Clinical features and visual outcomes of Japanese patients with scleritis

2010 ◽  
Vol 94 (11) ◽  
pp. 1459-1463 ◽  
Author(s):  
H. Keino ◽  
T. Watanabe ◽  
W. Taki ◽  
C. Nakashima ◽  
A. A. Okada
2018 ◽  
Vol 103 (2) ◽  
pp. 274-278 ◽  
Author(s):  
Makiko Nakayama ◽  
Hiroshi Keino ◽  
Takayo Watanabe ◽  
Annabelle A Okada

PurposeTo describe the clinical features, treatment and visual outcomes of Japanese patients with new-onset acute Vogt-Koyanagi-Harada (VKH) disease.MethodsClinical records of 111 patients who presented between 1999 and 2015 to the Ocular Inflammation Service of the Kyorin Eye Center, Tokyo, were reviewed.ResultsOf the 111 patients (68 women, 43 men), 16 had complete, 90 had incomplete and 5 had probable VKH disease. The median follow-up period was 36 months (4–175 months). The mean age at presentation was 41 years (19–74 years). Serous retinal detachment (202 eyes) and optic disc hyperaemia (89 eyes) were observed at presentation. Of the patients tested, 45/48 (93.8%) were human leucocyte antigen-DR4 positive and 63/77 (81.8%) had cerebrospinal fluid pleocytosis. Initial corticosteroid treatment consisted of pulse intravenous therapy in all patients. Sunset glow fundus was observed in 49.5% of eyes, and anterior and/or posterior segment recurrence of inflammation was observed in 25 patients (22.5%). Treatment was transitioned to cyclosporine in 17 patients (15.3%) for steroid sparing (6 patients) or recurrent inflammation (11 patients), with good subsequent control. Ocular complications were observed in 47 of 222 eyes (21.2%) (mostly cataract), and systemic complications were observed in 8.1% of patients (mostly hypertension and diabetes mellitus). Ninety-three percent of eyes (167 of 178 eyes) had a visual acuity of ≥1.0 at 1 year after presentation.ConclusionsAn aggressive corticosteroid treatment strategy in a large number of patients with new-onset acute VKH disease, with transitioning to cyclosporine in selected cases, resulted in excellent visual outcomes and low rates of recurrence.


2019 ◽  
Vol 28 (2) ◽  
pp. 209-216 ◽  
Author(s):  
Yoshimasa Ando ◽  
Hiroshi Keino ◽  
Makiko Nakayama ◽  
Takayo Watanabe ◽  
Annabelle A. Okada

2020 ◽  
Vol 64 (1) ◽  
pp. 28-34
Author(s):  
Virgilio Galvis ◽  
Angelica Pedraza-Concha ◽  
Alejandro Tello ◽  
M. Lina Plata ◽  
C. Luis Escaf ◽  
...  

2018 ◽  
Vol 196 ◽  
pp. 181-196 ◽  
Author(s):  
Ryo Ando ◽  
Wataru Saito ◽  
Atsuhiro Kanda ◽  
Satoru Kase ◽  
Kaoru Fujinami ◽  
...  

Genes ◽  
2019 ◽  
Vol 10 (9) ◽  
pp. 715 ◽  
Author(s):  
Sugiyama ◽  
Moteki ◽  
Kitajiri ◽  
Kitano ◽  
Nishio ◽  
...  

The OTOA gene (Locus: DFNB22) is reported to be one of the causative genes for non-syndromic autosomal recessive hearing loss. The copy number variations (CNVs) identified in this gene are also known to cause hearing loss, but have not been identified in Japanese patients with hearing loss. Furthermore, the clinical features of OTOA-associated hearing loss have not yet been clarified. In this study, we performed CNV analyses of a large Japanese hearing loss cohort, and identified CNVs in 234 of 2262 (10.3%, 234/2262) patients with autosomal recessive hearing loss. Among the identified CNVs, OTOA gene-related CNVs were the second most frequent (0.6%, 14/2262). Among the 14 cases, 2 individuals carried OTOA homozygous deletions, 4 carried heterozygous deletions with single nucleotide variants (SNVs) in another allele. Additionally, 1 individual with homozygous SNVs in the OTOA gene was also identified. Finally, we identified 7 probands with OTOA-associated hearing loss, so that its prevalence in Japanese patients with autosomal recessive hearing loss was calculated to be 0.3% (7/2262). As novel clinical features identified in this study, the audiometric configurations of patients with OTOA-associated hearing loss were found to be mid-frequency. This is the first study focused on the detailed clinical features of hearing loss caused by this gene mutation and/or gene deletion.


2017 ◽  
Vol 56 (22) ◽  
pp. 2971-2977 ◽  
Author(s):  
Akira Mizuki ◽  
Masayuki Tatemichi ◽  
Atsushi Nakazawa ◽  
Nobuhiro Tsukada ◽  
Hiroshi Nagata ◽  
...  

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