Secondary Osteoporosis

Emkey, Gregory R.

doi:10.1016/b978-0-12-801238-3.65820-8

Cited by 3 publications

(3 citation statements)

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“…Uzimajući u obzir prethodno navedeno, adekvatna i pravovremena terapija hepatičkih poremećaja mogla bi da ima pozitivan efekat na usporavanje progresije mikrostrukturnih oštećenja kosti kod ACJ pacijenata. Etiopatogenetski mehanizmi oštećenja kosti u alkoholnoj cirozi jetre Sekundarna osteoporoza, kao sistemsko oštećenje kosti poznatog uzroka, značajna je komplikacija pacijenata sa ACJ (45). Mehanizmi na kojima počiva razvoj osteoporoze kod bolesnika sa hroničnim bolestima jetre, a pogotovu kod bolesnika sa ACJ, još uvek su, međutim, nedovoljno rasvetljeni.…”

Section: Mineralna Gustina Kostiju U Alkoholnoj Cirozi Jetreunclassified

“…Mehanizmi na kojima počiva razvoj osteoporoze kod bolesnika sa hroničnim bolestima jetre, a pogotovu kod bolesnika sa ACJ, još uvek su, međutim, nedovoljno rasvetljeni. Etiopatogeneza skeletnog oštećenja se najčešće opisuje poremećajem procesa remodelovanja kosti, usled čega se resorpcija odvija brže od stvaranja kosti, pa se masa koštanog tkiva smanjuje uslovljavajući nastanak osteopenije/ osteoporoze (45). Većina vodećih naučnih timova smatra da etiopatogenetski mehanizmi gubitka kosti mogu biti varijabilni kod hroničnih oboljenja jetre različitih uzroka (9,16).…”

Section: Mineralna Gustina Kostiju U Alkoholnoj Cirozi Jetreunclassified

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Compromised bone strength in patients with alcoholic liver cirrhosis

Jadžić¹,

Đonić²

2020

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Osteoporoza i/ili osteopenija su česte komplikacije alkoholne bolesti jetre, sa posebnim značajem u njenom ireverzibilnom stadijumu (engl. alcoholic liver cirrhosis – ALC). U ovoj publikaciji je predstavljen pregled savremene literature o učestalosti osteoporoze, povećanom riziku od preloma kosti, promenama mineralne gustine i mikrostrukture kostiju, kao i o etio-patogenetskim mehanizmima koji dovode do smanjenja kvaliteta kosti kod pacijenata sa ALC-om. Zabeleženo je da osteoporoza može biti prisutna kod značajnog broja ALC bolesnika, naročito u slabinskom delu kičmenog stuba. Identifikovano je više faktora rizika, kao i etio-patogenetskih mehanizama povezanih sa gubitkom mineralne gustine kosti kod bolesnika sa alkoholnom i cirozama druge etiologije. Određeni autori tvrde da je dominantan mehanizam gubitka koštane mase usporeno osteoblastno stvaranje kosti, dok drugi rezultati sugerišu pojačanu razgradnju koštanog matriksa kao dominantniji mehanizam u nastanku skeletnih oštećenja kod ALC bolesnika. Povećana koštana fragilnost i sklonost ka patološkim prelomima značajno utiču na životni vek i kvalitet života pacijenata sa ALC-om. Stoga se preporučuje da osteološki skrining i procena rizika od frakture budu obavezni deo individualnog pristupa lečenju bolesnika sa alkoholnom cirozom jetre.

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Section: Mineralna Gustina Kostiju U Alkoholnoj Cirozi Jetreunclassified

Compromised bone strength in patients with alcoholic liver cirrhosis

Jadžić¹,

Đonić²

2020

Medicinski podmladak

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“…The mechanisms underlying the etiopathogenesis of bone changes in patients with alcoholic liver cirrhosis (ALC) are complex and still insufficiently understood. ALC‐induced skeletal damage is often described as a disorder of the bone remodeling process, which leads to a decrease in bone mass and mineral density (Culafić et al, 2014; López‐Larramona et al, 2013), thereby reducing bone strength and increasing fracture risk (Emkey, 2018; Otete et al, 2018). However, little is known as to whether increased bone resorption or decreased bone formation has a dominant role in the etiopathogenesis of ALC‐induced bone loss.…”

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confidence: 99%

The altered osteocytic expression of connexin 43 and sclerostin in human cadaveric donors with alcoholic liver cirrhosis: Potential treatment targets

et al. 2022

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Previous studies suggested that osteocyte lacunar network disruption could play a role in the complex pathophysiology of bone changes in aging and disease. Considering that particular research interest is lacking, we aimed to assess alcoholic liver cirrhosis (ALC)–induced changes in osteocyte lacunar network and bone marrow adiposity. Immunohistochemistry was conducted to assess changes in the micro‐morphology of osteocyte lacunar network and bone marrow adiposity, and expression of connexin 43 and sclerostin in vertebral and femoral samples collected from 40 cadaveric men (age range between 44 and 70 years) divided into ALC group (n = 20) and control group (n = 20). Furthermore, the assessment of the potential association between bone changes and the severity of the hepatic disorder (given by Knodell's pathohistologic scoring) was conducted. Our data revealed fewer connexin 43‐positive osteocytes per vertebral and femoral bone area (p < 0.01), suggesting defective signal transduction among osteocytes in ALC individuals. Moreover, we found an ALC‐induced increase in the number of adipocytes in the vertebral bone marrow (p = 0.038). Considering significant associations between the severity of liver tissue disturbances and impaired functionality of osteocyte lacunar network (Pearson's correlation analyses, p < 0.05), we may assume that timely treatment of the liver disease may delay bone impairment. ALC induced an increase in osteocytic sclerostin expression (p < 0.001), suggesting its role in mediating low bone formation among ALC individuals. Hence, medicaments targeting low bone formation may be beneficial to attenuate the bone changes among ALC patients. However, future clinical studies are required to verify the therapeutic utility of these findings.

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