia, unexplained weight loss, and nausea that are suggestive of adrenal insufficiency. Adrenal insufficiency should be considered in postoperative patients who exhibit signs of hypoadrenalism after fluticasone therapy has been withheld in the perioperative setting. Routine screening for hypoadrenalism in patients without clinical signs or symptoms of adrenal insufficiency after the discontinuation of inhaled fluticasone therapy is not indicated due to the apparently low incidence of adrenal insufficiency caused by fluticasone.

scholarly journals Tiered healthcare in South Africa exposes deficiencies in management and more patients with infectious etiology of primary adrenal insufficiency

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0241845
Author(s):  
Thabiso Rafaki Petrus Mofokeng ◽  
Kwazi Celani Zwakele Ndlovu ◽  
Salem A. Beshyah ◽  
Ian L. Ross
Keyword(s):  
South Africa ◽  
Adrenal Insufficiency ◽  
Online Survey ◽  
Management Strategies ◽  
Adrenal Crisis ◽  
Public Healthcare ◽  
Antibody Testing ◽  
Management Options ◽  
Primary Adrenal Insufficiency ◽  
The Public

Objective We wished to determine the prevalence, etiology, presentation, and available management strategies for primary adrenal insufficiency (PAI) in South Africa (SA), hypothesizing a prevalence greater than the described 3.1 per million. There is great inequity in healthcare allocation, as two parallel healthcare systems exist, potentially modifying PAI patients’ clinical profiles, private being better resourced than public healthcare. Methods An online survey of physicians’ experience relating to PAI. Results The physicians were managing 811 patients, equal to a prevalence of 14.2 per million. Likely causes of PAI in public/ academic vs private settings included: AIDS-related [304 (44.8%) vs 5 (3.8%); p<0.001], tuberculosis [288 (42.5%) vs 8 (6.0%); p<0.001], autoimmune disease [50 (7.4%) vs 88 (66.2%); p<0.001], malignancy [27 (4.0%) vs 7 (5.3%); p = 0.500], genetic including adrenoleukodystrophy (ALD) [5 (0.7%) vs 16 (12.0%); p<0.001], respectively. Overall, more patients presented with nausea [101 (74.3%) and vomiting 89 (65.9%), than diarrhoea 76 (58.9%); p = 0.008 and 126 (15.5%) in adrenal crisis. Features suggestive of a crisis were hypoglycaemia [40 (78.4%) vs 42 (48.8%); p = 0.001], shock [36 (67.9%) vs 31(36.9%); p<0.001], and loss of consciousness [25 (52.1%) vs 27 (32.9%); p = 0.031]. Greater unavailability of antibody testing in the public vs. the private sector [32 (66.7%) vs 30 (32.1%); p = 0.001], [serum-ACTH 25 (52.1%) vs 16 (19.5%); p<0.001] and glucocorticoids were [26 (54.2%) vs 33 (40.2%); p = 0.015]. Many patients, 389(66.7%) were not using identification, indicating that they need steroids in an emergency. Conclusion A survey of South African physicians suggests a higher prevalence than previously reported. Patients presented with typical symptoms, and 15.5% presented in adrenal crisis. Significant disparities in the availability of physicians’ expertise, diagnostic resources, and management options were noted in the public versus private settings. Greater awareness among health practitioners to timeously diagnose PAI is required to prevent a life-threatening outcome.

scholarly journals Reduction in daily hydrocortisone dose improves bone health in primary adrenal insufficiency

2016 ◽  
Vol 174 (4) ◽  
pp. 531-538 ◽  
Author(s):  
Julia Schulz ◽  
Kathrin R Frey ◽  
Mark S Cooper ◽  
Kathrin Zopf ◽  
Manfred Ventz ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Adrenal Crisis ◽  
Mineral Density ◽  
Primary Adrenal Insufficiency ◽  
Group Reduction ◽  
Group 3 ◽  
Group 2 ◽  
Over Time ◽  
Group 1

