scholarly journals Thyrotoxicosis leading to adrenal crises reveals primary bilateral adrenal lymphoma

Author(s):  
Catarina Roque ◽  
Ricardo Fonseca ◽  
Carlos Tavares Bello ◽  
Carlos Vasconcelos ◽  
António Galzerano ◽  
...  

Summary Primary adrenal lymphoma is a rare malignancy. It frequently presents bilaterally and with symptoms of adrenal insufficiency. Amiodarone may induce secondary organ dysfunction, and thyrotoxicosis develops in 15% of cases. The symptomatology of both conditions is nonspecific, especially in the elderly, and a high suspicion index is necessary for appropriate diagnosis. A 78-year-old female presented to the emergency department with confusion, nausea and vomiting. She had recently been to the emergency department with urinary tract infection, vomiting and acute hypochloremic hyponatremia. Upon re-evaluation, the leukocyturia persisted and because of TSH 0.01 µU/mL and free-T4 68 (10–18) pmol/L, she was admitted to the Endocrinology ward. Further evaluation supported amiodarone-induced thyroiditis type 2. Sepsis ensued, in the setting of nosocomial pneumonia. Hemodynamic instability, hyponatremia, hypoglycemia and vomiting raised the suspicion of adrenocortical insufficiency. Fluid resuscitation and hydrocortisone led to clinical improvement, and adrenal insufficiency was admitted. The thoracoabdominal tomography suggested an endobronchic primary lesion with hepatic and adrenal secondary deposits (6.6 and 7 cm), but this was confirmed neither on pleural effusion nor on bronchofibroscopic fluid analyses. The adrenals were not accessible for biopsy. Despite high-dose hydrocortisone maintenance, the patient died before definite diagnosis. The autopsy confirmed primary non-Hodgkin lymphoma. Learning points: Primary adrenal lymphoma is a rare cause of adrenal insufficiency, but progression can be fast and fatal. Hyperpigmentation is frequently absent. The presenting symptoms are nonspecific and might mimic infection. Disproportion of the general state with signs of specific organ symptomatology is a diagnostic clue. Infection may precipitate adrenal crisis and worsen thyroid function with further adrenal insufficiency exacerbation. In the context of thyrotoxicosis, there may be little clinical response to a therapeutic trial with standard dose glucocorticoids. High-dose glucocorticoid substitution may be required to achieve clinical stability in thyrotoxic patients.

Author(s):  
Casey M Hay ◽  
Daniel I Spratt

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.


Author(s):  
Kaja Grønning ◽  
Archana Sharma ◽  
Maria Adele Mastroianni ◽  
Bo Daniel Karlsson ◽  
Eystein S Husebye ◽  
...  

Summary Primary adrenal lymphoma (PAL) is a rare cause of adrenal insufficiency. More than 90% is of B-cell origin. The condition is bilateral in up to 75% of cases, with adrenal insufficiency in two of three patients. We report two cases of adrenal insufficiency presenting at the age of 70 and 79 years, respectively. Both patients had negative 21-hydroxylase antibodies with bilateral adrenal lesions on CT. Biopsy showed B-cell lymphoma. One of the patients experienced intermittent disease regression on replacement dosage of glucocorticoids. Learning points: Primary adrenal lymphoma (PAL) is a rare cause of adrenal insufficiency. Bilateral adrenal masses of unknown origin or in individuals with suspected extra-adrenal malignancy should be biopsied quickly when pheochromocytoma is excluded biochemically. Steroid treatment before biopsy may affect diagnosis. Adrenal insufficiency with negative 21-hydroxylase antibodies should be evaluated radiologically.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A108-A109
Author(s):  
Nani Oktavia ◽  
Chici Pratiwi ◽  
Jerry Nasaruddin ◽  
Muhammad Ikhsan Mokoagow ◽  
Marina Epriliawati ◽  
...  

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.


