Unilateral Nevoid Telangiectasia Clinical Presentation

  • Author: Rajani Katta, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Aug 1, 2011
 

History

Cutaneous lesions are asymptomatic and may go unrecognized. Inquiry into possible stimulus for development may include relation to puberty, pregnancy, contraceptive use, or hepatic diseases.

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Physical

Patches of superficial, blanchable telangiectasias may be small to large and few to numerous. They are disposed predominantly in a unilateral linear distribution. Note the image below.

Unilateral nevoid telangiectasia on the neck. Unilateral nevoid telangiectasia on the neck.

The third and fourth cervical dermatomes are the most common sites, but the thoracic dermatomes and scattered distant sites may also be involved.

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Causes

The pathogenesis of unilateral nevoid telangiectasia remains unknown.

The occurrence of acquired unilateral nevoid telangiectasia in certain settings characterized by elevations of estrogen suggests hormonal causes. Such settings include puberty, pregnancy, and during oral contraceptive use. The other major setting in which this has been reported to occur is in states of hepatic dysfunction. Unilateral nevoid telangiectasia has been reported in patients with chronic liver disease due to alcoholism or hepatitis C, and one case was described in a patient with liver metastases from carcinoid tumor.[5]

Uhlin et al documented increased levels of estrogen and progesterone receptors in involved areas compared with normal skin[6] ; however, other reports have not been able to reproduce this finding.

Because unilateral nevoid telangiectasia has been noted in cases in which no underlying hormonal or hepatic pathology has been found, other mechanisms probably play a role in the pathogenesis.

Although reported cases often involve a dermatome or a group of dermatomes, distribution following the lines of Blaschko suggests that a postzygotic somatic mutation leads to a distinct cell population in the affected site (mosaicism).

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Contributor Information and Disclosures
Author

Rajani Katta, MD  Associate Professor, Department of Dermatology, Baylor College of Medicine; Director, Contact Dermatitis Clinic

Rajani Katta, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Abdul-Ghani Kibbi, MD  Professor and Chair, Department of Dermatology, American University of Beirut Medical Center, Lebanon

Disclosure: Nothing to disclose.

Michael J Wells, MD  Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Van Perry, MD  Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

Van Perry, MD is a member of the following medical societies: American Academy of Dermatology and American Society for Laser Medicine and Surgery

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References

  1. Happle R. Loss of heterozygosity in human skin. J Am Acad Dermatol. Aug 1999;41(2 Pt 1):143-64. [Medline].

  2. Happle R. Mosaicism in human skin. Understanding the patterns and mechanisms. Arch Dermatol. Nov 1993;129(11):1460-70. [Medline].

  3. Wilkin JK, Smith JG Jr, Cullison DA, Peters GE, Rodriquez-Rigau LJ, Feucht CL. Unilateral dermatomal superficial telangiectasia. Nine new cases and a review of unilateral dermatomal superficial telangiectasia. J Am Acad Dermatol. Apr 1983;8(4):468-77. [Medline].

  4. Hynes LR, Shenefelt PD. Unilateral nevoid telangiectasia: occurrence in two patients with hepatitis C. J Am Acad Dermatol. May 1997;36(5 Pt 2):819-22. [Medline].

  5. Beacham BE, Kurgansky D. Unilateral naevoid telangiectasia syndrome associated with metastatic carcinoid tumour. Br J Dermatol. Jan 1991;124(1):86-8. [Medline].

  6. Uhlin SR, McCarty KS Jr. Unilateral nevoid telangiectatic syndrome. The role of estrogen and progesterone receptors. Arch Dermatol. Mar 1983;119(3):226-8. [Medline].

  7. Kavak A, Kutluay L. Unilateral nevoid telangiectasia and hyperthyroidism: a new association or coincidence?. J Dermatol. May 2004;31(5):411-4. [Medline].

  8. Kreft B, Marsch WC, Wohlrab J. Unilateral nevoid telangiectasia syndrome. Dermatology. 2004;209(3):215-7. [Medline].

  9. Cliff S, Harland CC. Recurrence of unilateral naevoid telangiectatic syndrome following treatment with the pulsed dye laser. J Cutan Laser Ther. Apr 1999;1(2):105-7. [Medline].

  10. Sharma VK, Khandpur S. Unilateral nevoid telangiectasia--response to pulsed dye laser. Int J Dermatol. Aug 2006;45(8):960-4. [Medline].

 
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Unilateral nevoid telangiectasia on the neck.
 
 
 
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