Skip to main content
Open Access Publications from the University of California

Dermatology Online Journal

Dermatology Online Journal bannerUC Davis

Unilateral nevoid telangiectasia syndrome: a case report and review of the literature

Main Content

Unilateral nevoid telangiectasia syndrome: A case report and review of the literature
Scott F Wenson MD1, Farhana Jan MD2, Alireza Sepehr MD1
Dermatology Online Journal 17 (5): 2

1. Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts.
2. Department of Dermatology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts


We report on a 43-year-old Caucasian female who presented with bright red macules in a unilateral distribution in the left C5-8 and L3-5 dermatomes. Histopathologic examination showed superficial papillary dermal telangiectasia with minimal chronic inflammation. Immunohistochemical stains for estrogen and progesterone receptors (ER/PR) were negative. A diagnosis of unilateral nevoid telangiectasia syndrome (UNTS) was given. UNTS is an uncommon disorder first described by Alfred Blaschko in 1899. It is comprised of telangiectasias occurring in a predominantly unilateral dermatomal distribution and often affecting the trigeminal, cervical, and upper thoracic dermatomes. It can be either congenital or acquired and has a 2:1 female:male ratio. UNTS has been reported in relation to hyperestrogenic states, with half of the reported cases related to pregnancy, puberty, or liver disease. However, the vast majority of cases show no increase in estrogen and progesterone receptors in lesional skin. UNTS may be more common than previously believed, and shows some response to vascular laser therapy. Differential diagnoses include hemangioma, angioma serpiginosum, and rarely, nevus flammeus.


Unilateral nevoid telangiectasia syndrome (UNTS) is a rare cutaneous disorder first described by Alfred Blaschko in 1899 [1]. UNTS is characterized by superficial dermal telangiectasias that occur unilaterally in a dermatomal distribution and commonly involve the trigeminal nerve as well as cervical and upper thoracic nerve distributions (C3-T2). Many different names have been used to describe this syndrome acquired spider telangiectasias [2], microtelangiectasia essential progressive unilateral [3], unilateral nevoid telangiectasia [4], linear telangiectasia [5], unilateral spider nevi [6], unilateral telangiectasia [7], and unilateral dermatomal superficial telangiectasia syndrome [8]. Whereas the latter term, unilateral dermatomal superficial telangiectasia syndrome coined by Wilken et al in 1978, is perhaps the best descriptive term for the syndrome, UNTS has become the most widely accepted name and also the most recognizable. The term nevoid in the diagnosis refers to the likeness to other congenital blaschkoid cutaneous lesions and does not connote a specific morphology of the telangiectasias. Early reports of UNTS appear to highlight a disease of women occurring primarily in hyperestrogenic states such as puberty or pregnancy. However, recent reports show a more heterogeneous presentation. Although originally believed to be a rare syndrome, the increasing frequency of reports of UNTS in recent years suggests this syndrome may be more common than previously thought. We report a case of UNTS presenting in a 43-year-old female and briefly review the literature.

Case report

Figure 1Figure 2
Figure 1. Continuous distribution of telangiectasias along lateral left arm and forearm in the C7-C8 dermatomes.

Figure 2. Left upper arm with dermatomal distribution of grouped telangiectasias.

We report on a 43-year-old female patient who presented complaining of a reddish eruption on her left arm and left leg. She reports that the eruption had been present on the left upper arm for greater than 20 years. She was seen 5 years prior at the same clinic at which time the eruption was noted to be consistent with benign nevoid telangiectasia (UNTS). The patient reports that in cold weather the eruption extends distally onto the left forearm and hand, as well as the left leg and is non-pruritic. The patient has had no successful therapies to date. Her past medical history was significant only for heavy menstrual bleeding and uterine fibroids.

Figure 3Figure 4
Figure 3. Extension of telangiectasias into lateral left hand and 5th digit in C8 dermatome.

Figure 4. Close-up of telangiectasias on left lateral hand.

Figure 5Figure 6
Figure 5. Close up of telangiectasias on left upper arm.

Figure 6. Faint telangiectasias on the left thigh involving L4-L5 dermatomes.

Dermatologic exam revealed bright red macules in a blaschkoid distribution involving the left upper arm. The left forearm, left dorsal hand, and left thigh showed similar but fewer scattered lesions (Figures 1 through 6). A 4 mm punch biopsy was obtained from lesional skin of the left upper arm and histopathological examination of the biopsy showed superficial papillary dermal telangiectasia with minimal perivascular chronic inflammation (Figures 7 through 10). Immunohistochemical stains for estrogen receptors (ER) and progesterone receptors (PR) were negative with adequate controls (not shown). The histopathologic findings were consistent with UNTS in the appropriate clinical setting.

