PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 7715435

[Alcoholic osteopathy].

M Sarli·H Plotkin·J R Zanchetta
View original source ↗Export metadata ↓

Abstract

Alcohol intake is one of the multiple risk factors for developing osteoporosis. Alcohol has direct toxic effects on osteoblasts which determines lower osteocalcin levels at an early stage, and histomorphometric changes later on. Some authors found not only diminished bone formation in alcoholics, but also increased bone resorption. The effect of alcoholism on calciotropic hormones includes fall of PTH serum levels after an acute or moderate alcohol intake, causing transient hypoparathyroidism. In chronic alcoholism, serum levels of vitamin D and its metabolites are decreased independently of any liver disease, probably related to alcohol influence on enzymatic systems. The mineral homeostasis of alcoholics is affected: hypocalcemia is found in acute intoxication, with hypo or hypermagnesemia. In chronic alcoholism the serum calcium values tend to be normal. Alcohol intake causes multiple endocrine changes that lead to hypogonadism in both sexes. The stimulation of hypothalamus-hypophyseal-adrenal axis contributes to the alcoholic bone disease, because of the adverse effects of corticoids on bone. Caloric and protein malnutrition, in addition to a dissipated life style are additional risk factors for the development of osteoporosis.

Explore related subjects

AlcoholismAnimalsBone DensityEndocrine GlandsEthanolHomeostasisHumansOsteoporosisRatsEnglish AbstractJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Sarli, H Plotkin, J R Zanchetta. 1994. [Alcoholic osteopathy].. https://pubmed.ncbi.nlm.nih.gov/7715435/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2007

How does alcohol impair neuronal migration?

Maternal alcohol consumption during pregnancy can cause serious birth defects, of which fetal alcohol syndrome (FAS) is the most devastating. Recognized by characteristic craniofacial abnormalities and growth deficiency, this condition produces severe alcohol-induced damage in the developing brain. FAS children experience ataxia; deficits in intellectual functioning; and difficulties in learning, memory, problem solving, and attention. Multiple aspects of central nervous system development can be affected by alcohol exposure, but the most striking abnormalities are neuronal and glial migration. Little is known about cellular mechanisms by which alcohol affects the migration of immature neurons. Recently, it has been found that Ca(2+) signaling and cyclic nucleotide signaling are the central targets of the action of alcohol in neuronal cell migration. Most importantly, the aberrant migration of immature neurons caused by alcohol exposure is significantly ameliorated by controlling the activity of these second-messenger pathways. In this Mini-Review, we first describe how alcohol exposure impairs the migration of cerebellar granule cells and then discuss the signaling mechanisms involved.

Alcoholism↗
PubMed2007

The alcoholic lung: epidemiology, pathophysiology, and potential therapies.

Epidemiological evidence gathered only in the past decade reveals that alcohol abuse independently increases the risk of developing the acute respiratory distress syndrome by as much as three- to fourfold. Experimental models and clinical studies are beginning to elucidate the mechanisms underlying this previously unrecognized association and are revealing for the first time that chronic alcohol abuse causes discrete changes, particularly within the alveolar epithelium, that render the lung susceptible to acute edematous injury in response to sepsis, trauma, and other inflammatory insults. Recent studies in relevant animal models as well as in human subjects are identifying common mechanisms by which alcohol abuse targets both the alveolar epithelium and the alveolar macrophage, such that the risks for acute lung injury and pulmonary infections are inextricably linked. Specifically, chronic alcohol ingestion decreases the levels of the antioxidant glutathione within the alveolar space by as much as 80-90%, and, as a consequence, impairs alveolar epithelial surfactant production and barrier integrity, decreases alveolar macrophage function, and renders the lung susceptible to oxidant-mediated injury. These changes are often subclinical and may not manifest as detectable lung impairment until challenged by an acute insult such as sepsis or trauma. However, even otherwise healthy alcoholics have evidence of severe oxidant stress in the alveolar space that correlates with alveolar epithelial and macrophage dysfunction. This review focuses on the epidemiology and the pathophysiology of alcohol-induced lung dysfunction and discusses potential new treatments suggested by recent experimental findings.

Alcoholism↗