Differences between radioactive iodine-induced sialadenitis and chronic obstructive parotitis.

The purpose of this study was to clarify the differences in the diagnosis and treatment outcomes between radioactive iodine-induced sialadenitis (RAIS) and chronic obstructive parotitis (COP). The study cohort comprised 47 consecutive patients diagnosed with RAIS and 50 patients with COP. All patients were treated by interventional endoscopy. Clinical, sialography, and endoscopy characteristics and treatment outcomes were compared between the two groups. Compared with the COP group, the RAIS group included more females (male:female ratio 1:8.4 vs 1:2.1; P = 0.011) and had a younger onset age (42 vs 50 years; P = 0.001) and shorter disease duration prior to hospital visit (5.4 vs 34.8 months; P < 0.001). In the RAIS group, sialography revealed obliteration of the main duct (20.4% vs 0%; P < 0.001), non-visualization of the main gland (23.7% vs 0%; P < 0.001), and incomplete contrast filling of the main gland (19.4% vs 6.4%; P = 0.008), which were scarcely observed in the COP group. Endoscopy revealed a higher percentage of duct atresia in RAIS compared to COP (20.4% vs 0%; P < 0.001). During follow-up, a higher percentage of RAIS patients had duct atresia and gland atrophy (49.5% vs 1.1%, P < 0.001). Compared with COP, RAIS more commonly involves younger females and has a shorter disease duration. Atresia of the main duct and atrophy of the gland parenchyma occur more often despite the use of interventional endoscopy.

Incidence and risk factors for radioactive iodine-induced sialadenitis.

BACKGROUND: Radioactive iodine (131I) is one of the treatments of hyperthyroidism and differentiated thyroid carcinoma (DTC). Swelling of salivary glands are one of the possible side effects of this treatment, known as radioactive iodine-induced sialadenitis (RAIS). The prevalence of RAIS varies widely and no specific risk ratio has been established. OBJECTIVES: To determine the incidence of RAIS, analysing the epidemiological data and tumour- and treatment-related factors that may influence the development of the disease. MATERIAL AND METHODS: 197 patients who received radioiodine treatment between 2015 and 2017 were studied (76.6% women). The variables studied were age, gender, weight, height, and body mass index; presence of high blood pressure, dyslipidemia, diabetes, and thyroid diseases; cumulative radioiodine dose, presence of sialadenitis, affected salivary gland, and the time of onset. RESULTS: 14 patients developed sialadenitis (78.6% women), all with DTC. The incidence of sialadenitis was 3.4% overall and 6.3% among DTC patients. Furthermore, we found that higher cumulative radioiodine doses confer a greater risk of developing sialadenitis, with a hazard ratio of 1.009 (p = .001). No association was found between the epidemiologic data studied and sialadenitis. CONCLUSIONS: In this series, a dose-dependent relationship was found between radioiodine treatment and sialadenitis.

Non-ionic iodinated contrast-induced sialadenitis with parotid gland sparing in patient of hepatocellular carcinoma.

61-years-old male patient presented with complain of neck swelling and soreness following contrast-enhanced (CE) CT examination with resolution of symptoms in 36-48 hours. He is diagnosed with hepatitis C virus and hepatocellular carcinoma (HCC); already treated with radiofrequency ablation for HCC. He had already undergone two CECT examinations before he was referred to our institution for disease staging/treatment. He also underwent three triphasic CT scan examinations at our institution during the course of treatment for treatment response and staging. Patient remained undiagnosed up to his fourth CT scan due to inability to relate symptoms with contrast administration. The patient was offered close monitoring on fifth CT exam and ultrasound of neck revealed enlarged and echogenic bilateral submandibular glands, however, thyroid and bilateral parotid glands appear unremarkable. This represents transient iodinated contrast induced sialadenitis with sparing of parotid glands.

A Mouse Model for Dietary Xenosialitis: ANTIBODIES TO XENOGLYCAN CAN REDUCE FERTILITY.

Humans can incorporate the xenoglycan N-glycolylneuraminic acid (Neu5Gc) from the diet into reproductive tissues and secretions. Most humans also have circulating antibodies specific for this dietary xenoglycan. The potential for inflammation induced by incorporated Neu5Gc and circulating anti-Neu5Gc antibodies, termed xenosialitis, has been discussed as a factor influencing several human diseases. Potential effects of xenosialitis on human fertility remain unknown. Here, we investigate possible adverse effects of the presence of Neu5Gc on sperm or endometrium combined with anti-Neu5Gc antibodies in semen or uterine secretions in a mouse model. We use Cmah(-/-) mice, humanized for Neu5Gc deficiency. We find that the viability, migration, and capacitation of sperm with incorporated Neu5Gc are negatively affected when these are exposed to anti-Neu5Gc antibodies. In addition, we find that after copulation, activated uterine neutrophils and macrophages show increased phagocytosis of sperm in the presence of anti-Neu5Gc antibodies via the complement receptor 3 (C3R) and Fcγ I/II/III (Fc receptor). Furthermore, Neu5Gc in endometrial cells combined with the presence of anti-Neu5Gc antibodies alters the receptivity and decidualization of endometrial explants. These studies provide mechanistic insights on how Neu5Gc on sperm and/or endometrium combined with anti-Neu5Gc antibodies in semen and uterine fluid might contribute to unexplained human infertility.

