A 21-year-old male presented with painful parotid and SMG swelling for the past 10 days. Although his parotid pain subsided after taking nonsteroidal antiinflammatory drug, painful SMG swelling continued until presentation. He was healthy without a history of any disease including allergic or metabolic disease. On physical examination, both SMGs were enlarged without a notable enlargement of lymph node. Contrast CT revealed that both Wharton’s ducts were dilated, showing a strong enhancement along with the duct (Fig. 1A). Under suspicion of acute sialadenitis, antibiotics (cefditoren 100 mg three times per day for 7 days) and prednisolone (5 mg twice a day for 5 days) were prescribed. We encouraged the patient to have frequent hydration and SMG massage for facilitating drainage of saliva. SMG swelling and pain subsided one week later. Since he wanted to know the cause of disease, laboratory tests for diabetes mellitus, autoimmune disease (anti-SS-A/Ro Ab, anti-SS-B/La Ab, rheumatoid factor [RF], antinuclear Ab [ANA], antineutrophil cytoplasmic Ab, complement component 3 and 4, immunoglobulin G [IgG]), and thyroid function were performed. Only serum eosinophilia showed a high level at 6.8% (normal range: 0%-5%). Other results were within normal limits. We again recommended frequent hydration and salivary gland massage without medication. During the following week, he complained of gradually progressive swelling and pain in both SMGs. We additionally checked multiple antigen simultaneous test. Only elevated total IgE at 403.4 IU/mL (normal limit: 100 IU/mL) was found. We performed ultrasonography (US) followed by core needle biopsy (CNB) for SMG parenchyma. US showed symmetric enlargement, inhomogeneous echogenicity, and dilated ducts of SMG (Fig. 1B). Mild lymphocytic infiltration between slightly dilated intralobular ducts was found on histologic evaluation (Fig. 1C). IgG4-positive cells were not found using immunohistochemistry (Fig. 1D). During the time period between the examination and tests, symptoms were relieved by 10 mg of prednisolone once a day for a week. We suspected this disease as eosinophilic sialodochitis. Thus, we prescribed 5 mg levocetirizine for two weeks. SMG pain and swelling subsided by antihistamine medication. After four more weeks of medication, sizes of both SMGs were nearly normal without aggravation. Blood examination revealed a normal eosinophil level (4.4%). His symptoms were well controlled by taking antihistamine medication intermittently for 7 months.

A 39-year-old male presented with symptoms of recurrent swelling of both SMG and parotid glands with pain for the past 10 years. When salivary glands swelled up, he complained of an itching sensation on the overlying skin of salivary glands. He reported no history of underlying disease including allergic disease. On physical examination, both SMGs and parotid glands were enlarged without tenderness. There was no palpable cervical node. CT revealed enhancement of both SMG parenchyma (Fig. 2A) and dilatation of both Wharton’s ducts. Dilation of both Stensen’s ducts was also observed on CT (Fig. 2B). Results of laboratory test showed elevated serum amylase (111 U/L, normal range: 28-100 U/L) and serum eosinophilia (5.3%, normal range: 0%-5%) without IgE elevation. Other laboratory tests for autoimmune diseases (anti-SS-A/Ro Ab, anti-SS-B/La Ab, RF, ANA, IgG, and IgG subclass IV) all showed negative finding. US followed by CNB were performed. US showed heterogenous echogenicity of both SMGs and dilatation of the intraglandular ducts (Fig. 2C). Histologic evaluation of SMG parenchyma revealed moderate lymphocytic infiltration with many eosinophils around a markedly dilated interlobular duct (eosinophil count up to 70/high-power field) (Fig. 2D). We prescribed 5 mg levocetirizine for two weeks under the suspicion of eosinophilic sialodochitis. Both SMG and parotid swelling as well as the itching sensation improved. Over a period of six months, his symptoms improved without recurrence.