ECE2023 Poster Presentations Adrenal and Cardiovascular Endocrinology (72 abstracts)
Relative adrenal insufficiency in liver cirrhosis: a common but often forgotten critical condition
Tijana Petkovic 1 , Ljiljana Marina 1,2 , Dunja-Simona Petkovic 1 , Jelena Martinov Nestorov 2,3 , Djordje Culafic 2,3 , Jelena Jovanovic 3 , Miomira Ivovic 1,2 , Antoan Stefan Sojat 1 , Natalija Antic 1 , Kristina Saravinovska 1 , Zorana Arizanovic 1 & Svetlana Vujovic 1,2
1Clinic for Endocrinology, Diabetes and Metabolic Diseases, University Clinical Centre of Serbia, National Centre for Infertility and Endocrinology of Gender, Belgrade, Serbia; 2Faculty of Medicine, University of Belgrade, Belgrade, Serbia; 3Clinic for Gastroenterology and Hepatology, University Clinical Centre of Serbia, Hepatology Department, Belgrade, Serbia
Introduction: Relative adrenal insufficiency (RAI) is common in critically ill patients and is characterized by the normal adrenal reserve for homeostatic demands and inadequate cortisol response in acute stress situations. RAI can also occur in patients with liver cirrhosis, both compensated and decompensated. However, it is often forgotten and difficult to diagnose due to the overlap between clinical symptoms of adrenal insufficiency and decompensated liver disease. Also, hypothalamic pituitary adrenal axis analysis in patients with cirrhosis is not performed routinely so many of these cases remain undiagnosed or misdiagnosed.
Case report: A male patient, 54 years of age, was admitted to Hepatology Department, Clinic for Gastroenterology and Hepatology due to a alcoholic liver cirrhosis (Child B) with esophageal varices grade 2/3 and refractory ascites. He was initially diagnosed in 2017 and had daily ascites drainage through permanent peritoneal catheter placed in his regional medical centre in 2021. At admission, he complained of abdominal pain, fatigue, nausea and diarrhea. Biochemical and hormonal evaluation showed hyponatremia 124 mmol/l, hyperkalemia 5.9 mmol/l, normal renal function, very low cholesterol 2.08 mmol/l, high TSH 13 mIU/L, with low fT4 8.1 pmol/l, low ACTH 0.6 pmol/l with low-normal cortisol 233 nmol/l, which is why he was sent for an endocrinological evaluation. In the physical examination, the patient was awake, communicative, afebrile, and hypotensive with no signs of haemorrhagic syndrome and besides hypotension of 80/50 mmHg, no other typical clinical sign of hypocortisolism. Based on electrolyte status, low ACTH, low normal cortisol and hypotension the Synacthen test was performed which showed an inadequate cortisol response: 237 nmol/l (0 min), 323 nmol/l (30 min) and 385 nmol/l (60 min). Hydrocortisone treatment was initiated and after two days all reported complaints resolved along with electrolyte and blood pressure normalization. Also, levothyroxine supplementation was initiated.
Conclusion: Diagnosis and treatment of RAI in cirrhotic patients remains controversial. Empiric glucocorticoid treatment is not recommended in asymptomatic patients. However, patients who are symptomatic benefit from glucocorticoid replacement as it was the case in our patient. These patients should have a close and careful follow up for sings of cortisol overtreatment and/or infection.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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