ObjectiveIndividuals with primary adrenal insufficiency (PAI) or congenital adrenal hyperplasia (CAH) receive life-long glucocorticoid (GC) replacement therapy. Current daily GC doses are still higher than the reported adrenal cortisol production rate. This GC excess could result in long-term morbidities such as osteoporosis. No prospective trials have investigated the long-term effect of GC dose changes in PAI and CAH patients.MethodsThis is a prospective and longitudinal study including 57 subjects with PAI (42 women) and 33 with CAH (21 women). Bone mineral density (BMD) was measured by dual energy X-ray absorptiometry at baseline and after 2 years. Subjects were divided into three groups (similar baseline characteristics) depending on changes in daily hydrocortisone equivalent dose (group 1: unchanged 25.2±8.2 mg (mean±s.d., n=50); group 2: increased 18.7±10.3 to 25.9±12.0 mg (n=13); group 3: decreased 30.8±8.5 to 21.4±7.2 mg (n=27)).ResultsSubjects in group 1 showed normal lumbar and femoral Z-scores which were unchanged over time. Group 2 subjects showed a significant decrease in femoral neck Z-scores over time (−0.15±1.1 to −0.37±1.0 (P<0.05)), whereas group 3 subjects showed a significant increase in lumbar spine and hip Z-scores (L1–L4: −0.93±1.2 to –0.65±1.5 (P<0.05); total hip: −0.40±1.0 to −0.28±1.0 (P<0.05)). No changes in BMI over time were seen within any group. Reduction in GC dose did not increase the risk of adrenal crisis.ConclusionThis study demonstrates for the first time that cautious reduction in hydrocortisone equivalent doses leads to increases in BMD, whereas dose increments reduced BMD. These data emphasize the need for the lowest possible GC replacement dose in AI patients to maintain health and avoid long-term adverse effects.

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 SUN-164 Adrenal Crisis in Early Pregnancy

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jenny Carolina Bello ◽  
Xiaolei Chen ◽  
Kenneth K Chen
Keyword(s):  
Adrenal Insufficiency ◽  
Normal Pregnancy ◽  
Nausea And Vomiting ◽  
Adrenal Crisis ◽  
Primary Adrenal Insufficiency ◽  
Early Presentation ◽  
Delay In Diagnosis ◽  
Medical Disorders ◽  
Free Cortisol ◽  
In Pregnancy

Abstract Nausea and vomiting are common symptoms in pregnancy, ranging from occasional nausea to fulminant and intractable vomiting. Many underlying metabolic disorders can mimic this, primary adrenal insufficiency (PAI) being one of them. Here, we present a case of adrenal insufficiency early in pregnancy. A 28 year old lady G1P0 at 8 weeks of gestations, with a past medical history of Grave’s Disease, presented to our hospital on 3 occasions over one week with severe intractable nausea and vomiting. On prior visits, she had received intravenous fluids and discharged home. Laboratory work-up was ordered on the third visit and she was found to have severe hyponatremia with level of 111mMol/L. TSH and FT4 levels were both within the reference range. AM cortisol level was low at 2.3mcg/dL. ACTH and renin were both significantly elevated confirming diagnosis of PAI. Intravenous hydrocortisone was commenced immediately with rapid resolution of her symptoms and correction of her hyponatremia. She was followed at the endocrinology clinic, with appropriate up-titration of glucocorticoid and mineralocorticoid doses throughout her pregnancy. Diagnosis of PAI is usually established prior to pregnancy. Presentation during pregnancy is not common, but it should be considered as a differential diagnosis when symptoms are out of proportion to the gestational status. Normal pregnancy is accompanied by progressive increase in circulating CRH and ACTH, increasing the levels of free cortisol as early as 7 weeks of gestation, rising up to 20-fold by the end of pregnancy. These physiologic changes could explain early presentation of adrenal crisis given insufficient glucocorticoid production. A delay in diagnosis and treatment increases the risk of maternal and fetal morbidity and mortality significantly. Management of PAI during pregnancy can be challenging as there are no established guidelines and they have mainly been based on observational studies (1). The appropriate selection and dose of the glucocorticoid is important for the treatment of PAI to minimize adverse effects on mother and baby (2). At the time of active labor and delivery, stress doses of glucocorticoids need to be administered to prevent adrenal crisis (3). In conclusion, early diagnosis and appropriate management of PAI during pregnancy is necessary to sustain a healthy pregnancy. Bibliography 1 Husebye ES, Allolio B, Arlt W, et al. Consensus statement on the diagnosis, treatment and follow-up of patients with primary adrenal insufficiency. J Intern Med 2014; 275: 104– 15. 2 Bandoli G, Palmsten K, Forbess C, et al. A review of systemic corticosteroid use in pregnancy and the risk of select pregnancy and birth outcomes. Rheum Dis Clin North Am. 2017; 43(3): 489–502 3 Chen K, Powrie R. Approach to the use of Glucocorticoids in Pregnancy for Nonobstetric Indications. de Swiet’s Medical Disorders in Obstetric Practice: Fifth Edition. 736-741.

