Sialoangiography: x-ray visualization of major salivary glands.
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The benign lymphoepithelial lesion of salivary glands is now considered the histological hallmark of a variety of clinical and pathological disorders affecting salivary tissues. Malignancy arising in the lesion is uncommon, but may take origin in either the epithelial or lymphoreticular components. Lymphomas and pseudolymphomas associated with salivary gland lymphoepithelial lesions have been predominately extra-salivary and strongly correlated with Sjögren's syndrome. Epithelial malignancy has not been associated with autoimmunity and with few exceptions has been of the anaplastic type. This report presents two patients with intra-salivary lymphomas arising in a benign lymphoepithelial lesion of salivary glands and a patient with anaplastic carcinoma arising in the epithelial islands of the lesion. The fourth patient manifested pseudolymphomatous lymphoreticular hyperplasia in lung and submandibular gland and illustrates the possible multiple organ involvement that may occur in patients with benign lymphoepithelial lesion, even without clinical evidence of concommitant autoimmune disorders.
Fine-needle aspiration cytology has been used as a routine diagnostic instrument in patients with salivary gland lesions during 1966-1972. A retrospective analysis of the primary cytologic reports correlated with the revised final diagnoses in 461 patients where a pathologic report is available, shows exact agreement in 63 percent, good and not misleading agreement in a further 18 percent, while false reports were initially given in 8 percent, and unsatisfactory specimens were obtained in 11 percent of the patients. On revision of the false reports it is found that with the present experience acquired over several years these can be reduced to under 5 percent. This analysis has also given indications upon which types of specimens are likely to cause diagnostic difficulties.
Between January 1, 1973, and December 31, 1988, the authors or their associates performed 552 fine-needle aspiration biopsies on patients with clinically significant masses of the salivary glands. All patients presented at the Medical College of Virginia Hospitals or Clinics of Virginia Commonwealth University; they were followed for periods ranging from 1 to 16 years. When available, the fine-needle aspiration diagnoses were correlated with histologic diagnoses and long-term patient outcomes. The sensitivity for a neoplasm was 93.3%; the specificity for the absence of a neoplasm was 99%. Diagnostic efficiency was 96.4%, and predictive value of a positive aspiration for a neoplasm was 98.3%. With fine-needle aspiration, surgical excision of salivary gland masses is often unnecessary. In patients with primary and metastatic neoplasms involving the salivary glands, fine-needle aspiration aids the surgeon in mapping the extent of the surgical procedure and in preoperatively preparing the patient. The procedure is cost-effective.
The pathogenesis of peritonsillar abscess is described in textbooks as being a direct communication and progression of acute exudative tonsillitis. Little study has been done on the true etiology and pathogenesis of peritonsillar abscess. This paper focuses on the pathogenesis of peritonsillar abscess. A group of salivary glands (Weber's glands) proven to be located in the supratonsillar space have been shown to be implicated in the pathogenesis of peritonsillar abscess. A review of peritonsillar abscess has been undertaken, and evidence has been presented to support the premise that the true cause for peritonsillar abscess is not necessarily an extension of an acute exudative tonsillitis, but an abscess formation of Weber's salivary glands in the supratonsillar fossa.
The three most common known causes of salivary gland dysfunction are medication usage, radiation therapy and Sjogren's syndrome. Current therapeutic options to treat salivary dysfunction are limited. Clinical considerations as well as the outlook for individuals experiencing salivary dysfunction are discussed.
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A modification of the swab method for sialometry is described. The individual secretions from the right parotid gland, left parotid gland and both submandibular glands together were collected, by use of cotton swabs after submaximal stimulation by citric acid. Five evaluation parameters and their normal ranges and variances are described from a material of 150 control individuals without sign of salivary gland impairment. The measurement is performed within five minutes, it is simple and convenient both for the patient and the staff. Therefore the method described is well suited for routine clinical use.
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In addition to its potent antileukemic properties, cyclocytidine has a sialogogue action that depends on stimulation of beta adrenergic ereceptors of salivary glands. Furthermore, when chronically administered (for 3 days), cyclocytidine caused enlargement of parotid and submaxillary glands and heart that resembled the hypertrophy caused by chronic isoproterenol administration. The salivas evoked by cyclocytidine also closely resembled those evoked by isoproterenol, and were extremely viscous, and high in K+, (121 plus or minus 5.6, for submaxillary, and 42 plus or minus 2.9, for parotid), low in flow rate (0.007 mg/min times mg) and parotid saliva contained high concentrations of amylase (805 plus or minus 33 mg/mg gland). Cyclocytidine also caused marked emptying of parotid gland amylase. The cyclocytidine-induced salivary flow and gland emptying of amylase were prevented for 90 min when propranolol (but not dibenzyline or atropine) was administered prior to injection of the cyclocytidine. In addition, when the superior cervical ganglion was acutely removed, administration of cyclocytidine elicited salivary flow from the denervated as well as the innervated glands. These findings suggest that cyclocytidine does not affect salivary glands through indirect central or ganglionic actions. Cyclocytidine action does not exclusively involve beta receptors, since even in the presence of propranolol, secretory flow was evident after 90 min but when dibenzyline was given with the propranolol, complete blockade of cyclocytidine-stimulated saliva was effected. The dominant effect is, however, a beta adrenergic one. The undesirable side effects of cyclocytidine (parotid pain, postural hypotension, and cardiac hypertrophy) probably stem chiefly from its beta adrenergic properties and might be eliminated (or at least modified) by administration of propranolol with the cyclocytidine.
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