Owing to the use of iodine-containing intravenous contrast agents, sialadenitis rarely occurs with a sudden expansion of the salivary glands. Contrast-induced sialadenitis (iodide mumps) was first described in 1956. The actual incidence is unknown, and fifty-two cases have been reported until 2015. Its pathogenesis is uncertain, but it appears to be the result of an idiosyncratic reaction or accumulation of iodine in the ductal system of the salivary gland ( 1 , 2 ). In this article, we aimed to present a case of contrast-induced sialadenitis after an iodine-containing contrast agent.

Case Presentation Ad i i A sixty-six-year-old male with a history of the abdominal aortic aneurysm was referred for Computed Tomography (CT) angiography. The patient had long-term arterial hypertension and chronic renal failure (stage 2 chronic kidney disease). Before this administration, he had a contrast-enhancement CT evaluation twice within 5 years. He had no history of allergy before. CT angiography of thoracic and abdominal aorta was performed by 90cc Iopromide (Ultravist300,ScheringAG, Germany), a non-ionic low-osmolar contrast material containing about 300mg iodine/ml. No adverse effects were experienced during administration and the stay at the radiology department. Around 8-10 hours after administration, the patient had referred to emergency service with mildly tenderness, pain, and swelling in the bilateral submandibular region. Physical examination also revealed mildly enlarged bilateral submandibular glands, with no fever. There was no erythema, ulcer, and no symptom in both the oral and oropharyngeal mucosa. He had a regular heart rate of 80bpm and blood pressure of 140/80 mmHg. There was no feature on the other system's examinations. On the laboratory tests, there was no feature, the patient had no leukocytosis, and his C-reactive protein was in a normal range. Ultrasonograph y(US) was preferred to evaluate submandibular glands. It performed bilateral diffuse homo geneous expansion of the submandibular salivary glands (Figure 1). There was no abscess and sialolithiasis. Bilateral level 1 (nearly sub mandibular gland) lymph nodes of the cervical region were normal. Doppler US performed a mildly increase in central vascularisation. The parotid glands were normal, and no sialolithiasis was seen. In the light of clinical and radiological findings, contrast-induced non suppurative sialadenitis was considered.

Then, the patient was treated conservatively, with analgesic/anti-inflammatory drugs. There was complete resolution of submandibular glands swelling in 3days after administration. On follow-up, sialadenitis was not repeated (Figure 2). A written patient consent is present. Discussion Ad i i Adverse reactions to intravascular contrast material are not frequent. Recent estimates of adverse reactions to iodinated contrast material range from 1 to 12%, with severe reactions comprising only 0,01 to 0,2% of total reactions. Katayama et al. ( 3 ) reported 337,647 cases of adverse reactions to ionic and nonionic contrast material are about 12% and 3%, for all that no cases of sialadenitis reported in that study. Adverse reactions are generally classified as either idiosyncratic or chemotoxic.

Idiosyncratic (anaphylactoid reactions) occur unpredictably and independently of the dose or concentration of the agent. Conversely, chemotoxic-type effects relate to dose, the molecular toxicity of each agent, and the physiologic characteristics of the contrast agents (i.e., osmolality, viscosity, hydrophilicity, calcium-binding properties, and sodium) ( 4 ). Sialadenitis is a rare adverse effect of iodinated contrast material. The mechanism of this complication is not well known but it is believed to be caused by iodine contrast, as an idiosyncratic (i.e., anaphylactoid) reaction or due to its toxic accumulation which causes the inflammation of mucous membranes and duct obstruction due to the concentration through the sodium iodide symporter of salivary gland tissue.5 98% of iodine is excreted by the kidney and the remaining 2% by the salivary sweat and lacrimal glands. Increasing iodine concentration creates a risk of iodine accumulation in salivary glands after the administration of iodinated contrast material ( 6 ). As known, substantially of reported cases participate in chronic renal failure or repetitive exposure to iodinated contrast material. Therefore, it is supposed that chronic kidney disease (as also our patient had) could be a risk factor for the development of this complication. The incidence of this adverse effect is not known. Until now, there were many extensive studies about acute and reverse effects of contrast administration but they had no cases of contrast-induced sialadenitis ( 2 , 3 , 5 , 6 ). McCullough et al.( 7 ) reported that 18 of 1381 patients who had i.v. contrast administration had parotitis of which had unilateral in the most of the cases in their study. It supports that although we have few cases in the literature clinically or radiological for this adverse effect, the true incidence is more than generally assumed.The course of postcontrast sialadenitis (iodide mumps) is substantially benign. The symptoms occur within a few minutes to up to 5 days after the administration. Complete resolution always occurs, in most cases within 2 or 3 days ( 8 ).

There were no fatal reactions associated with iodide mumps that have been reported in the literature until today. Facial paralysis, pancreatic mumps-global enlargement of the pancreas-, localized erythema, enlargement of the thyroid gland and the lacrimal glands, conjunctivitis, photophobia, coryza, generalized puffiness of the face, vague abdominal pain, slight dysphagia, and mild stridor and dyspnea reported association with iodide mumps in the literature ( 8 , 9 ). Our presented case had no additional symptoms with sialadenitis.

The US might help us for diagnosis; diffuse homogenous size increasing, dilate hyper echoic ducts, and increasing central vascular activity of the submandibular gland could be seen. There must be no abscess, sialolithiasis, and superlative lymphadenopathy in the US. The US also contributes to the differential diagnosis of other causes that enlarge the submandibular gland. US findings can be unilateral or bilateral. In our case, US findings were bilateral. Increased vascularization in the central part of the gland in Doppler US indicates hyperemia in the acute stage. Cross-sectional imaging methods such as CT and MRI can also be used in diagnosis. Especially in CT, the decrease in the density of the submandibular glands indicates the presence of edema ( 1 , 9 ). In the differential diagnosis, Sjogren’s syndrome, sialadenosis, sarcoidosis, and other causes of infectious sialadenitis should be thought ( 2 , 5 , 9 ). Treatment is conservative, however sialadenitis complete resolution within 2 or 3 days without treatment, patients can be supported by analgesic on demand. There is no evidence of the benefits of steroid and antihistamine ( 1 , 4 , 5 ).

In conclusion, nonsuppurative sialadenitis is a rare adverse effect of contrast material administration, which true incidence is unknown. Although non-ionic and low-osmolar agents are more reliable than ionic and high-osmolar ones, as our case had, there were few cases reported iodide mumps after nonionic low-osmolar agents. Chronic kidney failure and repeated dose of contrast material are risk factors for this complication. We think that this adverse effect deserves more attention, and follow-up, and prevention for recurrence because its long-term importance is unknown.