QJM Advance Access originally published online on July 31, 2008
QJM 2008 101(11):899-900; doi:10.1093/qjmed/hcn098
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Clearance of acanthosis nigricans associated with insulinoma following surgical resection
From the Department of Endocrinology, Institute of Post Graduate Medical Education & Research, Calcutta, India
Address correspondence to S. Ghosh, Department of General Medicine, Ayr hospital, Dalmellington road, Ayr, South Ayrhire, KA6 6DK, UK. email: drsujoyghosh{at}rediffmail.com
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Acanthosis nigricans is said to be a marker of insulin resistance. It is known to occur in patients with insulinoma where there is marked hyperinsulinaemia. We report a case wherein the acanthosis disappeared following surgical resection of insulinoma and this strengthens the hypothesis that hyperinsulinaemia is responsible for acanthosis.
A 35-year-old gentleman presented with episodes of blurred vision, confusion, altered consciousness and seizures, which were relieved on eating. He was non-diabetic not on any medication and had no known malignancies. He was obese (BMI = 31kg/m2) with acanthosis nigricans and skin tags (Figure 1).
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During a supervised fast he became symptomatic and had a plasma glucose of 36 mg/dl and inappropriately high serum insulin (79 mU/ml) and C-peptide (16 ng/ml) levels. Imaging revealed a mass at the junction of the head and body of the pancreas (1.5 cm x 1.2 cm). There was no evidence of other MEN1 tumours.
He underwent surgical enucleation of the mass, which was then histopathologically confirmed to be an insulinoma.
His plasma glucose normalized and he remained symptom free. At 8 weeks (post-op), we noticed that the acanthosis had disappeared. This had occurred even before his subsequent significant weight loss. Blood tests confirmed that his hyperinsulinaemic state had resolved. [Fasting glucose (85 mgl/dl) and insulin (6 mU/ml)].
Acanthosis nigricans is associated with numerous conditions including obesity, type 2 diabetes, polycystic ovarian syndrome and insulinoma.1
It is hypothesized that high levels of circulating unbound insulin binds to IGF-1 receptors on keratinocytes and fibroblasts and leads to proliferation of epidermis resulting in acanthosis nigricans.2
The resolution of the acanthosis even before significant weight loss further strengthens our belief that the surgical resection (with resolution of hyperinsulinaemia) was responsible for disappearance of the acanthosis.
A similar phenomenon has been described following partial pancreatectomy in a case of HAIR-AN syndrome.3
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1. Matsuoka LY, Wortsman J, Gavin JR, Goldman J. Spectrum of endocrine abnormalities associated with acanthosis nigricans. Am J Med (1987) 83:719–25.[CrossRef][Web of Science][Medline]
2. Cruz PD, Hud JA. Excess insulin binding to insulin-like growth factor receptors: proposed mechanism for acanthosis nigricans. J Invest Dermatol (1992) 98(Suppl. 6):82S–5S.[CrossRef][Medline]
3. Peifer SLE, Wilson RM, Gawkrodger DJ. Clearance of acanthosis nigricans associated with the HAIR-AN syndrome after partial pancreatectomy: an 11 year follow-up. Postgrad Med J (1999) 75:421–22.
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