Impairment of bone mass development in children with chronic cholestatic liver disease

Taveira, Adriana Távora de Albuquerque; Fernandes, Maria Inez Machado; Galvão, Lívia Carvalho; Sawamura, Regina; Vieira, Enaldo de Mello; Paula, Francisco José Albuquerque de

doi:10.1111/j.1365-2265.2007.02765.x

Cited by 25 publications

(25 citation statements)

References 35 publications

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“…We observed a strong association between bone mass and serum IGF-I levels in a previous study of cholestatic children (8). The present data support these data indicating that the persistent reduction of hepatic IGF-I produc-tion seems to be a factor that perpetuates the impairment of bone mass development in cholestasis.…”

Section: Discussionsupporting

confidence: 81%

“…We recently observed that, even in the early stage of chronic cholestatic disease (CCD), bone mass development is impaired in children (8). However, the design of the previous study was cross-sectional and therefore unsuitable for evaluating the evolution of bone mass of patients with this disease.…”

Section: Introductionmentioning

confidence: 89%

“…The etiopathogeny of hepatic osteodystrophy is not fully understood. During the terminal phase of slowly progressive liver disease, hepatic osteodystrophy is the result of a set of factors that are being incorporated along the process of declining hepatic function (2,18): a) nutritional factors (anorexia, weight loss, changes in body composition, and vitamin D deficiency) (18); b) hormonal factors (hypogonadism (18), vitamin D (17) and IGF-I deficiencies (8,18); c) metabolic alterations typical of hepatic insufficiency (acidbase disequilibrium, disorders of intermediate metabolism, and cholestasis) (18), and d) inflammatory state (production of cytokines and interleukins) (19). The present study shows Figure 1.…”

Section: Discussionmentioning

confidence: 99%

“…In our first study conducted in 2004-2005, we evaluated 36 children and adolescents, 13 of them with CCD (77% with low bone mass) and 23 controls (8). Of the 23 control subjects, 10 moved to other addresses.…”

Section: Methodsmentioning

confidence: 99%

“…Low BMD was defined using the criteria of the International Society of Clinical Densitometry, i.e, a Z-score of -2.0 or less adjusted for age and gender (14). Bone age was determined by the method of GraulichPyle, as described (8).…”

Section: Methodsmentioning

confidence: 99%

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Longitudinal evaluation of hepatic osteodystrophy in children and adolescents with chronic cholestatic liver disease

Taveira

Pereira

Fernandes

et al. 2010

Braz J Med Biol Res

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Longitudinal evaluation of hepatic osteodystrophy in children and adolescents with chronic cholestatic liver disease

Taveira

Pereira

Fernandes

et al. 2010

Braz J Med Biol Res

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Reduced Serum IGF-1 Associated With Hepatic Osteodystrophy Is a Main Determinant of Low Cortical but Not Trabecular Bone Mass

Liu

Han

Werner

et al. 2017

Journal of Bone and Mineral Research

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Hepatic osteodystrophy is multifactorial in its pathogenesis. Numerous studies have shown that impairments of the hepatic growth hormone/insulin-like growth factor-1 axis (GH/IGF-1) are common in patients with non-alcoholic fatty liver disease, chronic viral hepatitis, liver cirrhosis, and chronic cholestatic liver disease. Moreover, these conditions are also associated with low bone mineral density (BMD) and greater fracture risk, particularly in cortical bone sites. Hence, we addressed whether disruptions in the GH/IGF-1 axis were causally related to the low bone mass in states of chronic liver disease using a mouse model of liver-specific GH-receptor (GHR) gene deletion (Li-GHRKO). These mice exhibit chronic hepatic steatosis, local inflammation, and reduced BMD. We then employed a crossing strategy to restore liver production of IGF-1 via hepatic IGF-1 transgene (HIT). The resultant Li-GHRKO-HIT mouse model allowed us to dissect the roles of liver-derived IGF-1 in the pathogenesis of osteodystrophy during liver disease. We found that hepatic IGF-1 restored cortical bone acquisition, microarchitecture, and mechanical properties during growth in Li-GHRKO-HIT mice, which was maintained during aging. However, trabecular bone volume was not restored in the Li-GHRKO-HIT mice. We found increased bone resorption indices in vivo as well as increased basal reactive oxygen species and increased mitochondrial stress in osteoblast cultures from Li-GHRKO and the Li-GHRKO-HIT compared with control mice. Changes in systemic markers such as inflammatory cytokines, osteoprotegerin, osteopontin, parathyroid hormone, osteocalcin, or carboxy-terminal collagen cross-links could not fully account for the diminished trabecular bone in the Li-GHRKO-HIT mice. Thus, the reduced serum IGF-1 associated with hepatic osteodystrophy is a main determinant of low cortical but not trabecular bone mass.

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Osteoporosis and Hepatic Steatosis: 2 Closely Related Complications in Short‐Bowel Syndrome

Parreiras-e-Silva

Araújo

Elías

et al. 2020

J Parenter Enteral Nutr

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Background Osteoporosis has scarcely been prospectively investigated in short‐bowel syndrome (SBS). This prospective study was designed to evaluate incretins, adipokines, bone mass, and lipid deposits from marrow adipose tissue (MAT), visceral adipose tissue (VAT), subcutaneous adipose tissue (SAT), and liver (IHLs). Methods The study comprised 2 groups matched by gender, height, and age: the control group (CG) (9 males, 9 females) and the SBS group (SBSG) (6 males, 5 females). The SBSG was evaluated twice in an interval of 1 year (SBSG0 and SBSG1). The biochemical evaluation included incretins, leptin, and adiponectin. Dual‐energy x‐ray absorptiometry and magnetic resonance were, respectively, used to measure BMD and lipid deposits. Results Bone mineral density (BMD) was lower in the SBSG than in the CG, but there was no difference between SBSG0 and SBSG1. There was no difference in MAT, SAT, and VAT, but IHL was lower in CG than in SBSG0 and SBSG1. A negative correlation between MAT and third lumbar vertebrae BMD was found in the CG but not in SBSG0 or SBSG1. There was a negative association between IHL and bone mass considering all participants (CG and SBSG0) (R2 = 0.38; P < .05). Conclusion Appropriate nutrition assistance recovers body composition, reverts the relationship of bone mass and MAT, and mitigates bone loss in SBS. In spite of this, osteoporosis seems to be an early and persistent complication in SBS. Curiously, SBS seems to be a highly vulnerable condition for the development of hepatic steatosis and shows an association between bone mass and IHL.

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Impairment of bone mass development in children with chronic cholestatic liver disease

Abstract: These results indicate that CCLD limits bone mass gain in children. A reduction in hepatic IGF-1 production might be responsible, at least in part, for the low bone mass of these patients.

Cited by 25 publications

References 35 publications

Longitudinal evaluation of hepatic osteodystrophy in children and adolescents with chronic cholestatic liver disease

Longitudinal evaluation of hepatic osteodystrophy in children and adolescents with chronic cholestatic liver disease

Reduced Serum IGF-1 Associated With Hepatic Osteodystrophy Is a Main Determinant of Low Cortical but Not Trabecular Bone Mass

Osteoporosis and Hepatic Steatosis: 2 Closely Related Complications in Short‐Bowel Syndrome

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