ArticleEndocrine connections2014
Liver status in congenital, untreated, isolated GH deficiency.
Article in Endocrine connections, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Adult Growth Hormone Deficiency and Metabolic Dysfunction-Associated Steatotic Liver Disease.Current obesity reports · 2026Review
- The distinct hepatic metabolic profile and relation with impaired liver function in congenital isolated growth hormone-deficient rats.Endocrine connections · 2024Article
- Relationship between the Stimulated Peak Growth Hormone Level and Metabolic Parameters in Children with Growth Hormone Deficiency.Ewha medical journal · 2023Article
- The state of Sergipe contribution to GH research: from Souza Leite to Itabaianinha syndrome.Archives of endocrinology and metabolism · 2022Review
- Disruption of the GHRH receptor and its impact on children and adults: The Itabaianinha syndrome.Reviews in endocrine & metabolic disorders · 2021Review
- Growth Hormone Deficiency: Health and Longevity.Endocrine reviews · 2019Review
- Article
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
Abstract
Nonalcoholic fatty liver disease (NAFLD) is known to be associated with insulin resistance, atherosclerosis, and low serum IGF1 levels. We have described a large cohort of patients with isolated GH deficiency (IGHD) due to the c.57+1G→A mutation in the GHRH receptor gene. These subjects have increased insulin sensitivity (IS), delayed atherosclerosis, and normal longevity. We hypothesized that, despite visceral obesity, NAFLD would be absent or mild due to the increased IS. To assess the prevalence and severity of NAFLD in adult subjects with lifetime, congenital, untreated IGHD, we studied 22 IGHD adults and 25 controls (COs) matched for age and sex. NAFLD was assessed by a comprehensive liver function panel, and ultrasonographic pattern (hyperechogenic pattern, HP) coded as follows: 0, absent; 1, mild; 2, moderate; and 3, severe. Compared with COs, IGHD individual had lower serum IGF1 (P<0.0001), higher total cholesterol (P=0.027), lower prothrombin time (P=0.017), and similar activated partial thromboplastin time and fibrinogen values. Alanine transaminase (ALT) values were similar in the two groups, but aspartate transaminase was higher in IGHD (P=0.013). However, more IGHD subjects (7/22) than COs (3/23) had ALT above the upper limit of normal (P=0.044). The prevalence of NAFLD was higher in IGHD than COs (61 vs 29%, P=0.032), and the HP score was higher in IGHD than COs (P=0.041), but severe NAFLD was not observed in any IGHD (or CO) individual. Liver HP score is increased in lifetime, untreated, congenital IGHD, but the increase in transaminases is mild, suggesting a lack of advanced forms of NAFLD.
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