PubMed · 16502886
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Tim Emerton. 2005. AOD expertise.. https://pubmed.ncbi.nlm.nih.gov/16502886/
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In utero exposure to alcohol can have numerous adverse effects on a developing fetus. These effects represent a spectrum of structural anomalies and neurocognitive and behavioral disabilities that have recently been termed fetal alcohol spectrum disorders (FASD). Children at the most severe end of this spectrum and displaying the complete phenotype of characteristic facial anomalies, growth retardation and developmental abnormalities of the central nervous system are defined as having fetal alcohol syndrome (FAS). While FAS is the most readily clinically recognized form of FASD, other categories within the continuum of adverse effects due to prenatal alcohol exposure are becoming better defined. These include partial fetal alcohol syndrome (PFAS), alcohol-related birth defects (ARBD) and alcohol-related neurodevelopmental disorder (ARND). As more is learned regarding the exact manifestations of alcohol on brain development, these classifications may be expanded and/or refined. Because FASD represents a major public health concern, early recognition of at-risk children is important for initiating interventional strategies. Thus, the purpose of this report is to educate practicing physicians about the recognizable phenotypes of FASD in order to accurately identify these children and implement the most appropriate management plans.
The influence of ethanol (EtOH) on multiple dendritic cell (DC) subsets, in the steady state or following their mobilization in vivo, has not been characterized. Herein, generation of mouse bone marrow-derived DC (BMDC) in response to fms-like tyrosine kinase 3 ligand was inhibited by physiologically relevant concentrations of EtOH with selective suppression of plasmacytoid (p)DC. EtOH reduced surface expression of costimulatory molecules (CD40, CD80, CD86) but not that of coinhibitory CD274 (B7-H1) on resting or CpG-stimulated DC subsets. Interleukin (IL)-12p70 production by activated DC was impaired. Consistent with these findings, EtOH-exposed BMDC exhibited a reduced capacity to induce naïve, allogeneic T cell proliferation and impaired ability to prime T cells in vivo. DC subsets freshly isolated from EtOH-fed mice were also examined. Liver DC, inherently immature and resistant to maturation, exhibited little change in their low surface cosignaling molecule expression, whereas splenic DC showed reduced expression of surface costimulatory molecules in response to CpG stimulation in vivo. These splenic DC elicited reduced naïve, allogeneic T cell proliferation in vitro, and the stimulatory capacity of resting but not CpG-activated liver DC was reduced by chronic EtOH administration. T cells from animals primed with EtOH-exposed DC produced elevated levels of IL-10 following ex vivo challenge with donor alloantigen. Thus, EtOH impairs cytokine-driven differentiation and function of myeloid DC and pDC in vitro. Hepatic DC from chronic EtOH-fed mice are less affected than splenic DC, which exhibit impaired functional maturation following CpG stimulation. These results indicate a potential mechanism by which alcohol consumption is associated with immunosuppression.
Approximately 20% of medical and surgical patients in hospital have an alcohol use disorder (AUD). Diagnosis of chronic alcohol abuse is performed by specific medical history, examination and validated tests. Biomarkers are a means of diagnosing chronic alcoholism in sedated, intubated and emergency patients. Chronic alcohol consumption damages the central nervous and cardiovascular system, the liver and the immune system. In medical ICUs more than 50% of liver injuries and chronic pancreatitis are due to chronic alcohol abuse. The alcohol withdrawal syndrome is emerging in 25% of AUD patients in intensive care after reduction of sedative drugs. Long term alcohol abuse also leads to cardiac arrhythmias, dilatative cardiomyopathy and hypotonic circulatory dysregulation. Bleeding complications are two-fold increased during and after surgery. Immune suppression results in an increased incidence of infectious complications like pneumonia, wound infection and urinary tract infection. In particular, septic encephalopathy is often misinterpreted as alcohol withdrawal syndrome. Due to the fact that AUD patients show a two to five-fold higher rate of postoperative complications they require increased attention to avoid latency of treatment and the development of multiple organ failure. Prophylaxis in terms of drug therapy or abstinence intervals and brief intervention strategies can help to prevent or ease some of these complications and can decrease the rate of long-term injuries.