The sinonasal tract may give rise to a broad range of neoplasms that share a "small round blue cell" tumor (SBRCT) appearance on routine histology, but treatment strategies depend on precise tumor classification. Immunohistochemistry for p63 is often employed in the sinonasal SRBCT differential diagnosis because it is highly sensitive for squamous cell carcinoma (SCC). However, p63 staining may be observed in other tumor types, a potential diagnostic pitfall. P40 is a more squamous-specific isoform of p63, and it may be more useful in distinguishing poorly differentiated SCC from its mimickers in the sinonasal tract. Immunohistochemistry for p40 and p63 was performed on 171 sinonasal neoplasms with SRBCT morphology: 73 SCCs (67 poorly differentiated, non-keratinizing, or basaloid types and 6 nasopharyngeal carcinomas), 46 esthesioneuroblastomas, 11 sinonasal undifferentiated carcinomas (SNUCs), 11 lymphomas, 9 melanomas, 7 alveolar rhabdomyosarcomas, 4 solid adenoid cystic carcinomas, 4 NUT midline carcinomas, 4 primitive neuroectodermal tumors (PNETs), and 2 small cell carcinomas. P40 was positive in 72 of 73 SCCs, and showed a diffuse distribution in all but one positive case. P40 immunoexpression was also observed in 13 of 46 (28 %) esthesioneuroblastomas, 6 of 11 (55 %) SNUCs, 2 of 4 (50 %) adenoid cystic carcinomas, 3 of 4 (75 %) NUT midline carcinomas, 1 of 2 (50 %) small cell carcinomas, and 1 of 4 (25 %) PNETs; in the non-SCC tumors, p40 staining was focal in most cases. P63 was positive in every p40-positive tumor. In addition, a p63+/p40- phenotype was seen 5 of 11 (45 %) lymphomas, 4 of 7 (57 %) alveolar rhabdomyosarcomas, 1 of 4 (25 %) PNETs, and 3 of 46 (7 %) esthesioneuroblastomas. All sinonasal melanomas were negative for both markers. In the sinonasal SRBCT differential diagnosis, both p40 and p63 are highly sensitive for SCC, but p40 is more specific. Notably, p40 is consistently negative in lymphomas and alveolar rhabdomyosarcomas, two tumors that are frequently p63-positive. It must be remembered, however, that even diffuse p40 immunostaining is not entirely specific for the squamous phenotype, and therefore it should be utilized as part of an immunohistochemical panel.
Intestinal-type adenocarcinoma (ITAC) is a rare form of sinonasal cancer characterized by an association with exposure to industrial dusts, aggressive clinical behavior, and histologic/immunophenotypic similarity to tumors of the gastrointestinal tract. ITAC is sometimes very poorly differentiated and difficult to distinguish from other sinonasal neoplasms, particularly in a limited biopsy. CDX-2 and cytokeratin 20 are consistently immunoreactive in ITAC and as a result, these immunostains are often used to support the diagnosis. However, CDX-2 and cytokeratin 20 have not been tested on a broad range of sinonasal tumors, so their specificities remain unknown. Immunohistochemistry for CDX-2 and cytokeratin 20 was performed on 6 sinonasal ITACs as well as 176 nonintestinal-type sinonasal neoplasms. CDX-2 and cytokeratin 20 were positive in all 6 cases of ITAC. CDX-2 immunoexpression was also observed in 17 of 176 (10 %) non-intestinal-type tumors including 6 of 16 (38 %) sinonasal undifferentiated carcinomas, 8 of 81 (10 %) squamous cell carcinomas (including 5 of 39 non-keratinizing variants), 2 of 20 (10 %) salivary-type adenocarcinomas, and 1 of 2 (50 %) small cell carcinomas. In contrast, among non-intestinal types of sinonasal tumors, cytokeratin 20 was only focally observed in 1 of 176 non-intestinal tumors (a non-keratinizing squamous cell carcinoma). All cases of non-intestinal surface-derived adenocarcinoma and esthesioneuroblastoma were negative for both markers. Both CDX-2 and cytokeratin 20 are highly sensitive for the diagnosis of sinonasal ITAC, but cytokeratin 20 is more specific. CDX-2 staining may be observed in other high grade tumor types, especially sinonasal undifferentiated carcinoma and non-keratinizing squamous cell carcinoma. As a result, in the setting of a poorly differentiated sinonasal carcinoma the diagnosis of ITAC should not be based on CDX-2 immunoexpression alone. Clear-cut glandular differentiation and cytokeratin 20 immunoexpression are more reliable features.
Lichen planus is an inflammatory dermatosis with a prevalence of approximately 1%. Recent meta-analyses show that patients with hepatitis C virus have a 2.5- to 4.5-fold increased risk of developing lichen planus. Lichen planus has also followed vaccinations and has specifically been attributed to the hepatitis B vaccine, the influenza vaccine, and the tetanus–diphtheria–acellular pertussis vaccine. We describe a case of lichen planus in a hepatitis C virus–infected African American male occurring in temporal association with the administration of the tetanus–diphtheria–acellular pertussis vaccine. The patient’s presentation was clinically consistent with lichen planus and confirmed by biopsy. It is likely that many cases of vaccine-induced lichen planus have gone unpublished or unrecognized. In areas with high prevalence of hepatitis C virus infection, we may expect to see more cases of vaccine-induced lichen planus especially in light of the updated Centers for Disease Control and Prevention tetanus–diphtheria–acellular pertussis vaccination recommendations. This case serves to educate healthcare providers about vaccine-induced lichen planus and, in particular, the need to counsel hepatitis C virus–infected patients about a potential risk of developing lichen planus following vaccination. We also reflect on current theories suggesting the T-cell–mediated pathogenesis of lichen planus and the role that hepatitis C virus and toxoid or protein vaccines may play in initiating the disease.
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