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Contrast material containing Iodine can cause parotitis. Here we present A 70 year's old man admitted to United Hospital Limited, Gulshan, Dhaka, Bangladesh on 5th May 2021 with the complaints of chest pain and shortness of breath and he was diagnosed as NSTEMI with ALVF. He was Covid 19 positive two weeks back. He underwent PCI to LM to LAD, LCX and RCA two years back. He had hypertension, diabetes mellitus and dyslipidemia. He was taking dual antiplatelet, beta-blocker, ACE inhibitor, statin, diuretic and anti-diabetic medication. His physical examination findings were reasonably normal. An electrocardiogram revealed bi-fascicular block and echocardiogram showed inferior wall and basal segment of inferior-lateral wall were hypokinetic. His high sensitive Troponin I was raised and serum creatinine was normal. This case report contains a case of bilateral parotitis following coronary angioplasty, subsided with conservative management. Possible reasons may be the direct toxicity or idiosyncratic reaction of the iodinated contrast agent.

A 67-year-old woman received induction chemotherapy comprising vincristine, daunorubicin, cyclophosphamide, L-asparaginase and prednisolone for acute lymphoblastic leukemia with a common B-cell phenotype. The administration of L-asparaginase at 3,000 U/m 2 for 6 days was planned. Before the fourth administration on day 16, left parotid swelling was identified along with increased serum amylase (991 U/L; 94% derived from salivary glands). An enlarged left parotid gland was apparent on computed tomography. The symptoms resolved after cessation of L-asparaginase, with serum amylase normalizing by day 20. This rare adverse event should be recognized as improving within a week after ceasing L-asparaginase.

Background: Sialadenitis by iodinated contrast medium (i.c.m) oriodine mumps (IM) is a rare and late benign manifestation that occurs independently of intravenous or endoarterial administration modality. If renal function is normal, i.c.m. does not reach salivary glands concentrations able to induce sialadenitis. However, a critical glomerular filtration reduction may lead to salivary ducts edema and glandular swelling after i.c.m. injection. We report a rare case report of IM in a patient on chronic hemodialysis., Methods: A 72-year-old woman affected by chronic kidney disease on chronic hemodialysis, underwent to endoscopic removal of a rectal cancer. For disease staging, a total body TC with i.c.m. was performed. The following morning, patient showed a soft and aching bilateral paroditidis swelling. Salivary glands ultrasound was diagnostic for sialadenitis. The patient was rapidly treated with betamethasone following by a 240 minutes post-dilution online hemodiafiltration session., Results: Within the next 24h, a complete remission of IM was obtained., Conclusion: In our patient, a compensatory hyperactivity of the sodium / iodine symporter (NIS) on salivary gland cells may have played a crucial role in IM induction. An high efficiency hemodialysis session within the few following hours after i.c.m injection is a fundamental tool in patients on renal replacement treatment to prevent IM that is an epiphenomenon of i.c.m. accumulation., (Copyright by Società Italiana di Nefrologia SIN, Rome, Italy.)

Case Presentation: Mr. S is a 32-year-old male with schizophrenia. Due to poor responses to various antipsychotic medications, he was started on clozapine with the dose titrated to 300 mg/day during a 4-week period. The weekly checks of the complete blood cell count showed gradual increases in the eosinophil count from normal values to 4320 per mm(3). Mr. S did not have any symptoms except some increased salivation. Clozapine was suspended, and eosinophils gradually began to decline to the normal range. Clozapine was subsequently re-started and there were no changes in eosinophil counts. Mr. S exhibited improvement of symptoms but complained of acute auricular pain and increased salivation, 8 weeks after clozapine rechallenge. He also developed a swelling of his both parotid glands. The diagnosis of clozapine-induced parotitis was suggested. Symptomatic medication was prescribed with a favorable outcome., Conclusion: We report a case of a patient who developed eosinophilia shortly after clozapine use, and then developed parotitis. There is debate in the literature over how to manage these complications of clozapine treatment. Generally they do not warrant clozapine discontinuation.

