Borsanyi S, Blanchard CL. Coronavirus Resource Center. Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy Continue. Twitter Facebook. This Issue. September 3, Steven Borsanyi, M. Blanchard, M. Author Affiliations Baltimore. Access through your institution. Add or change institution. Save Preferences. Privacy Policy Terms of Use. Access your subscriptions. This suggests that cirrhosis of the liver, irrespective of its etiology, may be the predisposing factor that was shared by the patients who had developed sialadenosis.
Initial reports dating back to the s observed that sialadenosis frequently occurred in malnourished and vitamin deficient populations [ 3 , 4 ]. Subsequently, sialadenosis has been associated with eating disorders and diabetes [ 1 , 7 , 28 ] which have significant nutritional interactions.
Since patients with these conditions as well as cirrhosis are likely develop multiple nutritional deficits, malnutrition or related metabolic complications may be the underlying pathophysiologic processes that patients with sialadenosis have in common.
The frequent association between sialadenosis and cirrhosis may also be attributed to the likelihood and possible confounding effect of patients having both liver disease and diabetes. The liver plays an essential role in the metabolic interrelationships and interdependence among glucose, glycogen, and insulin. Hepatocytes convert glucose to amino acids, fatty acids, and glycogen. Destruction of hepatocytes results in a decreased storage of glycogen, increased serum fatty acids, and decreased uptake of glucose by muscles.
This results in hyperglycemia as well as insulin resistance [ 29 ]. As a consequence, diabetes can develop as a complication of cirrhosis, and occurs most frequently in patients with chronic hepatitis C and non-alcoholic fatty liver disease steatohepatitis [ 30 ]. Hemochromatosis is likely to affect the liver and leads to diabetes mellitus because of iron damage to the islet cells [ 31 ]. Conversely, diabetes, particularly type 2, can cause liver disease due to altered metabolism of lipids that leads to an increase in serum lipids resulting in fatty infiltration of the liver non-alcoholic steatohepatitis [NASH].
This condition is similar to alcoholic liver disease and can progress to cirrhosis. Liver disease can also result from the hepatotoxic effects of some oral hypoglycemic drugs [ 31 ]. At the time of this study, however, we did not determine if these transplant candidates also had diabetes. Although the pathogenesis of sialadenosis has not been established, a neuropathic process that affects the autonomic innervation of the salivary glands has been suggested [ 2 , 9 , 32 — 34 ].
This hypothesis is based on ultrastructural analyses of parotid tissue obtained from controls and patients with sialadenosis who had liver disease or diabetes [ 33 ].
Sialadenosis was associated with acinar cells that were twice as large as compared with control specimens. In addition, there was evidence of axonal and myoepithelial cell degeneration with swelling of the axon fibers and vacuolization [ 33 ]. These alterations were similar to the appearance of axons from rats that were exposed to high doses of ethanol [ 35 ].
Axonal abnormalities have also been identified by electron microscopy in diabetic rats [ 36 ]. Autonomic neuropathies develop in patients with alcoholic as well as non-alcoholic liver disease, cirrhosis, and diabetes [ 37 — 39 ].
Nutritional dysfunctions that accompany these diseases, in addition to the eating disorders, may lead to neuropathy of autonomic fibers that innervate the parotid glands.
This concept, first proposed in , [ 40 ] could, therefore, explain the development of sialadenosis in these patients. The diagnostic criterion for sialadenosis in this study was based on visual evidence of bilateral parotid gland enlargement.
Although new technology is available for imaging the salivary glands, it has not been determined that this methodology is useful for the evaluation of sialadenosis in the absence of any structural or functional abnormalities in the glands. The sialadenosis literature appears to have relied primarily on clinical manifestations of sialadenosis, and to ensure the validity of comparisons with the present study, the same diagnostic criteria were applied.
Among 28 liver transplant candidates who had sialadenosis, 17 had non-alcohol-related liver diseases. This suggests that all types of cirrhosis may contribute to the development of sialadenosis. Metabolic derangements resulting in malnutrition are common in cirrhosis and may, therefore, represent the underlying pathophysiologic mechanism for sialadenosis in patients with liver diseases as well as diabetes and eating disorders.