Effect of recombinant human thyroid-stimulating hormone or levothyroxine withdrawal on salivary gland dysfunction after radioactive iodine administration for thyroid remnant ablation.

BACKGROUND: The purpose of this study was to examine the incidence of sialadenitis and xerostomia within a year after radioactive iodine administration for thyroid remnant ablation after preparation with recombinant human thyroid-stimulating hormone (rhTSH) or levothyroxine (LT4 ) withdrawal. METHODS: The study has included 121 patients, divided into 4 groups: group A (rhTSH = 100 mCi), group B (rhTSH = 70 mCi), group C (LT4 withdrawal = 100 mCi), and group D (LT4 withdrawal = 70 mCi). Study outcomes were Summated Xerostomia Inventory score and number of sialadenitis episodes after radioactive iodine administration. RESULTS: Salivary gland dysfunction was reported in 31% and 12% of patients, at the end of months 1 and 12, respectively. There was significantly lower incidence in groups A and B in comparison with groups C and D (p = .002 and .021, respectively). CONCLUSION: The use of rhTSH for preparation of radioactive iodine ablation as opposed to LT4 withdrawal reduces the incidence of salivary gland dysfunction. © 2015 Wiley Periodicals, Inc. Head Neck 38: E227-E230, 2016.

Does tocilizumab contribute to elevation of rheumatoid factor and induction of paradoxical syaloadenitis in rheumatoid arthritis patients?

A 56-year-old woman, treated with tocilizumab (TCZ) for 8 months for severe rheumatoid arthritis (RA), was admitted to the hospital due to the swelling and tenderness of parotid glands. The patient was diagnosed with seropositive erosive RA in 1988, and treated with different disease modifying antirheumatic drugs (DMARDs) that were used together with a low dosage of glucocorticoides, followed by biologic therapy with infliximab and adalimumab which also proved to be inefficient. The patient had an excellent initial response on TCZ therapy. After 8 months, she was presented with an extreme enlargement of parotid glands. Bacterial, viral, and granulomatous diseases were excluded. A spectrum of autoantibodies including anti-Ro and anti-La showed normal values, expect for slightly elevated anti-cyclic citrullinated peptide (anti-CCP) and extreme elevation of the rheumatoid factor (RF) to 10,100 IU/ml. The biopsy of salivary glands was done and histological specimen showed limphoplasmocytic syaloadenitis. Tocilizumab therapy was stopped and the dosage of glucocorticoids and methotrexate (MTX) was raised. After 6 weeks, the patient was in better condition with slightly lower levels of RF (9,010 IU/ml). We hypothesise that in this patient, TCZ stimulated RF hyper production which can induce a paradoxical secondary syaloadenitis in RA.

Sialendoscopy for the management of obstructive salivary gland disease: a systematic review and meta-analysis.

OBJECTIVE: To conduct a systematic review with meta-analysis to determine the efficacy and safety of sialendoscopy in the treatment of obstructive diseases of the salivary glands in adults. DATA SOURCES: MEDLINE, EMBASE, and the Cochrane Library (no lower limit to October 2010). Reference lists were searched for identification of relevant studies. STUDY SELECTION: Prospective or retrospective studies of adult patients treated with interventional sialendoscopy for the management of salivary gland obstruction were selected. Outcome measures included rates of success (symptom-free and absence of residual obstruction), sialadenectomy, and complications. Non-English publications were excluded. DATA EXTRACTION: Two independent review authors screened eligible studies, extracted relevant data, and resolved discrepancies by consensus when applicable. Weighted pooled proportion, 95% confidence intervals, and test results for heterogeneity are reported. DATA SYNTHESIS: Twenty-nine studies were included in the analysis. The weighted pooled proportion of success rates were 0.86 (95% CI, 0.83-0.89) for studies involving 1213 patients undergoing sialendoscopy alone and 0.93 (95% CI, 0.89-0.96) for the 374 patients undergoing sialendoscopy with a combined surgical approach. Outcomes following interventional sialendoscopy for radioiodine-induced sialadenitis were reported in 3 studies, and success rates were variable. Rates of sialadenectomy were low, and few major complications were reported. CONCLUSION: Findings from the present systematic review and meta-analysis suggest that sialendoscopy is efficacious, safe, and gland preserving for the treatment of obstructive major salivary gland disease.

