Membranous basal cell adenoma (MBCA) is a rare benign salivary gland neoplasm. It is difficult to diagnose MBCA based on fine-needle aspiration (FNA) cytology due to rare reporting of its FNA cytology and overlapping of its FNA cytologic features with some benign and malignant entities. We present a case of MBCA in a 67-year-old female that was originally misinterpreted as adenoid cystic carcinoma (ACC) on FNA cytology. The FNA smears showed numerous uniform small basaloid epithelial cells with round or oval nuclei and inconspicuous nucleoli, and scant cytoplasm. The basaloid cells surround acellular, dense, homogenous material or are surrounded by acellular or paucicellular dense homogeneous material possibly containing bland spindle cells. The basaloid cells are present in variably sized three-dimensional clusters, acini, or sheets with variable cohesion. The dense homogenous material surrounded by basaloid cells may be interconnected. High power magnification reveals the homogeneous material to have a fibrillar texture. The edges of dense homogenous materials were well-demarcated. We describe the diagnostic pitfalls of FNA for MBCA, particularly versus ACC, basal cell adenoma, cellular pleomorphic adenoma, myoepithelioma, basal cell adenocarcinoma, and basaloid squamous cell carcinoma in hope of improving clinical management and patient treatment.
Sebaceous lymphadenoma (SLA) is a histologic variant of lymphadenoma or sebaceous adenoma of the salivary gland. The fine-needle aspiration (FNA) cytology of SLA has not been well-described. In this report, we reported a case that involved an 81-year-old male with a long-standing left parotid mass and was diagnosed on FNA cytology. The FNA smears showed clusters of three types of epithelial cells in a background of abundant lymphoid cells, macrophages and abundant proteinaceous materials. The predominant epithelial cells were large polygonal cells with abundant cytoplasm filled with multiple, uniform, small, and clear vacuoles, ill-defined cytoplasmic borders, and small centrally located round nuclei with finely granular chromatin, conspicuous nucleoli and indented nuclear membranes apparently imprinted by cytoplasmic vacuoles. These cells were surrounded by polygonal or flat cells with less or more dense cytoplasm, indistinct cell borders and round or oval small nuclei with smooth nuclear membranes, which correspond to germinative or basaloid cells. Some cells had granular cytoplasm. Large three dimensional clusters of nonkeratinized squamous cells have oval nuclei containing evenly distributed chromatin, and scant to moderate dense cytoplasm that were arranged in a "stream of fish" pattern. Rare granulomas and cystic contents (degenerated cells, inflammatory cells, macrophages, and abundant granular debris/proteinaceous material) were also seen. The diagnosis of SLA was confirmed by the surgical resection.
Hageman factor 1 with contact from collagen can be sufficient to convert the zymogen. Fitzgerald's 2 not needed, but often has speeded the addition of "a" to XI. When your body's subjected to contusing, factor XI can help stop the bruising. With calcium's aid, factor IXa 3 is made, and from here on it gets more confusing. You may think all this stuff is insipid, but with calcium, VIIIa, and some phospholipids, 4 tenase is formed as per the norm, and at prothrombinase, 5 intrinsic has ended. Extrinsic: If you're dying from a traumatic hemorrhage, your body can make its own bandage. Factor III is released, and calcium completes the VIIa 6 and TF 7 assemblage. Common: The common pathway's where it all comes together and saves you from the brink of the nether. Factors X, V 8 , and IV 9 put their foot in the door and then thrombin 10 starts building the anchor. This one can be a tough customer: factor II 11 converts I 12 to a monomer. Factors V and VIII swoop in positive feedback loops 13 and XIIIa 14 transmutes fibrin polymer.
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