Hyperammonium in Patients With Precirrhosis Stage: Clinical Reality?

Ильченко, Л. Ю.; Никитин, И. Г.

doi:10.20514/2226-6704-2018-8-3-186-193

Cited by 10 publications

(4 citation statements)

References 12 publications

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“…If the detoxifying function of the liver is reduced, the conversion of ammonia into urea is hindered and alternative metabolic pathways for this purpose are activated in the muscular system, astrocytes of the central nervous system, and kidneys [8][9][10]. Skeletal muscle tissue and nervous tissue are the main ammonia detoxifi ers [11].…”

Section: Excreted Urea Consists Of "Ammonia" Nitrogen and Aspartic Ac...mentioning

confidence: 99%

“…Hyperammonemia induces autophagy, where damaged proteins are broken down but not processed [17,18]. The presence of sarcopenia is one of the prognostic factors of death in patients with liver cirrhosis (low Model for End-Stage Liver Disease [MELD] scores -a tool for scoring terminal stages of liver disease and predicting preimplantation survival) [11,19].…”

Section: Excreted Urea Consists Of "Ammonia" Nitrogen and Aspartic Ac...mentioning

confidence: 99%

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Russian Consensus on “Hyperammonemia in Adults”: The 2021 Version (in English)

Лазебник

Голованова

Алексеенко

et al. 2022

jour

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Hyperammonemia is an acute or chronic intoxication with ammonia and ammonium associated with elevated ammonia levels in serum due to either its increased production and/or decreased detoxification. Hyperammonemia can result from a variety of causes and clinically presents with unspecific signs and symptoms, including asthenia, encephalopathy, liver steatosis or fibrosis, and sarcopenia. With impaired liver function, hyperammonemia most frequently manifests in (micro)encephalopathy. Thus in case of unexpect change in mental status hyperammonemia must be excluded as fast as possible. An express method of photometric assay is informative enough to determine the ammonia levels. The following hyperammonemia classification is proposed: a) by ammonia levels (normal level: ≤ 60 μmol/L; mild (Grade 1): ≤ 100 μmol/L; moderate (Grade 2): ≤ 200 μmol/L; and severe (Grade 3): > 200 μmol/L); b) by etiopathogenesis (hereditary (congenital), functional (physiological), acquired (hepatic, extrahepatic, mixed)); c) by clinical presentation (transient, recurrent or persistent, constant (stable, without treatment), covert). Treatment for hyperammonemia is aimed at treating the primary disease and includes a diet that is restricted in animal protein but contains sufficient vegetable protein, limited physical activities, and use of intestinal non-absorbable antibiotics (rifaximin- alpha) as well as pre- and probiotics. L-ornithine- L-aspartate (LOLA) is a baseline therapeutic product administered in a number of scenarios to correct the level of hyperammonemia.

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Section: Excreted Urea Consists Of "Ammonia" Nitrogen and Aspartic Ac...mentioning

confidence: 99%

Section: Excreted Urea Consists Of "Ammonia" Nitrogen and Aspartic Ac...mentioning

confidence: 99%

Russian Consensus on “Hyperammonemia in Adults”: The 2021 Version (in English)

Лазебник

Голованова

Алексеенко

et al. 2022

jour

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“…Это связывают со способностью аммиака активировать звездчатые клетки печени, снижать клеточный метаболизм, активировать профиброгенный, провоспалительный профиль звездчатых клеток, нарушать внутрипеченочную гемодинамику, стимулировать эндоретикулярный стресс и индуцировать образование активных форм кислорода [3,4]. Больше всего работ посвящено изучению роли аммиака у лиц с неалкогольной жировой болезнью печени (НАЖБП) [5,6]. В некоторых исследованиях упоминается о возможности развития гипераммониемии у лиц с метаболическим синдромом (МС).…”

Section: ростовский государственный медицинский университет ростов-нunclassified

Increased ammonia levels and its association with visceral obesity and insulin resistance

Шавкута

Shnyukova

Колесникова

et al. 2020

jour

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Hyperammonemia is considered as a significant trigger factor in the progression of liver diseases, starting from the stage of steatosis. There is also a link between high levels of ammonia and metabolic syndrome. The article discusses the relationship of hyperammonemia with a violation of carbohydrate metabolism. It is likely that an increase in ammonia is associated with an increase in visceral fat and may be a predictor of the development of insulin resistance as a key factor in carbohydrate metabolism disorders.

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“…Для коррекции гипераммониемии при заболеваниях печени длительное время применяется L-орнитина-L-аспартат (LOLA), который активирует работу орнитинового цикла детоксикации. Применение LOLA у пациентов с МАЖБП снижает выраженность цитолиза и дислипидемии [7,8]. Однако еще не было изучено, может ли применение этого препарата уменьшить выраженность стеатоза и фиброза печени.…”

Section: Introductionunclassified

Влияние Курсового Приема L-Орнитин- L-Аспартата На Фиброз И Стеатоз Печени У Больных Ассоциированной С Нарушениями Метаболизма Жировой Болезнью Печени (Неалкогольной Жировой Болезнью Печени), Имеющих Гипераммониемию

Garanina¹

2021

Rossijskij žurnal gastroènterologii, gepatologii, koloproktolog

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Introduction. Hyperammonaemia develops both in cirrhosis and earlier fibrotic stages during metabolic-associated fatty liver disease (MAFLD). Besides neurotropic, ammonia exerts the hepatotoxic and profibrotic effects. L-ornithine-L-aspartate (LOLA) has been proved effective in treatment for hyperammonaemia in cirrhosis patients.Aim. An impact study of the LOLA course therapy on inflammation, steatosis and liver fibrosis biomarkers in MAFLD.Materials and methods. A total of 90 patients were divided between two cohorts. The control cohort included patients with liver steatosis S0–S1, absent liver fibrosis, normal liver function tests, clean history of liver disease, while MAFLD cohort gathered liver steatosis S2–S3 and METAVIR fibrosis F1. Steatosis and fibrosis were assessed with a Fibroscan 502 unit with CAP measurement. All patients had ammonia estimated from whole blood. At high ammonia, LOLA was ordered at 9 g/day for 8 weeks, with control of blood ammonia, AST, ALT, GGT, CRP and ferritin, as well as fibrosis and steatosis post-therapy.Results. The study enrolled 45 patients of the MAFLD and 45 — of control cohort. Hyperammonaemia was revealed in 26 (58 %) MAFLD and 3 (7 %) control patients (p <0.001). MAFLD-hyperammonaemic patients also had the significantly higher male ratio, type 2 diabetes and severer hepatic steatosis rates vs. hyperammonaemia-negative MAFLD individuals. In 8 weeks of LOLA therapy, the ALT, AST, GGT, ferritin and CRP levels decreased significantly, and blood ammonia attained normal range (p <0.001). Elastometry liver stiffness decreased in 22 (85 %) patients, reaching F0 values in 6 cases (p <0.001). The steatosis grade reduced in 18 (69 %) individuals.Conclusion. LOLA normalises blood ammonia levels and reduces the severity of inflammation, steatosis and liver fibrosis.

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Hyperammonium in Patients With Precirrhosis Stage: Clinical Reality?

Cited by 10 publications

References 12 publications

Russian Consensus on “Hyperammonemia in Adults”: The 2021 Version (in English)

Russian Consensus on “Hyperammonemia in Adults”: The 2021 Version (in English)

Increased ammonia levels and its association with visceral obesity and insulin resistance

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