Effect of HAART on salivary gland function in the Women's Interagency HIV Study (WIHS).

OBJECTIVE: To determine the impact of highly active antiretroviral therapy (HAART) on salivary gland function in human immunodeficiency virus (HIV) positive women from the Women's Interagency HIV Study (WIHS). DESIGN: Longitudinal cohort study. SUBJECTS AND METHODS: A total of 668 HIV positive women from the WIHS cohort with an initial and at least one follow-up oral sub-study visit contributed 5358 visits. Salivary gland function was assessed based on a dry mouth questionnaire, whole unstimulated and stimulated salivary flow rates, salivary gland enlargement or tenderness and lack of saliva on palpation of the major salivary glands. MAIN OUTCOME MEASURES: Changes in unstimulated and stimulated flow rates at any given visit from that of the immediate prior visit (continuous variables). The development of self-reported dry mouth (present/absent), enlargement or tenderness of salivary glands (present/absent), and absence of secretion on palpation of the salivary glands were binary outcomes (yes/no). RESULTS: Protease Inhibitor (PI) based HAART was a significant risk factor for developing decreased unstimulated (P = 0.01) and stimulated (P = 0.0004) salivary flow rates as well as salivary gland enlargement (P = 0.006) as compared with non-PI based HAART. CONCLUSIONS: PI-based HAART therapy is a significant risk factor for developing reduced salivary flow rates and salivary gland enlargement in HIV positive patients.

[Sweet's syndrome and phenylbutazone-induced sialadenitis]. / Syndrome de Sweet et sialadénite à la phénylbutazone.

BACKGROUND: Phenylbutazone frequently induces a range of potentially dangerous adverse reactions. We report a case of Sweet's syndrome with sialadenitis induced by phenylbutazone. CASE-REPORT: A 54-year-old woman presented lumbar pains treated with phenylbutazone for three days. Six days later, she exhibited inflammation of the submaxillary and parotid salivary glands, followed by an erythematous, oedematous, pustular and febrile eruption, with failure of antibiotic therapy. Laboratory data showed leukocytosis and neutrophilia, anaemia, an elevated platelet count and liver dysfunction. The infectious and autoimmune tests were negative. The skin biopsy confirmed Sweet's syndrome. Clinical and biological abnormalities resolved on administration of systemic steroids. DISCUSSION: Phenylbutazone-induced sialadenitis is rare and presents unrecognized adverse effects that may be associated with a systemic reaction. In the present case report, Sweet's syndrome met the criteria for drug-induced Sweet's syndrome. There appears to have been a systemic reaction caused by a hypersensitivity mechanism, in the same way as sialadenitis.

Valproic acid-associated sialadenosis of the parotid and submandibular glands: diagnostic and therapeutic aspects.

Sialadenosis has been defined as a non-inflammatory, parenchymatous salivary gland disease causing recurrent, bilateral swelling of the salivary glands. As an adverse drug reaction of valproic acid, sialadenosis is very rare. To our knowledge, it has been reported only once in the world literature to date. We present herein the case of a patient with valproic acid-associated sialadenosis of both the parotid and submandibular glands. This appears to be the first published case of a patient who received surgical treatment. On light and electron microscopy of all the affected salivary glands, granular sialadenosis with predominantly moderate electron-dense secretory cytoplasmatic granules was observed. No relevant degenerative alterations were seen. There was no histological evidence of peripheral neuropathy of the nerve supply, leading to disordered activity of acinar cells by loss of neurosecretory granules. Lateral parotidectomy, performed under neuromonitoring control for safety reasons, is the treatment of choice for chronic recurrent parotitis that does not respond to conservative therapy, particularly if the cosmetic deformity is unacceptable to the patient. If the submandibular glands are involved, partial removal is recommended.

Induction of C-reactive protein, serum amyloid P component, and kininogens in the submandibular and lacrimal glands of rats with experimentally induced inflammation.

