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Unlabelled: Between the sialosis' etiologic agents, we can find the chronic alcoholism and diabetes. Both nosologic entities are described using a similar histopathologic pattern., Objectives: The purpose of this work has been analyzing and comparing the histopathological differences between the diabetic and alcoholic sialosis., Study Design: We studied 7 parotid glands samples of diabetic patients and 4 samples of normal glands obtained from surgical material were used as a control. For the comparative study, we used 12 parotid glands from chronic alcoholic patients with clinical diagnosis of cirrhosis and 6 autopsies on individuals who had died from alcoholic hepatic cirrhosis. This material was fixed in formaline, processed for embedding in paraffin, standard coloration techniques and immunotechnique for cytokeratin EA/1 y EA/3., Results: In the cases of diabetics, the parotid gland was characterised by the presence of small acini, a bigger number of lipid intracytoplasmic droplets in the acinar and ductal cells, as well as an abundant adipose infiltration in the stroma when compared to the alcoholics. We observed that the cytokeratins' expression was heterogeneous at the acinar level, and very positive in the hyperplasic ducts, compared to the alcoholic and control groups., Conclusions: These qualitative valorations indicate the differences between the histopathologic pattern of sialosis with different origins.

The association between the class I and class II histocompatibility antigens (HLA) and the severity of alcoholic liver disease was studied in 102 alcoholic patients (64 males and 38 females) with liver disease. According to histologic diagnosis 41 patients had a mild hepatic lesion (12 with minimum changes, 15 with steatosis and 14 with fibrosis) and 61 patients had severe hepatic lesion (13 with alcoholic hepatitis, 35 with cirrhosis and 13 with cirrhosis and alcoholic hepatitis). No differences were found between the two groups in regards to sex, quantity and length of alcohol consumption, although the patients with mild hepatic lesion were younger than those with severe hepatic lesion (41.2 +/- 8.2 and 47.8 +/- 11.6 years, respectively). The prevalence of the A30, B16, B47, Bw56, Cw1, Cw5 and Cw7 antigens was higher in the alcoholics than in the controls, although only the A30 (12.7% vs. 4.4%, p < 0.04) and the Bw56 antigens (3.9% vs 0.1%, p < 0.001) remained significant when the p value was corrected by the number of antigens studied. These differences were due to a greater prevalence of the A30 antigens (17.0% vs. 4.4%, p < 0.001), B16 (24.3% vs. 7.5%, p < 0.01) and Bw56 (7.3% vs 0.1%, p < 0.001) in patients with mild hepatic lesion versus the controls. In contrast, these antigens were present in similar numbers in patients with severe hepatic lesion and in the controls. On the other hand, no differences were observed regarding the prevalence of the class II HLA antigens between the alcoholics and the controls, or between the two alcoholic groups. These data suggest that the alcoholics with A30, B16 and Bw56 antigens are less susceptible to developing severe liver disease.

A qualitative and quantitative histological analysis of minor salivary glands was carried out in 60 alcoholics and 20 matched control patients. Minor salivary glands biopsies were obtained and samples were processed for conventional light microscopy. A quantitative morphometrical assessment was carried out by counting the number of acinar cells present in an area by means of a squared grid eye piece. Neither hipertrophic nor atrophic responses were found in the quantitative analysis. Histological changes such as acinar degeneration, hyperemia, mononuclear inflammatory and fat infiltration were found in both experimental and control samples. None of these findings reached statistical significance. Eleven adult alcoholics without liver damage (ASD) presented duct dilatation. On the other hand, only 3 adult alcoholics with liver damage (ACD) developed this response. This difference was statistically significant (p = 0.02). Perhaps no difference was found when we compared ASD group with its respective control group (p = 0.699). We could not differentiate if this change was due to alcoholism or another undeterminated factor. At least under the scope of this study, we may conclude that minor salivary glands are scarcely affected by alcoholism even when liver damage has been established.

