A hallmark of mucoid otitis media (MOM, i.e., chronic otitis media with mucoid effusion) is mucus accumulation in the middle ear cavity, a condition that impairs transduction of sounds in the ear and causes hearing loss. The mucin identities of mucus and the underlying mechanism for the production of mucins in MOM are poorly understood. In this study, we demonstrated that the MUC5B and MUC4 were major mucins in MOM that formed distinct treelike polymers (mucus strands). The MUC5B and MUC4 mRNAs in the middle ear mucosa with MOM were up regulated 5-fold and 6-fold, compared with the controls. This upregulation was accompanied by the extensive proliferation of the MUC5B-and MUC4-producing cells in the middle ear epithelium. Further study indicated that the mucin hyperproduction was significantly linked to CD4 + and CD8 + T cells and/or CD68 + monocyte macrophages. It suggests that MUC5B and MUC4 expression may be regulated by the products of these cells.

Toll-like receptor 2 (TLR2) plays a key role in the host defense against Gram staining positive (Gram ϩ ) bacteria and their cell wall envelope components. However, little is known about the expression of TLR2 in the middle ear under otitis media (OM) conditions, and its role in the persistent otitis media with effusion (OME). In this study, we demonstrated that the pneumococcal cell wall component, peptidoglycan-polysaccharides (PGPS), activated the expression of TLR2 in the middle ear epithelial cells through the nuclear factor kappa B (NF-B)-cytokine signaling pathway while I kappa B alpha mutant (IB␣M), a dominant negative inhibitor of NF-B, abrogated the expression of TLR2 induced by PGPS. This study suggests that the existence of residual PGPS may maintain a low profile of cytokine production in the middle ear mucosa and thus contribute to the pathogenesis of OME. (Pediatr Res 69: 101-105, 2011)

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A 56-yr-old man was admitted to our university hospital for severe back pain one month after a resection for lung adenocarcinoma (stage IIIA) without evidence of the adrenal mass. Computed tomography (CT) of the abdomen showed bilateral bleeding of adrenal tumors. Endocrinological laboratory studies showed high plasma ACTH and normal serum cortisol levels with the loss of circadian rhythm. Although plasma ACTH levels increased, there was no cortisol response to administration of human corticotropichormone (hCRH). Core-needle biopsy was performed on the right adrenal tumor and revealed adenocarcinoma cells mimicking a primary lung tumor previously examined. We diagnosed retroperitoneal hemorrhage due to bilateral adrenal gland metastasis from lung adenocarcinoma with adrenal insufficiency. Adrenal metastases most commonly originate from a primary lung tumor, followed by stomach, esophagus and liver/bile ducts. Bilateral adrenal metastases were noted in approximately half of all adrenal metastases patients. Clinically significant adrenal hemorrhage by metastasis is exceedingly rare and non-specific symptoms, such as abdominal, chest or back pain, nausea and vomiting, confusion, weakness, hypotension, shock and high fever, are often observed in these patients. We present a case of massive retroperitoneal hemorrhage and adrenal insufficiency due to adrenal gland metastasis from adenocarcinoma of lung.

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