The mRNAs for acute-phase proteins and kininogens were found to be increased in the submandibular gland (SMG) and extraorbital and intraorbital lacrimal gland (ELG and ILG) in response to experimentally induced inflammation in rats; i.e., 24 hours after subcutaneous injection of turpentine oil, mRNAs for C-reactive protein (CRP), serum amyloid P component (SAP), and H- and T-kininogens were induced in the SMG, ELG, and ILG of rats, whereas these mRNAs were not detected in the same tissues of normal control rats. The induction of mRNAs for these inflammatory proteins by turpentine oil was preceded by a transient increase in the level of mRNA for tumor necrosis factor-alpha (TNF-alpha) at 6 hours after subcutaneous injection of the oil. This was confirmed by injection of another inflammation inducer, lipopolysaccharide (LPS), which induced the TNF-alpha mRNA in the same way at 6 hours as turpentine oil did. The up-regulation of acute-phase proteins including kininogens in the SMG, ELG, and ILG suggest the existence of a strict defense system in the exocrine glands.

Oral mucosal injury caused by denture cleanser tablets: a case report.

A case of chemical injury to the oral mucosa that resulted in obstructive sialadenitis of the submandibular glands is presented. The injury occurred when a patient chewed, swished, and expectorated an immersion-type denture-cleansing tablet attempting to clean a fixed bridge. The literature is reviewed for similar oral mucosal injury caused by improper use of denture-cleansing products. Suggestions for the prevention of such injuries are made.

Liver injury related to amoxycillin-clavulanic acid: interlobular bile-duct lesions and extrahepatic manifestations.

We report eight cases of liver injury related to amoxycillin-clavulanate. Liver biopsy performed in seven patients revealed varying degrees of injury to interlobular bile ducts in all cases. Lesions included irregularity of the nuclei, vacuolization of the cytoplasm, lymphocytic infiltration, destruction and endothelialization of the bile duct epithelium. Ductopenia was not observed. In two patients liver injury was accompanied by prominent extrahepatic manifestations (acute interstitial nephritis in one and acute lacrimal gland inflammation and sialadenitis with prolonged xerostomia in the other). We conclude that interlobular bile-duct lesions of varying severity are a common feature in liver injury related to amoxycillin-clavulanate. Side effects of the drug include acute interstitial nephritis and sialadenitis.

Production of microliths and sialadenitis in rats by a short combined course of isoprenaline and calcium gluconate.

The relationship between microliths and sialadenitis in man is unclear, so an attempt was made to investigate it experimentally in rats with the use of isoprenaline and calcium gluconate either alone or combined. The acini of the submandibular and parotid glands of rats that were given isoprenaline were enlarged, and degenerate acinar cells were seen, with extravasated secretions in the submandibular gland. Similar changes were seen in the submandibular and parotid glands of rats that were given isoprenaline combined with calcium gluconate; in addition, ductal microliths with regions of atrophic sialadenitis were observed. The results suggest that there is temporary obstruction to the salivary flow after isoprenaline is injected, and in the rats that were also given calcium gluconate some of the stagnant saliva calcified to form microliths, which produced a lasting obstruction and obstructive sialadenitis. This supports the possibility that microliths, which are present in normal salivary glands of man, are a primary etiologic factor in sialadenitis.

[Cytostatic-induced stomatitis]. / Zytostatika-induzierte Stomatitis.

45 patients with oral cancer preoperatively received regional intraarterial chemotherapy (RIAC). All patients developed stomatitis or glossitis limited to the region of cytostatic perfusion. Between 1 and 19 days (median 4 days) after RIAC the tumor was removed by hemiglossectomy, partial resection of the floor of the mouth etc. The tissue alterations induced by chemotherapy in these surgical specimens were analyzed histomorphologically. Stomatitis due to RIAC was characterized by necrosis, ulceration and severe epithelial dysplasia of mucous membranes. Approximately 2 weeks after chemotherapy both the inflammatory changes and the dysplasia had disappeared completely. The differences between spontaneous premalignant dysplasia of the oral cavity and dysplasia induced by RIAC are discussed.

[Sialadenosis of the parotid gland after chronic nicotine use]. / Sialadenose der Glandula parotis nach chronischem Nikotinkonsum.

The effect of chronic nicotine consumption on the morphology of the rat parotid gland was investigated. After nicotine-loading for 90 days with an average serum nicotine concentration of 78 +/- 10 ng/ml a significant increase of acinar cell volume was observed. The acinar cells contained an increased number of enlarged light, immature secretory granules. These findings were confirmed by morphometric analysis. Further an increase of the granular endoplasmatic reticulum, an enlargement of the Golgi complexes and an oedematous swelling of intraglandular autonomous nerves were found. Similar findings have been observed in the parotid gland of animals and also of humans chronically treated with the beta-adrenergic drugs aludrin and isoproterenol, and have been termed "sialadenosis". It seems likely that the observed morphological alterations are caused by a stimulation of glandular beta-adrenoceptors via a nicotine-induced release of catecholamines from the adrenals.