# S28.1 CLINICAL FEATURES OF CO-MORBID ALCOHOL DEPENDENCE, ANXIETY AND DEPRESSION {#article-title-2}
Anxiety disorders include a range of conditions including panic disorder, agoraphobia, specific phobias, social phobia, post-traumatic stress disorder, obsessive - compulsive disorder, acute stress disorder and generalized anxiety disorder. This family of anxiety disorders is common, prevalence rates range from ∼9-14% and vary by gender. Importantly, anxiety disorder is a common co-morbidity with alcohol use related problems. Alcohol use problems are prevalent in industrialized countries, with a point prevalence rate of ∼17% in the US general population. This presentation will compare the course of alcohol dependence and anxiety disorders by gender in a sample highly vulnerable to alcohol use problems and anxiety symptoms. Data will come from the Collaborative Study on the Genetics (COGA), a US multisite extended family study of alcoholism. COGA contains more than 2255 families with more than 17,682 individuals. Participants were interviewed using a structured diagnostic interview covering Axis I diagnoses, including Antisocial Personality Disorder. Preliminary findings indicate that subjects with alcohol dependence reported an earlier use of tobacco and marijuana, a higher prevalence anxiety symptoms and an increased prevalence of major depression and PTSD compared to nonalcoholic persons. Interestingly, nonalcoholic COGA subjects reported an earlier age of onset of earlier onset of OCD and social phobia but a later onset of panic and agoraphobia than alcoholic subjects. Persons with alcohol dependence also reported a higher utilization of mental health services. Additional analyses will compare the onset of both alcohol use and anxiety disorders, the severity of both conditions, and the prevalence of other comorbid conditions.
# S28.2 BASIC ASPECTS OF ALCOHOL USE DISORDER COMORBID WITH DEPRESSIVE DISORDER {#article-title-3}
Among several candidates for the common mechanisms in pathophysiology of alcohol use disorders and depression, recent studies suggest that neurogenesis plays an important role in these conditions. We have preciously demonstrated that alcohol influenced neural stem cells (NSCs) function and decreased neurogenesis and that antidepressants rescued the alcohol-induced suppression of neurogenesis. An association between depression and endoplasmic reticulum (ER) stress has been suggested recently. Our in vitro study using NSCs obtained from rat embryos indicated that ER stress decreased neuronal differentiation and that antidepressants changed the expression of GRP78, which might be involved in cell differentiation mechanisms. All these findings suggest that alcohol use disorder and depression have some common underlying mechanisms. The neuro-adaptive changes associated with alcohol exposure involve markers such as BDNF, which promotes neurogenesis. Variations in BDNF levels in the circulation were found to be associated with psychiatric pathologies. Serum levels of BDNF have been reported to decrease in patients with depression and also in alcoholic patients. We have investigated the platelet BDNF release in response to adding antidepressants in vitro using samples of washed platelets prepared from rat blood. BDNF was released from platelet by antidepressant treatment and this release was suppressed by TrkB inhibitor. Ethanol suppressed this effect. These results may point to an involvement of platelet BDNF release dysfunction in the mechanism of serum BDNF decrease suggesting that the alteration of trophic factor function not only in the brain but also in the peripheral blood may be linked to impaired neurogenesis.
# S28.3 ALCOHOL COMORBIDITY IN HEPATIC AND GASTROENTEROLOGICAL DISORDERS {#article-title-4}
Chronic alcohol consumption may cause and/or aggravate multiple diseases within the gastrointestinal tract. Apart from several cancers of the upper aerodigestive tract, liver and colorectum, which will be covered elsewhere, chronic alcohol, abuse is a major cause of gastroesophageal reflux disease, and thus esophagitis. Acute alcohol intoxication can lead to acute gastritis with nausea and vomiting, which can occasionally be the reason of an upper gastrointestinal bleeding. In addition, chronic alcohol abuse can deteriorate small bowel diseases including celiac disease and lactose intolerance by inducing villous atrophy. The liver is by far the most prominent target organ of alcohol-related toxicity and besides pure alcoholic liver disease, concomitant non-alcoholic liver diseases including chronic viral hepatitis B and C, as well as obesity-related chronic liver lesions and iron overload can be worsened by chronic alcohol consumption. Chronic pancreatitis is alcohol-related in the vast majority of cases, and causes substantial morbidity and mortality in severely diseased patients by malnutrition, diabetes mellitus und associated complications. All these conditions have in common that they contribute to the miserable nutritional status of many alcoholics, but also are reversible once alcohol consumption is ceased.
# S28.4 EFFECT OF ALCOHOL COMORBIDITIES IN METABOLISM IN THE CARDIOVASCULAR SYSTEM INCLUDING BLOOD PRESSURE {#article-title-5}
The heart and vascular system are frequently affected by alcohol misuse, with a by-modal dose-dependent cardiovascular effect, which is beneficial at low-dose but detrimental at high-dose. Since ethanol induces systemic and synchronic noxious effects, the frequent presence of alcohol-related comorbidities may increase the final cardiovascular damage. Ethanol induces direct acute and chronic toxic effect either on excitatory and metabolic cells. This effect is mediated by disturbances in [Ca ++] transients, apoptosis, ionic, nutritional, energy, metabolic, immuno-inflammatory and endocrine regulation. The sum of these systemic and local effects induces reversible dysfunction and evolves to permanent structural cardiovascular damage. Chronic liver disease clearly increases the risk to develop alcohol dilated cardiomyopathy. There is direct clinical relationship between alcohol-induced skeletal, neurologic, cardiac and vascular damage. Caloric and protein malnutrition, vitamin (B,C,D,E) deficiencies and oxidative damage increase the risk of left-ventricular dysfunction and arrhythmias. Ionic derangement (K + , Ca ++, P +++ , Mg + +) and dyslipemia, increases the risk of arrhythmia and hypertension. Obesity and diabetes increases the risk of hypertension, cardiac dysfunction and ischemic stroke. Concurrent viral (C virus, HIV) and bacterial infection, as well as tobacco and cocaine consumption increases the risk of alcohol-related cardiovascular damage. Since ethanol has a systemic dose-dependent damaging effect and most pathogenic mechanisms are common to different organs, the presence of other sites of organ damage (liver, brain, muscle) forces to study possible cardiovascular involvement. This cardiovascular damage sometimes is subclinical, and potentially reversible with abstinence. Control of alcohol-related comorbidities is relevant in alcoholism and may decrease the global cardiovascular involvement.
A 52-year-old man was admitted to our hospital because of an abnormal shadow on chest X-ray. Chest computed tomography scan and broncho-fiberscopic examination revealed a tumor at the left main bronchus. The tumor was removed completely by partial resection of the left main bronchus with thoracotomy. Historical finding of the resected specimen revealed a benign pleomorphic adenoma of the bronchus. The postoperative course was un-eventful for 9 years. We reported a rare case of pleomorphic adenoma of the bronchus.