1997 ◽  
Vol 24 (3-4) ◽  
pp. 363-367 ◽  
Author(s):  
Mark Pimentel ◽  
James B. Johnston ◽  
Donald R. Allan ◽  
Howard Greenberg ◽  
Charles N. Bernstein

HORMONES ◽  
2004 ◽  
Vol 3 (1) ◽  
pp. 68-73 ◽  
Author(s):  
Evanthia Diamanti-Kandarakis ◽  
Pantelis Chatzismalis ◽  
Frangiskos Economou ◽  
Stefanos Lazarides ◽  
Athena Androulaki ◽  
...  

2019 ◽  
Vol 104 (6) ◽  
pp. e55.3-e56
Author(s):  
V Stachanow ◽  
J Melin ◽  
R Michelet ◽  
O Blankenstein ◽  
U Neumann ◽  
...  

BackgroundPatients with congenital adrenal hyperplasia (CAH) have low to no biosynthesis of cortisol and require lifelong cortisol replacement. Optimisation of hydrocortisone (HC, synthetic cortisol) therapy in this population is important, since too low or high cortisol concentrations increase the risk of adrenal crisis or Cushing’s syndrome1. HC has nonlinear pharmacokinetics (PK) caused by saturable binding to corticosteroid binding globulin (CBG)2. The objective of this analysis was to extend an established paediatric HC PK-model3 with dried blood spot (DBS) data in order to further characterise the binding behaviour of HC in children.MethodsA semi-mechanistic adult PK model for a novel HC formulation4 has previously been reduced to a paediatric model using sparse plasma samples from a phase III study in 24 patients with adrenal insufficiency5. Plasma and DBS concentrations of cortisol were collected and additional DBS HC concentrations were obtained from a follow-up study. The relation between plasma and DBS samples was characterised by a graphical evaluation, after which nonlinear mixed-effects modelling was applied using NONMEM 7.4.ResultsPlasma concentrations of cortisol were substantially higher than the corresponding DBS concentrations. The plasma/DBS ratio ranged between 2 to 8 within and between children, while the relation between the cortisol DBS concentrations and cortisol plasma concentrations showed nonlinear behaviour mirroring the nonlinear binding kinetics to CBG.ConclusionsOur graphical analysis identified substantial differences and high inter- and intraindividual variabilities between plasma and DBS samples. A nonlinear mixed-effects model is being set up to quantify these findings and allow for further prediction of HC exposure. Afterwards, effect biomarkers can be included in order to evaluate cortisol replacement therapy and to optimise the HC treatment in paediatric patients.ReferencesSpeiser PW, et al. J Clin Endocrinol Metab 2010;95(9):4133–4160.Lentjes EG, WM, et al:J Clin Endocrinol Metab. 1999;84(2):682–687.Melin J:Dissertation 2017.Melin J, et al:Clin Pharmacokinet. 2018;57(4):515–527.Neumann U. et al:Clin Endocrinol. 2018;88(1):21–29.Disclosure(s)Nothing to disclose


2018 ◽  
Author(s):  
Jason J Lewis ◽  
Richard E Wolfe

Nondiabetic endocrine emergencies are less frequent but equally concerning as diabetic emergencies. The diagnosis of adrenal crises, pheochromocytoma, or pituitary deficiencies can be difficult in the emergent setting given the nonspecific findings frequently confused with other presenting illnesses. Although the differential is broad for patients presenting with shock and hypotension, as seen in adrenal crises, hypertensive emergencies in pheochromocytoma, or a litany of potential symptoms in pituitary abnormalities, the diagnosis should be considered in a patient presenting to the emergency department with severe metabolic abnormalities, undifferentiated shock, or cardiovascular lability. This review demonstrates how to recognize and manage acute adrenal crisis, pheochromocytoma, and pituitary deficiencies in the acute care setting. Patients with nondiabetic endocrine emergencies may present in extremis, and immediate stabilization, typically without confirmatory testing, is necessary. Early intervention is key in treating such presentations. This review contains 1 figure, 2 tables and 21 references Key words: adrenal crisis, adrenal insufficiency, catecholamine surge, pheochromocytoma, pituitary deficiency


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