The risk factors for hepatic steatosis in patients with primary aldosteronism

Shibayama, Yuki; Wada, Norio; Baba, Shuhei; Obara, Shin’ya; Sakai, Hiromu; Usubuchi, Hiroaki; Terae, Satoshi; Nakamura, Akinobu; Atsumi, Tatsuya

doi:10.1507/endocrj.ej19-0600

Cited by 7 publications

(4 citation statements)

References 32 publications

(29 reference statements)

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“…The remaining 783 records were screened further in titles and abstracts and 85 candidates were subsequently examined in full text for eligibility. After exclusion of studies using overlapped samples or lacking sufficient data, 21 articles 13 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 remained eligible and successfully incorporated into the meta‐analysis. A detailed flow chart of study selection is displayed in Figure 1 .…”

Section: Resultsmentioning

confidence: 99%

Meta‐analysis of blood parameters related to lipid and glucose metabolism between two subtypes of primary aldosteronism

Zhu

2022

J of Clinical Hypertension

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It remains unclear whether metabolic profiles differ within the subtypes of primary aldosteronism (PA). This meta‐analysis aimed to compare the blood parameters related to lipid and glucose metabolism at baseline between unilateral PA and bilateral PA. A search was performed using PubMed, Web of Science, and Sciencedirect databases, supplemented by hand‐searching of related references. Standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated for each parameter. Twenty‐one studies involving 4197 patients with PA were included. Compared with bilateral PA groups, unilateral PA groups demonstrated significantly lower low‐density lipoprotein cholesterol (LDL‐C, SMD: −.14 mmol/L, 95% CI: −.20, −.07), total cholesterol (TC, SMD: −.16 mmol/L, 95% CI: −.23, −.09), triglyceride (TG, SMD: −.22 mmol/L, 95% CI: −.29, −.16), fasting blood glucose (FBG, SMD: −.11 mmol/L, 95% CI: −.18, −.04), hemoglobin A1c (HbA1c, SMD: −.21%, 95% CI: −.30, −.13), and homeostasis model assessment‐insulin resistance (HOMA‐IR, SMD: −.40, 95% CI: −.58, −.23). No significant difference was found in high‐density lipoprotein cholesterol (HDL‐C) level between the two groups (SMD: .40 mmol/L, 95% CI: −.02, .11). To sum up, comparison of several blood metabolic parameters between the two subtypes suggested that the bilateral PA may associate with a higher prevalence of impaired glucose and lipid metabolism than unilateral PA; however, results should be treated with caution. Additional well‐designed studies are needed to prove the present results and better elucidate the link between metabolic abnormalities and etiologies of each PA subtype.

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Section: Resultsmentioning

confidence: 99%

Meta‐analysis of blood parameters related to lipid and glucose metabolism between two subtypes of primary aldosteronism

Zhu

2022

J of Clinical Hypertension

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“…156 Activation of the mineralocorticoid receptor by aldosterone leads to impaired insulin sensitivity in skeletal muscle and adipocytes by stimulation of inflammatory and oxidative stress metabolic pathways 157,158 . PA has been reported to increase the risk of metabolic syndrome and NAFLD [159][160][161] . Thus, there may be merit in screening patients with PA for NAFLD.…”

Section: Miscellaneousmentioning

confidence: 99%

Pathophysiology of NASH in endocrine diseases

Gariani¹,

Jornayvaz

2021

Endocrine Connections

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Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the industrialized world. NAFLD encompasses a whole spectrum ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and cirrhosis. The latter can lead to hepatocellular carcinoma. Furthermore, NASH is the most rapidly increasing indication for liver transplantation in western countries and therefore represents a global health issue. The pathophysiology of NASH is complex and includes multiple parallel hits. NASH is notably characterized by steatosis as well as evidence of hepatocyte injury and inflammation, with or without fibrosis. NASH is frequently associated with type 2 diabetes and conditions associated with insulin resistance. Moreover, NASH may also be found in many other endocrine diseases such as polycystic ovary syndrome, hypothyroidism, male hypogonadism, growth hormone deficiency or glucocorticoid excess, for example. In this review, we will discuss the pathophysiology of NASH associated with different endocrinopathies.

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“…Активація альдостероном мінералокортикоїдного рецептора призводить до порушення чутливості до інсуліну в скелетних м'язах і адипоцитах через стимуляцію метаболічних шляхів запалення та окисного стресу. Встановлено, що ПА підвищує ризик метаболічного синдрому та НАЖХП, що може бути корисним при скринінгу пацієнтів з ПА на НАЖХП [49].…”

Section: ендокринні причини неалкогольного стеатогепатитуunclassified

Non-alcoholic steatohepatitis in patients with endocrine pathology. Review

Tkach¹,

Чеверда²

2021

CE&ES

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Non-alcoholic steatohepatitis (NASH) is a subtype of non-alcoholic fatty liver disease (NAFLD), which in the absence of treatment can progress to the development of cirrhosis and hepatocellular carcinoma, as well as to increased mortality associated with these diseases. The main risk factors for the development of NAFLD and NASH are the presence of insulin resistance and obesity. Quite often NAFLD and NASH are associated with so-called extrahepatic manifestations, such as obstructive sleep apnea, hypertension, dyslipidemia, intestinal dysbiosis, genetic predisposition, sedentary lifestyle and consumption of certain foods. However, NAFLD and NASH are also associated with some endocrine diseases and conditions, including type 2 diabetes, polycystic ovary syndrome, hypothyroidism, male hypogonadism, growth hormone deficiency or excess, hypercortisolism, vitamin D or prolactin deficiency. In many of these diseases, the key pathophysiological mechanism is insulin resistance. This review considers the putative pathophysiological mechanisms that play an important pathogenetic role in the development of NASH in these endocrine disorders.Unfortunately, our understanding of the pathophysiology of NAFLD in various endocrinopathies is far from complete. In addition, the natural course of NAFLD due to endocrine disorders compared to the course and consequences of “primary” NAFLD is still poorly understood. Therefore, in the coming years, further research into the pathophysiology and clinical features of NASH will be important to better understand the relationship between different endocrinopathies and NAFLD, which will help improve the treatment of this pathology.

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The risk factors for hepatic steatosis in patients with primary aldosteronism

Cited by 7 publications

References 32 publications

Meta‐analysis of blood parameters related to lipid and glucose metabolism between two subtypes of primary aldosteronism

Meta‐analysis of blood parameters related to lipid and glucose metabolism between two subtypes of primary aldosteronism

Pathophysiology of NASH in endocrine diseases

Non-alcoholic steatohepatitis in patients with endocrine pathology. Review

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