scholarly journals Obojestranska krvavitev v nadledvičnico: vzrok visoki zgodnji zlatenici in akutni primarni insuficienci nadledvičnic pri novorojenčku

2018 ◽  
Vol 87 (3-4) ◽  
Author(s):  
Petja Fister ◽  
Marta Žnidaršič Eržen ◽  
Primož Kotnik ◽  
Mojca Tomažič
Keyword(s):  
Gestational Diabetes ◽  
Adrenal Insufficiency ◽  
Clinical Case ◽  
Adrenal Glands ◽  
Clinical Signs ◽  
Term Neonate ◽  
Primary Adrenal Insufficiency ◽  
Acute Adrenal Insufficiency ◽  
Life Threatening ◽  
Threatening Situation

Adrenal bleeding in a newborn is rare. The cause of bleeding is unknown, most likely due to several factors. Bleeding may be minimal with no clinical signs or fulminant with acute adrenal insufficiency, which is a life-threatening situation that requires immediate detection and treatment.In this paper we represent a clinical case of a term neonate born to the mother with gestational diabetes, who was hospitalised due to high early hyperbilirubinemia. Significant bleeding in both adrenal glands was identified by ultrasound and primary adrenal insufficiency diagnosed. We discuss possible causes, the diagnostic clues, the treatment of disease and its prognosis.

scholarly journals RECURRENT INVASIVE DUCTAL BREAST CARCINOMA PRESENTING AS PRIMARY ADRENAL INSUFFICIENCY WITH ADRENAL CRISIS

2020 ◽  
Vol 6 (2) ◽  
pp. e50-e53
Author(s):  
Mitha Madhava Naik ◽  
Michael James Nestasie ◽  
Murray B. Gordon
Keyword(s):  
Breast Carcinoma ◽  
Adrenal Insufficiency ◽  
Adrenal Crisis ◽  
Primary Adrenal Insufficiency ◽  
Invasive Ductal Breast Carcinoma ◽  
Ductal Breast Carcinoma ◽  
First Case ◽  
History Of ◽  
Recurrent Breast ◽  
Work Up

Objective: We report the first case of recurrent ductal breast carcinoma presenting as primary adrenal insufficiency. Methods: We describe a patient who developed a recurrence of invasive ductal breast carcinoma which went undetected until the patient presented with fulminant adrenal crisis. We describe here an overview of the clinical presentation, work-up, diagnosis, and treatment of adrenal crisis. Results: Adrenal crisis due to bilateral adrenal metastases secondary to invasive ductal breast carcinoma is an exceedingly rare occurrence. To our knowledge, this is the first case of recurrent breast carcinoma in which the presenting feature is primary adrenal insufficiency. Conclusion: Patients with a history of breast carcinoma and bilateral adrenal enlargement should be evaluated for the presence of primary adrenal insufficiency.

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