Pemphigus Vulgaris with Marked Stenosis of the Esophageal Orifice from an Osteoporosis Drug: a Case Study with Long-term Follow-up

Pemphigus vulgaris produces multiple and intractable erosions of the oral mucosa in the head and neck region. We describe a case of pemphigus vulgaris that showed erosions in the hypopharynx and stenosis of the esophageal orifice from an osteoporosis drug. A 73-year-old woman was admitted with oral intake difficulty and erosions in the hypopharynx. During the first admission, we could not make a definite diagnosis by biopsy or blood examination. The condition of the mucosa worsened subsequently; an esophagram showed marked stenosis of the esophageal orifice. As a possible factor exacerbating the stenosis, an osteoporosis drug was considered. The stenosis was improved by balloon expansion. One year after the first medical examination, we finally made a definite diagnosis of pemphigus vulgaris from the results of a blood examination in which anti-desmoglein 3 turned positive when the hypopharyngeal erosions and stenosis of the esophageal orifice became worse. Systemic treatment with a steroid was effective for the control of pemphigus vulgaris; restenosis of the esophageal orifice was recognized twice during a state of remission, and careful follow-up will be necessary in the future

Expression of transient receptor potential channel vanilloid (TRPV) 1–4, melastin (TRPM) 5 and 8, and ankyrin (TRPA1) in the normal and methimazole-treated mouse olfactory epithelium

Conclusion: It is suggested that TRPV1, 2, 3, and 4, TRPM5 and 8, and TRPA1 may play several roles in the olfactory epithelium (OE), contributing to olfactory chemosensation, olfactory adaptation, olfactory-trigeminal interaction, and OE fluid homeostasis. In patients with olfactory disturbance, TRPV1 and TRPM8 may be closely related to a high rate of recognition of curry and menthol odors, while TRPV2 may also play a crucial role in the regeneration of olfactory receptor neurons. Objective: Expression of TRPV1–4, TRPM5 and 8, and TRPA1 in the normal and methimazole-treated mouse OE was analyzed. Methods: The localization of TRPV1–4, TRPM5 and 8, and TRPA1 in the OE of normal and methimazole-treated CBA/J mice was investigated by immunohistochemistry. Results: Normal OE showed a positive immunofluorescent reaction to TRPV1–4, TRPM5 and 8, and TRPA1. In lamina propria, the nerve fibers displayed TRPV 1, 2, and 3, TRPM8 and TRPA1. In the pathological condition, the expression of TRPV3, TRPV4, TRPM5, and TRPA1 was markedly reduced and took a long time to recover. In contrast, expression of TRPM8 was scarcely affected, even in the pathological condition, while TRPV1 and TRPV2 showed early recovery following methimazole treatment

A new animal model for Ménière's disease

Conclusion. A new mouse model for Ménière's disease has been developed by the treatment with both LPS and aldosterone. The induction of vestibular dysfunction in the hydropic animals model may require additional stress such as reduced inner ear blood flow, acute changes of endolymph volume and/or pressure, etc. Objective. The aim of this study is to develop a more suitable animal model, which shows more resemblance to the pathophysiological process in Ménière's disease. Materials and methods. Adult CBA/J mice were treated with intratympanic injection of LPS, intraperitoneal injection of aldosterone or injection of both LPS and aldosterone. Morphological analysis was performed in the cochlea and endolymphatic sac. Results. All experimental animals showed mild to moderate endolymphatic hydrops. The animals treated with both LPS and aldosterone showed reversible vestibular dysfunction after the intratympanic injection of epinephrine

Protective effect of edaravone against tobramycin-induced ototoxicity

Conclusion. It is suggested that simultaneous treatment with the radical scavenger edaravone has an effective protective effect against tobramycin ototoxicity in rat. Even if the edaravone treatment is postponed for 7 days, it can still prevent hearing loss, but a 14 day delay cannot protect from ototoxicity. Objectives. With the aim of alleviating hearing loss caused by aminoglycoside ototoxicity, we performed a trial to assess the hearing protective efficacy of the radical scavenger edaravone. Materials and methods. In part one of the study, 21 male Sprague-Dawley albino rats were used; 2 rats served as controls for the safety of edaravone. Eight rats each received 10 subcutaneous injections (s.c.) of tobramycin (160 mg/kg b.w.) once daily and saline injection intraperitoneally for 2 weeks. Eleven rats were given 10 s.c. tobramycin injections simultaneously with an intraperitoneal injection of edaravone (3 mg/kg b.w.). In part two, tobramycin was injected in 13 rats (as above). Five of these received two edaravone injections 7 days later and four rats similarly 14 days later. Auditory brainstem response (ABR) was used to assess hearing. Results. All rats treated only with tobramycin showed a deterioration of hearing. None of the rats given simultaneous treatment with tobramycin and edaravone demonstrated hearing loss. A 7 day delay in edaravone injection still prevented hearing loss, but a 14 day delay had only a temporary prophylactic effect