Figure 7Figure 8
Figure 7. Scanning magnification showing unremarkable epidermis with superficial papillary dermal telangiectasias and unremarkable reticular dermis (H&E, x20).

Figure 8. Medium-power view demonstrating telangiectasias and mild perivascular chronic inflammation (H&E, x40).

Figure 9Figure 10
Figure 9. High-power view highlighting superficial papillary dermal telangiectasias and mild perivascular lympho-histiocytic inflammation (H&E, x200).

Figure 10. High-power view of superficial papillary dermal telangiectasia with mild perivascular lympho-histiocytic inflammation (H&E, x400).

Review of the literature

Including the present case there are slightly fewer than 100 reported cases of UNTS in the literature available for review [1-50, 51-59] (Table 1). In the reported cases, the age of presentation ranges from 0.4 to 83 years, with a mean of 28.1 years and a median of 25.0 years. The age of onset ranges from birth to 69 years, with a mean of 18.0 years and a median of 16.5 years. Sixty-three cases are female and 33 are male; in one case gender was not reported. Forty-five cases involve the left half of the body and 44 involve the right. Additionally, 2 are bilateral and 1 involves the central forehead; 6 do not report laterality. Fourteen cases involve the trigeminal distribution; 74 cases involve at least one cervical dermatome; 44 involve at least one thoracic dermatome; 9 involve at least one lumbar dermatome; 3 involve the sacral dermatomes. Association with pregnancy is reported in 26 cases and 23 with the onset of puberty. There are16 congenital cases and 10 cases are associated with hepatic cirrhosis or liver disease (including alcohol abuse, HBV infection, and HCV infection). Two cases develop following the initiation of hormonal contraceptive medication [5, 27]. The association with Becker melanosis [32] is seen in one case and one is associated with chemotherapy administration [51]. Other associations include hyperthyroidism in one case [46] and a metastatic carcinoid tumor in one example (notably to the liver) [33]. In one case a pyogenic granuloma developed within the area affected by UNT [43]. However, 16 cases either have no known association or no association is provided. Of the reported cases that were tested for estrogen and progesterone receptor status on histopathologic sections, only 1 case is positive for both ER and PR [10], 1 case shows trace ER positivity [11], and 1 case shows trace PR positivity [12]. The remaining cases, including the current reported case, are negative for either ER and/or PR in lesional skin.


UNTS is an uncommon vascular skin lesion which has been shown to affect a variable patient population. It is known to occur as both a congenital and as an acquired condition [17]. It consists of partially to completely blanchable telangiectasias occurring most often in a unilateral dermatomal distribution that frequently affects the trigeminal, cervical, and upper thoracic dermatomes. Histopathologic examination reveals a normal-appearing epidermis with underlying superficial dermal telangiectatic blood vessels with minimal inflammatory infiltrate [53]. Although originally described as a syndrome predominantly in the female population and in conjunction with hepatic cirrhosis, as more cases have been added to the literature the female-to-male ratio has decreased to approximately 2:1. Recently numerous cases have been reported in which there is no association with a known pathology [4, 39, 52, 53]. As the literature regarding UNTS has expanded it appears that the condition may not be as rare as previously described. UNTS may in fact be an underreported syndrome [21, 24].

Many of the original reports of UNTS indicate a high female predominance as well as an association with hyperestrogenic states such as puberty and pregnancy [5, 18, 28]. Half of all cases reported (48/96) involve puberty and pregnancy. An additional sixteen cases (15.5%) were congenital and it is possible that the development of lesions in utero may result from increased exposure to sex hormones such as estrogen or progesterone. Cases occurring in women during pregnancy have characteristically flared during pregnancy and often wane or resolve completely in the post-partum period, suggesting a direct relationship between the elevated hormonal milieu of pregnancy and the cutaneous lesions of UNTS [5, 6, 17, 35, 47, 48]. In 1972, Cunliffe et al [6] attempted to test this hypothesis in a patient who had experienced UNTS during her past pregnancy with post-partum resolution. Estrogen creams were applied to the previously affected areas in hopes of inducing a recurrence of telangiectasias in an artificial hyperestrogenic environment. However, the telangiectasias failed to recur under these conditions, suggesting estrogen may not be the only inciting factor [6]. No other studies have tested the hypothesis in this fashion.

