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SALIVARY GLANDS - ENDOCRINE ISSUES JUNE 1999
Diabetic sialosis is a persistent non-inflammatory bilateral painless
soft symmetric hypertrophy of the parotid glands, with infrequent
involvement of the submandibular salivary glands. A diabetic autonomic
neuropathy leads to impairment of salivary gland protein secretion
and synthesis. Intracellular zymogen (an amylase precursor) granule
engorgement results and causes the acinar hypertrophy that leads
to parotid enlargement. Parotid hypertrophy can also originate from
an increased fatty deposition secondary to diabetic disturbances
in lipid metabolism and hyperlipidemia.
The thyroid is often implicated in Sjogren's syndrome (SS), a chronic
autoimmune exocrinopathy of the lacrimal and salivary glands. With
the onset of xerophthalmia and xerostomia, a diagnosis of primary
SS is made. Secondary SS occurs when another connective tissue disease
(rheumatoid arthritis, lupus erythematosus etc) is present. Besides
a clinical history, diagnosis is based upon serologic evidence,
histologic examination of labial salivary glands, volumetric and
chemical evaluation of tears and saliva, and sialography. Serum
studies testify to the presence of characteristic antibodies - RF,
ANA, anti-SSA, anti-SSB. Labial salivary glands demonstrate a significant
lymphocytic infiltration. Decreased tear and salivary volumes (both
measurable) are accompanied by changes in their chemistry. Sialographically,
the abnormal pattern (sialectasis) is pathognomonic. Approximately
45-50% of patients with SS have subclinical evidence of hypothyroidism
while 24% of patients with some form of autoimmune thyroid disease
have a subclinical SS. Hashimoto's thyroiditis represents the usual
thyroid entity associated with SS. Not uncommonly, both SS and Hashimoto's
are prey to the development of a MALT lymphoma.
Following
surgery, therapeutic management of most thyroid cancers includes
radioactive iodine 131I, a radioisotope
with an affinity for thyroid tissue. After diagnostic scanning and
thyroid ablation with 131I, eradication
of residual carcinoma in the thyroid bed or in metastatic locations
is accomplished with elevated doses of 131I.
Unfortunately, normal salivary glands (particularly the parotid)
also selectively concentrate the 131I
and thereby suffer the sequelae of radiation. Immediate transient
parotid gland swelling and pain are to be expected. However, permanent
injury and a clinically persistent sialadenitis is not an unexpected
result.
Propylthiouracil therapy for hyperthyroidism prevents the organification
of iodine for thyroid hormone synthesis. The resulting elevated
serum iodide is actively secreted by the salivary glands. A work
hypertrophy with enlarged parotids can develop.
An increase in circulating progesterone and estrogen (pregnancy)
can be associated with sialorrhea. These hormones decrease lower
esophageal sphincter contractility. Gastric reflux occurs. The acids
cause esophageal irritation (heartburn). Effective clearance of
the acids is a protective function of the esophagosalivary reflex
mediated thru the vague. Sialorrhea results and serves to neutralize
the acids, ravage the esophageal wall and discourage esophageal
disease.
The Salivary Gland Center (SGC) was developed because a void existed
in the diagnostic and comprehensive care of patients with salivary
gland problems and/or secretory dysfunction. Since the diversity
of these salivary conditions presents challenges to the clinician,
the SGC is available for referrals.
Louis Mandel, DDS
Director, Salivary Gland Center
(212) 305-9982
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