Three Cases of Neck Swelling after FNAC (fine-needle aspiration cytology).

Fine-needle aspiration cytology (FNAC) is considered a safe procedure, but it causes massive neck swelling and airway obstruction rarely. Neck swelling after FNAC is caused by two mechanisms: by hematoma or by release of vasodilator substances in thyroid cells and nerve terminals. The latter condition was previously reported as an acute and frightening swelling of the thyroid, but is not named appropriately. For convenience, we therefore refer to the condition as dTSaFNA (diffuse thyroid swelling after fine-needle aspiration) in this report. dTSaFNA is usually transient and rarely results in airway obstruction. We report one case of thyroid hematoma and two cases of dTSaFNA. All three cases were treated in hospital and recovered completely.

[Eight cases of calcific retropharyngeal tendinitis/retropharyngeal calcific tendinitis].

Calcific retropharyngeal tendinitis/retropharyngeal calcific tendinitis is an inflammation of the longus colli muscle caused by calcium hydroxyapatite crystal depositon in the longus colli muscle tendon. The three major symptoms are neck pain, limitations of neck movement, and swallowing pain. We treated 8 cases of calcific retropharyngeal tendinitis/ retropharyngeal calcific tendinitis. Each patient complained of neck pain, limitations of neck movement, and swallowing pain. The only local finding was the smooth swelling of the posterior pharyngeal wall. CT imaging showed calcification of the tendon of the longus colli muscle and a low density area in the retropharyngeal space without ring enhancement, suggesting a retropharyngeal abscess. MR imaging showed the smooth swelling of the retropharyngeal space and an increased signal intensity on T2-weighted MR imaging. Calcific retropharyngeal tendinitis heals spontaneously, and treatment is not usually required. However, the clinical outcomes are similar and can be confused with retropharyngeal abscess and pyogenic spondylitis, so antibiotics are administrated in many cases. In our report, 7 patients were hospitalized and were treated with the intravenous administration of antibiotics, while 1 patient who refused hospitalization was treated with an oral antibiotic. Steroids were administrated in 2 cases. The 7 patients who were hospitalized were cured within 6 to 10 days.

Bcl6 regulates Th2 type cytokine productions by mast cells activated by FcepsilonRI/IgE cross-linking.

Bcl6-deficient (Bcl6-/-) mice displayed Th2 type inflammation, which caused by abnormality of non-lymphoid cells. However, initiators for the Th2 type inflammation were not clear. In order to elucidate the initiators, we investigated property and function of mast cells derived from Bcl6-/- mice. Mast cells were developed from bone marrow cells cultured with IL-3 (BMMCs). Although the development of BMMCs from Bcl6-/- mice was similar to that from wild-type mice, proliferation of Bcl6-/- BMMCs stimulated with IL-3 was slightly lower than that of wild-type BMMCs. When these BMMCs were stimulated by FcepsilonRI/IgE cross-linking, Bcl6-/- BMMCs produced Th2 cytokines more than wild-type BMMCs did. Thus, Bcl6-/- mast cells are one of the initiators for Th2 type inflammation in Bcl6-/- mice, and Bcl6 may be a molecular target for Th2 type allergic diseases.