Introduction: Clozapine is the drug of choice for patients with an unsatisfactory response to routine antipsychotic treatment. Side effects such as sedation, weight gain, hypotension and hypersialorrhea are frequently reported whereas clozapine-induced parotitis is a less known complication., Case Report: We report the case of a 32-year-old woman with a refractory schizoaffective disorder, bipolar type. The failure to respond to at least two well-conducted antipsychotic trials with flupentixol and risperidone, led clinicians to prescribe clozapine, which was started three years earlier. Since its introduction, clozapine induced sialorrhea, which has been managed until now with anticholinergic medication. Recently, Mrs B. was hospitalized for a new relapse. Once treatment compliance checked (good level of plasmatic dosage), we decided to increase the dose of clozapine from 350 mg/d to 500 mg/d. Twenty days later, Mrs B. exhibited improvement of symptoms but complained of acute bilateral auricular pain and odynophagia. The bilateral and comparative clinical exam displayed a bilateral filling of the retromandibular depression, the painful swelling of the parotid gland, along with ptyalism and a slight inflammatory oedema of the Stenon duct orifice. Mrs B. was apyretic, with physiological constants within the limits of normal values. The biological analyses displayed a discrete inflammatory syndrome (mild hyperleucocytosis and anemia), a negative mumps IgM test and positive mumps IgG test, and a 1050 ng/mL clozapine blood level. Once viral parotitis was ruled out, the involvement of clozapine was evoked. Symptomatic medication was prescribed with per os analgesic (paracetamol) and antiseptic mouthwash (Éludril). Clozapine dosage was lowered to 400 mg/d. A week later, clinical examination confirmed improvement of the medical and psychiatric conditions., Discussion: We report the case of a patient who developed a parotitis following clozapine dose adjustment. Clozapine induced parotitis was retained once the infectious and other organic etiologies had been ruled out. Previous cases of clozapine-induced parotitis have already been reported and we have some arguments to suspect this etiology in our case. First, Mrs B. experienced more hypersialorrhea with the increase in clozapine dosage. Second, the anticholinergic medication was interrupted 3 days before the episode of parotitis. Two main pathophysiological hypotheses, immune and inflammatory, have already been proposed to explain clozapine-induced parotitis. In the former, the immunomodulating properties of clozapine may sensitize the mononuclear blood cells, leading to the sialadenitis. The latter hypothesis is the more documented and proposes that clozapine-induced hypersialorrhea may be responsible for a chronic inflammatory state that can lead to the formation of a parotid lithiasis and consequently parotitis. This case report illustrates clozapine induced-parotitis, a poorly known complication of this compound. Clinicians should be aware of its hypersialorrhea and inflammatory consequences in order to better prevent the occurrence of this complication., (Copyright © 2013 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Carotid stenting is being increasingly used for revascularization of the moderate to severe carotid stenosis and thus its complications are increasingly being recognized. We report a rare complication of induced by iodine contrast in a patient undergoing carotid stenting. s. A 51 year old man after the second stenting developed multiple small infarcts in spite of the distal device. He also had painful parotid swelling which improved within a week. One should be aware of iodine parotitis s in the patients undergoing iodinated contrast study.

Nifedipine is a widely used anti-anginal and anti-hypertensive agent. It is associated with significant gingival changes attributed more to collagen hyperplasia than to enhancement of protein synthesis. We investigated the influence of nifedipine on morphological changes in the parotid glands of rats in a model of hypertension. Twenty-eight male Wistar rats (8-10 weeks; 200±15 g) were divided into four groups (A-D). Hypertension was induced by surgical means in groups C and D. Animals in groups B and D were treated with nifedipine (0.85 mg/kg) via a gastroesophageal catheter the day after surgery (experimental day-1) for 2 weeks. A significant difference was observed between the control group and nifedipine group and between the control group and hypertension group with regard to the weight of the parotid gland and its surface area. Histological findings demonstrated changes in the parotid glands of hypertensive animals with mild vessel dilatation and infiltration of inflammatory cells. These histological findings seemed to be due more to changes in venous function than to alterations in gland architecture.

Objective: To review the current literature on drug-induced parotitis., Data Sources: Literature was accessed through MEDLINE/PubMed (1980-May 2012), using the search terms sialadenitis/chemically induced and parotitis/chemically induced. EMBASE (1980-May 2012) was searched using the terms parotitis/diagnosis, sialadenitis/side effect, and parotitis/side effect. International Pharmaceutical Abstracts (1970-May 2012) was searched using the search terms parotitis and sialadenitis. All searches were limited to articles on humans written in English. Inclusion criteria were published letters, case reports, reviews, and clinical trials involving drugs that may be associated with parotitis. Articles pertaining to parotitis induced by iodine-containing drugs were excluded. References of all relevant articles were reviewed for additional citations., Study Selection and Data Extraction: Review articles, clinical trials, background data, and case reports of drug-induced parotitis were collected and case reports were assessed for causality., Data Synthesis: Parotitis is an uncommon adverse effect; however, signs and symptoms of parotitis have been noted in case reports as an adverse drug reaction related to various medications. Assessing causality of an adverse drug reaction such as parotitis is challenging. To help determine the probability of causality for these events, algorithms such as the Naranjo probability scale have been developed. Eighty-four case reports of drug-induced parotitis from 40 different drugs were reviewed using a modified Naranjo probability scale that included criteria specific for parotitis. Medications that met the criteria for establishing causality included l-asparaginase with 7 case reports, clozapine with 13 case reports, and phenylbutazone with 13 case reports., Conclusions: Drug-induced parotitis is a rare adverse drug reaction. Based on the quantitative and qualitative evidence collected from the case reports, medications that are associated with drug-induced parotitis include l-asparaginase, clozapine, and phenylbutazone. Many other drugs have been implicated in the development of parotitis; however, the evidence supporting this association is insufficient to determine causality at this time.

