Management of Liver Decompensation in Advanced Liver Disease (Renal Impairment, Liver Failure, Adrenal Insufficiency, Cardiopulmonary Complications)

Téllez, Luís; Guerrero, Antonio José Moreno

doi:10.1007/s40261-022-01149-3

Cited by 6 publications

(4 citation statements)

References 61 publications

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“…Therefore, only the measurement of free plasma cortisol or salivary cortisol can be used, and these should be measured in parallel with total cortisol to assess probable deficiency, with an average delay of 1 wk to 2 wk and limited availability in emergency services. Based on the above, we suggest measuring these in situations where the patient’s clinical condition raises doubts about the diagnosis[ 83 , 87 , 91 ].…”

Section: Diagnosismentioning

confidence: 99%

“…Intravenous hydrocortisone at a dose of 200 mg/d to 300 mg/d divided into 3 to 4 doses is indicated, with subsequent progressive titration based on the patient’s clinical evolution. For non-critically ill patients without symptoms, literature is limited; therefore, oral hydrocortisone at a dose of 15 mg to 20 mg divided into two doses per day is suggested, only in cases of persistent hypotension and hyponatremia[ 86 , 87 , 91 , 163 , 164 ].…”

Section: Treatmentmentioning

confidence: 99%

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From liver to hormones: The endocrine consequences of cirrhosis

Quiroz-Aldave,

Gamarra-Osorio,

Durand-Vásquez

et al. 2024

World J Gastroenterol

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Hepatocrinology explores the intricate relationship between liver function and the endocrine system. Chronic liver diseases such as liver cirrhosis can cause endocrine disorders due to toxin accumulation and protein synthesis disruption. Despite its importance, assessing endocrine issues in cirrhotic patients is frequently neglected. This article provides a comprehensive review of the epidemiology, pathophysiology, diagnosis, and treatment of endocrine disturbances in liver cirrhosis. The review was conducted using the PubMed/Medline, EMBASE, and Scielo databases, encompassing 172 articles. Liver cirrhosis is associated with endocrine disturbances, including diabetes, hypoglycemia, sarcopenia, thyroid dysfunction, hypogonadotropic hypogonadism, bone disease, adrenal insufficiency, growth hormone dysfunction, and secondary hyperaldosteronism. The optimal tools for diagnosing diabetes and detecting hypoglycemia are the oral glucose tolerance test and continuous glucose monitoring system, respectively. Sarcopenia can be assessed through imaging and functional tests, while other endocrine disorders are evaluated using hormonal assays and imaging studies. Treatment options include metformin, glucagon-like peptide-1 analogs, sodium-glucose co-transporter-2 inhibitors, and insulin, which are effective and safe for diabetes control. Established standards are followed for managing hypoglycemia, and hormone replacement therapy is often necessary for other endocrine dysfunctions. Liver transplantation can address some of these problems.

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Section: Diagnosismentioning

confidence: 99%

Section: Treatmentmentioning

confidence: 99%

From liver to hormones: The endocrine consequences of cirrhosis

Quiroz-Aldave,

Gamarra-Osorio,

Durand-Vásquez

et al. 2024

World J Gastroenterol

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“…Systemic hemodynamic complications are typical of portal hypertension (PHT) and cirrhosis. [1][2][3][4] PHT produces alterations in cardiovascular function and tone, with splanchnic arterial vasodilation, reduced systemic vascular resistance, and lower effective arterial blood volume along with arterial pressure reductions. 5 Effective hypovolemia, low perfusion pressure, and reduced glomerular filtration rate can lead to vasoconstriction within the kidney with subsequent sodium and water retention, resulting in hepatorenal syndrome-acute kidney injury (HRS-AKI).…”

Section: Introductionmentioning

confidence: 99%

OCE-205, a Selective V1a Partial Agonist, Reduces Portal Pressure in Rat Models of Portal Hypertension

Bukofzer¹,

Harris²,

Song³

et al. 2023

JEP

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Purpose Management of decompensated cirrhosis may include the use of vasoconstrictors that can lead to serious adverse events. OCE-205 was designed as a highly selective V1a receptor partial agonist, intended to have a wider therapeutic window than full vasopressin agonists. Methods We aimed to characterize the activity of OCE-205 treatment in two rat models of portal hypertension (PHT). For both models, OCE-205 was administered as a subcutaneous bolus injection. Thirty male Wistar rats were fed a methionine/choline-deficient (MCD) diet to model PHT. Animals received OCE-205 (10, 25, 100, or 500 µg/kg) or intra-arterial terlipressin (100 µg/kg). In a more severe model of PHT, 11 male Sprague Dawley rats had the common bile duct surgically ligated (BDL) and received OCE-205. Portal pressure (PP) and mean arterial pressure (MAP) were measured. Results For PP in the MCD model, MAP increased while PP decreased in rats treated with OCE-205 or terlipressin; the peak changes to MAP were 14.7 and 33.5 mmHg, respectively. Changes in MAP began to plateau after 10 min in the OCE-205 groups, whereas in the terlipressin group, MAP rapidly increased and peaked after 20 min. Across all treatment groups in the BDL model, a dose-related decrease from baseline in PP was observed following OCE-205, plateauing as the dose increased. In all treatment groups, PP change remained negative throughout the 30-min testing period. In both PHT rat models, a reduction in PP was coupled to an increase in MAP, with both plateauing in dose–response curves. Conclusion Data support OCE-205 as a promising candidate for further development. Institutional Protocol Number Procedures were approved by the Ferring Research Institute (FRI) Institutional Animal Care and Use Committee on July 13, 2011, under protocol FRI-07-0002.

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“…Decompensated cirrhosis and the associated serious hemodynamic complications remain an area unmet need for patients. Systemic hemodynamic complications are typical of portal hypertension (PHT) as a result of cirrhosis ( Tellez and Guerrero, 2022 ; Biggins et al, 2021 ; Smith et al, 2019 ; Moller and Bendtsen, 2018 ). The onset of decompensated cirrhosis leads to vasodilation of the splanchnic arteries, reduction in systemic vascular resistance, lower effective arterial blood volume, and reduced arterial pressure ( Ginès et al, 2018 ).…”

Section: Introductionmentioning

confidence: 99%