Ann Dermatol.  2016 Oct;28(5):637-639. 10.5021/ad.2016.28.5.637.

A Case of Hyperandrogenism, Insulin Resistance, and Acanthosis Nigricans Syndrome; Increase in Proliferating Cell Nuclear Antigen and Decrease in Loricrin in Acanthosis Nigricans

Affiliations
  • 1Department of Dermatology, Faculty of Medicine, Oita University, Oita, Japan. hatano@oita-u.ac.jp
  • 2Department of Endocrinology, Faculty of Medicine, Oita University, Oita, Japan.
  • 3Department of Gynecotocology, Faculty of Medicine, Oita University, Oita, Japan.

Abstract

No abstract available.


MeSH Terms

Acanthosis Nigricans*
Hyperandrogenism*
Insulin Resistance*
Insulin*
Proliferating Cell Nuclear Antigen*
Insulin
Proliferating Cell Nuclear Antigen

Figure

  • Fig. 1 Hypertrichosis on her face (A: eyebrows, B: chin) and hyperpigmented, velvety patches on her axilla (C), the nape of her neck (D) and the dorsal aspect of her phalangeal joints (E). Histological examination revealed epidermal papillomatosis and acanthosis with orthohyperkeratosis, and no significant inflammatory infiltrate (F). (F) H&E, ×40.

  • Fig. 2 Immunohistochemical staining on axilla of the patient revealed the conspicuous increase in proliferating cell nuclear antigen (PCNA)-positive cells, especially in basal layer and the reduced and abnormally expanding expression of loricrin in granular and upper spinous layers. (A) PCNA in a healthy volunteer, (B) PCNA in the patient. (C) loricrin in a healthy volunteer, (D) loricrin in the patient. A~D: ×100.


Reference

1. Elmer KB, George RM. HAIR-AN syndrome: a multisystem challenge. Am Fam Physician. 2001; 63:2385–2390.
2. Friedman CI, Richards S, Kim MH. Familial acanthosis nigricans. A longitudinal study. J Reprod Med. 1987; 32:531–536.
3. Cruz PD Jr, Hud JA Jr. Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for acanthosis nigricans. J Invest Dermatol. 1992; 98:6 Suppl. 82S–85S.
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4. Krane JF, Murphy DP, Carter DM, Krueger JG. Synergistic effects of epidermal growth factor (EGF) and insulin-like growth factor I/somatomedin C (IGF-I) on keratinocyte proliferation may be mediated by IGF-I transmodulation of the EGF receptor. J Invest Dermatol. 1991; 96:419–424.
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5. Sadagurski M, Yakar S, Weingarten G, Holzenberger M, Rhodes CJ, Breitkreutz D, et al. Insulin-like growth factor 1 receptor signaling regulates skin development and inhibits skin keratinocyte differentiation. Mol Cell Biol. 2006; 26:2675–2687.
Article
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