A significant reduction of the escape threshold to mechanical stimulation of the lateral facial skin was observed bilaterally at days 2 and 3 after unilateral complete Freund's adjuvant (CFA) administration into parotid gland. A slight reduction of mechanical escape threshold was also observed in rats with saline administration. The parotid gland inflammation was verified and quantified by measuring the tissue Evans' blue dye extravasation. The Evans' blue concentration in the parotid gland tissues was significantly greater in the CFA-injected rats than that of the saline-injected rats at 72 h after treatment. On day 10 after CFA administration into the parotid gland, the Evans' blue concentration was recovered to the control level. The administration of capsaicin into the parotid gland did not alter neuronal activities in the transition zone between the trigeminal spinal subnucleus interpolaris and caudalis (Vi/Vc). In contrast, capsaicin administration induced significant increases in the receptive field size and mechanical and cold responses of neurons located in superficial laminae of the C1/C2. The subgroup of C1/C2 neurons responded to mechanical distension of the parotid gland, whereas no Vi/Vc neurons responded to parotid distension.

Background: Several adverse events following immunization (AEFI) have been attributed to immunization with live attenuated measles, mumps, and rubella (MMR) vaccines. The MMR vaccine was introduced into the routine infant immunization schedule in 2003, followed by a second dose of vaccine at school-entry for children 4 to 6 years of age. The objective of this study was to characterize adverse reactions following MMR vaccination in Iran., Methods: Children who received the MMR vaccine and resided in five selected provinces of Iran were examined weekly for four weeks to detect well-known AEFIs that included: parotitis, fever and convulsions, convulsions without fever, encephalopathy, and anaphylactic reactions. Incidence of AEFIs were calculated and compared among recipients in both age groups., Results: During the follow-up period, trained providers reported 792 AEFIs. Parotitis was the most frequent event occurring in 1.8% of recipients. Of 14,109 children vaccinated at 12 months of age the following AEFIs occurred: parotitis (147), fever and convulsions (8), convulsions (7), encephalopathy (1), and anaphylactic reactions (1). Of 29,338 children vaccinated at 4 to 6 years of age, parotitis, fever and convulsions, encephalopathy, and anaphylaxis occurred in 626, 5, 1, and 1 child, respectively; no convulsions without fever were reported in this age group., Conclusion: Parotitis is the most frequent AEFI among MMR vaccine recipients in Iran. Incidence rates of AEFIs following MMR vaccination in Iran are similar to rates of AEFIs reported in other studies.

Adverse drug reactions to the sulfonamide antibiotics are uncommon. When they do occur, they usually manifest as a rash or urticaria. Our review of the recent literature found that while sialadenitis is listed as a possible side effect of sulfonamide use, no actual case has ever been reported until now. We describe a case of acute bilateral parotitis that arose as a side effect of sulfonamide antibiotic treatment. We also examine the relevance of such pathology to the proposed mechanisms of sialadenitis, and we briefly discuss sulfonamide-induced pancreatitis. Lastly, we review the controversy over the possibility that some adverse drug reactions may be caused by cross-reactivity among different classes of sulfonamides.

Objective: To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide-exposed rat parotid gland., Materials and Methods: Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration., Results: The myeloperoxidase activity of the lipopolysaccharide-exposed gland was 10-fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin-8 (10 or 25 μg kg(-1) , given twice intraperitoneally) or melatonin (10 or 25 mg kg(-1) x 2) the lipopolysaccharide-induced response was elevated 4.6- and 3.5-folds at the most. The cholecystokinin-A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin-8, while the melatonin 2-preferring receptor antagonist luzindole had no effect on the melatonin-induced inhibition. Unselective nitric oxide-synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide-synthase (of non-nervous origin) halved the inflammatory response., Conclusion: Some hormones may contribute to anti-inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide-synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide., (© 2010 John Wiley & Sons A/S.)