Morphologic and enzyme induction phenomena changes in the small bowel mucosa produced by excessive alcohol intake were studied. Both aspects may have nutritional repercussions in alcoholic patients. Three groups of patients were included in the study: group I made up of 20 healthy controls, group II with 30 alcoholic patients with active alcohol intake at the time of the study and group III made up of 30 alcoholics following abstinence. The nutritional status, possible existence of associated liver disease, intestinal morphology and the mucosal and serum gamma glutamyltranspeptidase (GGT) levels were evaluated. The morphologic changes observed under the study conditions, with normal levels of ingestion in alcoholic with active alcohol intake, were mild and could be related with the nutritional status and folate deficiency which some presented than being secondary to a direct toxic effect of the alcohol. Moreover, significant increases were observed in the GGT in the intestinal mucosa of alcoholics with active intake (3.97 +/- 1.37 mU/g of tissue) with respect to the control group (1.86 +/- 0.7 mU/g). The changes were rapidly reversible following abstinence and correlated with the changes observed in serum, thus suggesting an enzymatic induction mechanism.

The aim of this study was to look for pathological changes in the oral cavity in a group of 40 non cirrhotic male alcoholics, ranging in age from 30 to 40 years old. These subjects were compared with a group of 40 non alcoholic male subjects of similar age. The presence of lip, dental, periodontal, salivary gland and oral mucosa lesions was recorded. In alcoholics, pigmented lesions were observed in the lips in all the subjects (compared to 36% of controls), in the cheek mucosa in 65% and in the palate mucosa in 35.5%. Sixty five percent of alcoholics were partially edentate (compared to 32.5% of controls). It is concluded that the consideration of oral changes as a whole could be useful in the diagnosis of occult alcoholism. Moreover these patients have an important need of odontological attention that has to be considered.

Alcohol-induced brain damage is known since long, with classical descriptions of lesions. There is no constant correlation between them and any of the clinical presentations of chronic intoxication. New neuroimaging techniques, neuropsychology and basic investigation have supplied with new data. The so-called alcoholic dementia and its possible reversibility are major issues of this problem. This paper reviews radiological, pathological, vascular and neuropsychological studies related to this point.

Multiple symmetric lipomatosis (MSL) is characterised by nonencapsulated localised lipomatous accumules (type I) or diffused (type II). There is a high incidence in Mediterranean males with high alcohol intake. The biochemical blood alterations described are similar to those related to alcoholism or chronic hepatopathy. The disease can be associated with demyelinating peripheric or autonomic neuropathy and in MSL type I with mediastinal findings of 5 patients suffering from MSL type I, comparing them with the cases in the literature and insisting on the participation of alcoholism (early onset, important amount, and long-term habit) in the etiology of MSL and its contribution to the developing of neuropathy and abnormalities of lipidic metabolism.

The authors report on a comparative study of light and electron microscopy in the diagnosis of tissue obtained in 21 percutaneous liver biopsies in patients known to have cirrhosis. Using light microscopy twelve patients were ascertained to have post-necrotic cirrhosis and twelve had Laennec's cirrhosis. All of these patients were given phenobarbital, 65 mg. every twelve hours, during twenty-one days. A control group of five patients received placebos. With electron microscopic methods, in all of the cirrhotic patients both before and after treatment with phenobarbital, the authors observed bands of fibrous tissue made up of collagen fibers and fibroblasts which originate in the portal spaces and in the Kupffer cells. This makes up the mesenchymal reaction to the liver cell damage, which in the long run proves to be more important than liver cell regeneration. Phenobarbital treatment resulted in hyperplasia of the agranular endoplasmic reticulum in liver cells. The authors agree with other authors that this is related to metabolic activity of enzymes acting on extraneous drugs and chemical substances.

A case of toxic liver disease induced by cyanamide in a patient in treatment with this drug during 18 months, is presented. We reviewed the different liver cell alterations produced by a long-term treatment with cyanamide, which produces fibrosis and portal inflammation, as well as polished cells with different characteristic features. These alterations forced the establishing of close controls of patients in treatment with this type of anti-alcoholism drug, as well as the reduction of the duration of therapy, this questioning the efficacy of the treatment of chronic alcoholism with this aversive drug.