戸松 瑛介

38歳男性。全身の骨痛、歩行・起立障害を主訴に前医を受診した。腫瘍性骨軟化症(TIO)が疑われ、精査加療目的に当院へ紹介となった。FGF23の全身静脈サンプリングと68Ga-DOTATOC-PET/CTにより右鼻腔内の腫瘤がTIOの原因腫瘍であると診断し、内視鏡下に右鼻腔腫瘍摘出術が施行された。その結果、病理組織学的に鼻腔原発リン酸塩尿性間葉系腫瘍と診断され、術後5日で全身の骨痛は完全消失し、立位保持・歩行ともに可能となった。術後1年経過現在、腫瘍の再発や骨痛の再燃はなく、FGF23も正常範囲内である。

AIMS: Although skin manifestations are common in diabetic patients, its characteristics are poorly identified. This study explored the differentiation process of keratinocytes in type 2 diabetes mellitus (T2DM) in vivo. METHODS: Back skin of T2DM model KKAy/TaJcl mice (KKAy) and C57BL/6JJcl mice (control) aged 8 and 12 weeks was used. The mRNA expression of differentiation markers of keratinocytes was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of each marker in situ was examined immunohistochemically. RESULTS: KKAy mice showed hyperglycemia versus control mice. The histological findings showed increased thickness and structural impairment of epidermal tissue in KKAy mice. The qRT-PCR revealed that the expression of integrin beta 1 and keratin 14 in KKAy and control mice was identical. However, the expression of involucrin at 8 weeks, keratin 10 at 12 weeks, and filaggrin and loricrin at 8 and 12 weeks was decreased in KKAy mice. Immunohistochemical findings showed that filaggrin was markedly decreased in KKAy mice, though Ki-67 remained unchanged. CONCLUSION: The terminal differentiation process was impaired in the diabetic skin, while keratinocyte proliferation was preserved. Damaged terminal differentiation of keratinocytes may contribute to impairment of the skin barrier function in diabetic dermatoses.