We report a case of a 56-year old patient with coronary heart disease and subacute myocardial infarction who presented with acute sialadenitis after twice undergoing coronary angiography. Acute sialadenitis ('iodide mumps') after exposure to contrast medium is characterized by a fast, painless and bilateral swelling of the salivary glands. It is usually self-limiting but can occur after re-exposure to the contrast agent.

Drug induced acute parotitis is a very uncommon complication reported with a few drugs only. There is no case of acute bilateral parotitis reported previously with i.v. enalaprilat. We present here a female patient who developed acute bilateral parotitis within minutes of i.v. enalaprilat injection and recovered within 24 hours of stopping the drug and with symptomatic treatment.

Blockage of the salivary duct can produce pain and inflammation from the build up of saliva in the parotid gland. The processing of parotid inflammation-induced pain, however, is poorly understood. The purpose of this study was to clarify the functional involvement of the trigeminal subnucleus interpolaris/caudalis transition region (Vi/Vc) and upper cervical spinal cord (C1/C2) in processing nociceptive input relevant to parotitis. The effect of capsaicin-induced parotitis was examined on a total of 37 nociceptive neurons isolated from the Vi/Vc (n = 23) and C1/C2 (n = 14) regions. Eight of 23 Vi/Vc neurons responded to mechanical distention of the parotid gland, whereas no C1/C2 neurons responded to the parotid distention. Receptive field characteristics in all neurons were examined following capsaicin injections into the parotid gland. Mechanical and cold responses increased significantly in C1/C2 but not Vi/Vc neurons following capsaicin. Receptive field sizes also increased in C1/C2 but not Vi/Vc neurons. At the Vi/Vc transition region, pinch-evoked activity increased in neurons receiving convergent inputs from the parotid gland and facial skin when compared to non-convergent neurons. The present data indicate that the hyperalgesia and referred pain associated with parotitis may result from sensitization of C1/C2, but not Vi/Vc nociceptive neurons.

Acute pancreatitis due to pancreatic exocrine over-secretion induced by organophosphate poisoning has been previously reported but parotid gland involvement has not. This paper describes a case of acute organophosphate-induced parotitis in a patient with pre-existing sialolithiasis. The patient developed bilateral facial swelling in the pre-auricular area extending to the angle of the jaw and also developed elevated serum amylase on the second day of the poisoning. Serum lipase remained normal. Autopsy confirmed parotid gland inflammation and pre-existing ductal lithiasis. This case illustrates that organophosphate-induced parotitis can occur and should be considered in patients with organophosphate poisoning who have hyperamylasemia without elevation in serum lipase.

Although I-131 whole-body scanning is a useful method to evaluate and manage well-differentiated thyroid cancer, several causes of false-positive findings require careful evaluation. The authors describe a case of benign parotitis mimicking metastasis on an I-131 whole-body scan.

A wide variety of adverse effects of methimazole (MMI) have been reported. Here we report a new MMI-induced disorder, acute pancreatitis and parotitis. Three weeks after a woman started MMI treatment for Graves' disease, she developed a high fever, painful parotid swelling and dull pain in the upper abdomen with elevation of the serum levels of salivary and pancreatic enzymes. These abnormalities disappeared soon after the withdrawal of MMI. However, the same abnormalities were rapidly provoked when MMI was reintroduced. Marked increases in the leucocyte count and CRP were also observed during these episodes. The possible mechanisms of MMI-induced pancreatitis/parotitis are discussed.

In six patients, women of 49, 59, 71, 82, 76 and 64 years old, acute inflammation of parotid and submandibular salivary glands was diagnosed. All were using nitrofurantoin as treatment for urinary tract infection. The symptoms disappeared after the treatment was discontinued. There were no signs of hypersensitivity to nitrofurantoin. Three of the patients had similar complaints during previous treatment with nitrofurantoin.

In a boy with non-Hodgkin's lymphoma (NHL), two different complications developed concurrently associated with L-asparaginase (L-ASP) therapy. A non-ketotic hyperglycemic state was observed simultaneously with bilateral acute parotitis after the patient was subjected to L-ASP. The hyperglycemia with normal insulin levels and the absence of plasma and urine ketones was controlled with insulin therapy and no residual impairment of glucose tolerance was demonstrated later. Bilateral acute parotitis, which is a rare complication associated with L-ASP, resolved spontaneously within a week after cessation of L-ASP. The rarely observed toxic effects of L-ASP, such as parotitis, should be recognized as promptly as the better-known complications, e.g., hyperglycemia, to avoid the continuation of this antineoplastic agent.

