Bilateral corneal perforation caused by neurotrophic keratopathy associated with leprosy: a case report.

BACKGROUND: Neurotrophic keratopathy (NK) is a rare degenerative corneal disease caused by damage to the trigeminal nerve. We hereby describe a severe case with bilateral corneal perforation due to leprosy (Hansen's disease)-associated NK. CASE PRESENTATION: An 89-year-old man with a history of leprosy treated 40 years previously in our sanatorium developed bilateral corneal perforation due to NK. He had a history of bilateral persistent epithelial defects and bacterial keratitis. Although epithelialization was obtained with the use of autologous serum eye drops, progressive corneal thinning concomitant with stromalysis led to bilateral perforation. Over one month treatment with topical antibiotics, anti-inflammatory and lubricants resulted in healing of the epithelial defects and corneal perforations. A Cochet-Bonnet esthesiometer demonstrated a total absence of corneal sensation in both eyes. CONCLUSIONS: The present case indicated the irreversible nerve damage due to leprosy that had been cured 23 years ago, which can progress over the years and cause bilateral corneal perforations.

Expression and function of alternative splice variants of the mouse TGF-beta type I receptor.

Mouse TGF-beta type I receptor, Alk5, encodes two types of mRNA generated by alternative splicing of four amino acids in the extracellular region. In the present study, the expression and function of alternative splice variants of Alk5, i.e., Alk5-L (Alk5 with the four amino acids) and Alk5-S (Alk5 without the four amino acids), were examined. Expression of Alk5 was detected in all examined tissues, and no significant differences in the ratio of Alk5-S to Alk5-L were detected between tissues. Expression of Alk5 was also detected in various cells, with Alk5-L being especially abundant in A-6 ES cells when it was examined by RT-PCR and subsequent image analyses. No clear difference in Smad2 phosphorylation in response to treatment with TGF-beta(1) was detected between L17 cells expressing Alk5-S and those expressing Alk5-L. Consistent with these results, transcription mediated by Alk5-S in L17 cells treated with TGF-beta(1) was comparable to that mediated by Alk5-L. In addition, alternative splicing had no effect on transcriptional activation induced by GDF-8, a member of the TGF-beta family. The present results indicate ubiquitous expression of Alk5 isoforms in mouse tissues and cells, and insignificant effects of alternative splicing on signaling induced by TGF-beta(1) and GDF-8.

[Ocular impairment in leprosy].

Leprosy causes several ocular disorders, and it also causes aftereffect with high frequency in various ways. Primary impairment is the ocular disturbance caused with direct invasion of nerve and ocular tissue by Mycobacterium leprae. Secondary impairment is the complication of nerve paralysis and residual inflammation due to primary disorder. Main work at Japanese national leprosariums has been the control of primary and secondary impairment in recent years. Clinical ophthalmic study in the leprosarium revealed a increase of age-related ocular disease in addition to aftereffect of leprosy. Severe sequelae due to sensory and functional disturbance will require suitable applications of advanced clinical technologies.