It has been proposed that sialadenosis results from a neuropathic process that involves the autonomic innervation of the salivary glands.
This neuropathy may be a complication of nutritional abnormalities that are frequently associated with sialadenosis. National Center for Biotechnology Information , U.
Journal List Head Neck Pathol v. Head Neck Pathol. Published online Mar James Guggenheimer , 1 John M. Close , 2 and Bijan Eghtesad 3. John M. Author information Article notes Copyright and License information Disclaimer. Corresponding author. Received Jan 29; Accepted Mar This article has been cited by other articles in PMC. Abstract Sialadenosis sialosis has been associated most often with alcoholic liver disease and alcoholic cirrhosis, but a number of nutritional deficiencies, diabetes, and bulimia have also been reported to result in sialadenosis.
Introduction Sialadenosis sialosis is characterized by bilateral enlargement of the parotid glands that is asymptomatic, does not affect salivary gland function, and is not related to any inflammatory or neoplastic process [ 1 , 2 ]. Open in a separate window.
Results Sialadenosis was found in 28 subjects 9. Table 1 Characteristics of the 28 subjects with sialadenosis. Table 2 Features associated with nutritional deficits in end-stage liver disease [ 10 — 20 ]. Generalized malnutrition Reduced nutritional intake Nausea and anorexia Taste disturbances Dietary restrictions Cachexia Muscle wasting Loss of muscle strength Reduced protein synthesis and break down of protein leading to protein loss Loss of protein through drainage of ascitic fluid Increased nitrogen excretion Hypoalbuminemia Zinc deficiency Increased metabolism and energy expenditure Weight loss Reduced body mass index Decline in body cell mass Loss of body fat Generalized malabsorption Impaired absorption of fat soluble vitamins Reduced vitamin storage Increased insulin resistance Increased resistance to growth hormone Decreased hepatic glycogen storage.
Discussion In this study of candidates for liver transplantation, sialadenosis was not significantly related to alcoholic cirrhosis or other underlying liver disease. Conclusions Among 28 liver transplant candidates who had sialadenosis, 17 had non-alcohol-related liver diseases.
References 1. Mandel L, Surattanont F. Bilateral parotid swelling: a review. Peel RL. Diseases of the salivary glands. In: Barnes L, editor. Surgical pathology of the head and neck. New York: Marcel Dekker, Inc; Asymptomatic parotid swelling and isoproterenol.
Gill G. Metabolic and endocrine influences on the salivary glands. Otolaryngol Clin North Am. Alcoholic beer sialosis. J Oral Maxillofac Surg. Mandel L, Hamele-Bena D. Alcoholic parotid sialadenosis. J Am Dent Assoc. Rice DH. Salivary gland disorders. Neoplastic and nonneoplastic. Med Clin North Am.
Histological analysis of parotid and submandibular glands in chronic alcohol abuse: a necropsy study. J Clin Pathol. The effects of ethanol on salivary glands. Alcohol and the gastrointestinal tract. Donaghy A. Issues of malnutrition and bone disease in patients with cirrhosis.
J Gastroenterol Hepatol. Nutrition and chronic liver disease. J Clin Gastroenterol. Martin P, Rosen HR. Liver transplantation. Philadelphia: Saunders Elsevier; DeLegge MH. Nutrition in gastrointestinal diseases. Tessari P. Protein metabolism in liver cirrhosis: from albumin to muscle myofibrils. Nutritional aspects of liver disease and transplantation. Nutrition in liver disease. Pathogenesis and assessment of malnutrition in liver disease. Protein metabolism in alcoholism: effects on specific tissues and the whole body.
Utility of standard nutritional parameters in detecting body cell mass depletion in patients with end-stage liver disease. Liver Transpl. Ghany M, Hoofnagle JH. Approach to the patient with liver disease. New York: McGraw-Hill;
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