The largest nationwide active surveillance of four Measles-Mumps-Rubella (MMR) vaccines was conducted in Japan. A total of 1255 pediatricians actively participated in the study, which comprised 8.6% of all members of the Japanese Pediatric Society. The total number of registered recipients of MMR vaccines was 38 203. They were arbitrarily given one of the MMR vaccines produced by three makers (Takeda, Osaka city, Kitasato Minato-ku. Tokyo and Biken Suita city, Japan) or the standard MMR vaccine made of designated strains (Kitasato's measles-AIK-C, Biken's mumps-Urabe Am9 and Takeda's rubella-To336) produced by Takeda, Kitasato and Biken and were observed for 35 days. The rates of virologically confirmed aseptic meningitis per 10,000 recipients were 16.6, 11.6, 3.2 and 0 for the standard MMR, Takeda MMR, Kitasato MMR and Biken MMR vaccines, respectively. The incidence of convulsions between 15 and 35 days was the highest with the standard MMR vaccine and the incidence of fever associated with vomiting occurring between 15 and 35 days (symptoms relevant to aseptic meningitis) were also the highest with the standard MMR vaccine. The incidence of parotid swelling was the lowest with Takeda MMR vaccine. This surveillance revealed that incidences of aseptic meningitis after administration of the standard MMR vaccine and of Biken MMR vaccine were different. This posed questions about the manufacturing consistency of the Urabe Am9 mumps virus vaccines. On the other hand, the National Institute of Health found that the biological characteristics of the Urabe Am9 mumps virus contained in the standard MMR vaccine and in the Biken MMR vaccine were different. The Biken Company reported that the mumps vaccine in the standard MMR vaccine was a mixture of two Urabe Am9 mumps vaccine bulks; one identical to that contained in the Biken MMR vaccine and the other produced by a different manufacturing process.

In a patient affected by acute lymphoblastic leukemia (ALL) and subjected to therapy with Erwinia L-asparaginase, acute parotitis was observed. Microbiological studies excluded any infectious etiology. Regression of parotitis was spontaneous. This complication has not been previously reported and could be due to the same mechanism of pancreatic injury. The occurrence of acute parotitis needs to be promptly recognized in order to avoid the continuation of L-asparaginase.

Low doses of HgCl2 induce a genetically restricted autoimmune syndrome in Brown Norway (BN) rats (BN(Hg)). Part of the syndrome includes spontaneously developing mononuclear cell foci in salivary and lacrimal glands, morphologically similar to focal sialoadenitis in Sjögren's syndrome in man. In this study, we have shown that Hg-induced focal adenitis in BN rat is not female predominant and not solely dependent on Hg uptake in the glands. In BN(Hg), focal adenitis was found to develop in several different glands (parotid, submandibular, lacrimal, thyroid) as a specific manifestation of immunopathosis induced by Hg in the RT1n-haplotype-carrying BN. Such manifestations were absent in another strain, the Hg-resistant Lewis (RT1l). Also a potent contact sensitizer, DNFB, induced focal adenitis in isolated glands, provided that strong sensitization had occurred. Immunohistochemical characterization of focal adenitis in BN(Hg) with monoclonal antibodies showed that T cells and dendritic cells dominate the early infiltrates, whereas B cells were absent.

Drug-induced parotitis is a relatively uncommon adverse drug reaction. Most of the data on drug-induced parotitis consist of isolated case reports with few attempts at rechallenge to confirm the aetiology. Phenylbutazone and oxyphenbutazone have a significant number of reports suggesting that these drugs may be implicated in causing parotitis. Antipsychotics, particularly thioridazine, have been associated with parotitis. Most of these reports relate the anticholinergic oral drying as a predisposing factor in the development of a parotid gland infection. There is inadequate literature on the histamine (H2) receptor blockers, interferon-alpha, doxycycline, trimipramine, nifedipine, methyldopa, nitrofurantoin, nicardipine, isoproterenol or ritodrine to link them as aetiological agents in the development of parotitis.

We report a 60-year-old woman with renovascular hypertension who developed a severe cutaneous vasculitis 24 h after the injection of iopamidol during urography. A review of the literature suggests that her concomitant hydralazine therapy probably predisposed her to this reaction, as similar reactions have occurred in systemic lupus erythematosus, and hydralazine can induce a LE-like syndrome. We recommend that urography should be avoided in patients receiving hydralazine.