Several authors have noted an association between UNTS and liver disease, often hepatic cirrhosis [12-15, 23, 25, 41], but also rarely metastatic disease to the liver [33]. Hepatic failure and cirrhosis are known to cause hyperestrogenemia as a result of impaired estrogen metabolism and the correlation between liver disease and vascular abnormalities such as spider angiomata are well known [60]. Therefore, cases in which a patient’s known primary symptoms are hepatic failure or cirrhosis appear to strengthen the argument that UNTS is a process driven by increased levels of circulating estrogens, similar to cases presenting during puberty or pregnancy. Similarly, Kavak and Kutluay [46] report a single case of UNTS developing in a patient with hyperthyroidism, which is hypothesized by the authors to have caused a mildly hyperestrogenic state and subsequently the resulting telangiectasias.

Some authors refute estrogen as the causal agent underlying the telangiectasia development in UNTS [26, 39]. Many reports supporting the hormonal hypothesis cite a single case [27], which demonstrated increased estrogen and progesterone recepors in a lesional skin biopsy. Since the report by Uhlin and McCarty, the overwhelming majority of cases have shown little or no estrogen/progesterone receptor positivity in biopsies from patients with UNTS [31, 33, 35, 38, 39, 44-46, 49-51, 53, 56, 59]. Also, there have been no documented cases of increased serum or urine estrogen or progesterone levels outside of known pregnant patients. Our case showed no increased estrogen and progesterone receptors in the biopsy of lesional skin using immunoperoxidase staining methods.

However, the methods used by Uhlin and McCarty [27] to determine the estrogen and progesterone receptor levels in their case did not involve typical immunoperoxidase methods. Instead, the authors utilized quantitative evaluation of estrogen and progesterone receptors using a unique and complex radioactive labeling method. No other study has utilized a similar method and this may explain the negativity for estrogen and progesterone receptors in subsequent reports. Given the overwhelming lack of positivity for estrogen and progesterone receptors in the vast majority of patient samples, unless future investigators are able to duplicate the methods of Uhlin and McCarty [27], it seems reasonable to conclude that UNTS is not associated with increased estrogen or progesterone receptors in affected areas. It remains possible that the estrogen or progesterone receptors in the skin of patients with UNTS may be more sensitive to circulating sex hormones, but this theory has not been tested and the study performed by Cunliffe et al [6] suggests otherwise.

There have been several hypotheses regarding a possible underlying vascular pathogenesis of UNTS. Some authors favor that UNTS represents a congenital but generally latent, vascular nevus, which becomes active under certain physiologic triggers such as hepatic disease or hyperestrogenic states [12, 23, 41, 43, 45, 59]. Others have suggested that UNTS may represent a subclinical variant of nevus flammeus that may only become apparent under the appropriate pathophysiologic conditions [15, 20, 47]. Jucas et al [20] proposed that an as-yet-unknown epidermal angiogenic factor may be the causal agent of the telangiectasia development in UNTS. To date, no specific angiogenic factor has been elucidated. Kreft et al [47] demonstrated by laser-Doppler flowmetry that the areas of skin involved in UNTS show hyperperfusion, indicating a functional vascular defect. The development of the telangiectasias in the case reported by Beacham and Kurgansky [33] was associated with a warm flushing sensation in the affected area, possibly because of increased vascular flow to the affected areas resulting in ectatic blood vessels and the clinically apparent telangiectasias. Mazereeuw-Hautier et al [43] report a single case in which a pyogenic granuloma developed within the lesional skin affected by UNTS. Although most likely coincidental, it is possible that the vascular outgrowth of the pyogenic granuloma was related to the underlying vascular physiologic disturbance of the patient’s UNTS.

Several authors have suggested that chromosomal mosaicism is the underlying cause of UNTS [38, 52, 59], although to date there is no evidence to support this theory. Ortonne et al [19] describe a patient whose UNTS lesions showed a marked flare during an infection by the measles virus, although the authors do not associate this finding with the pathogenesis of UNTS.

There are only two reports that describe telangiectasias occurring in UNTS in organs other than the skin [15, 48]. Anderton and Smith [15] report a patient with known hepatic cirrhosis who had cutaneous findings consistent with UNTS as well as numerous gastric telangiectasias noted on endoscopy. Given that the patient had documented cirrhosis, the gastric telangiectasias could very well have been a consequence of increased splanchnic vascular pressure rather than the true nevoid telangiectasias seen in UNTS. In the case reported by Tang et al [48], the patient developed bilateral nevoid telangiectasias as well as gastric telangiectasias during pregnancy. Both the cutaneous and gastric findings resolved post-partum, consistent with UNTS, albeit bilateral in this case. It is unclear whether the gastric findings were truly related to the diagnosis of nevoid telangiectasia syndrome or were possibly related to vascular changes of pregnancy. Given the lack of additional reports of UNTS involving the gastrointestinal tract, we favor that these reports are evidence of coincidental gastrointestinal vascular lesions with a background of UNTS. However, these cases may represent a rare variant of UNTS with gastric involvement.

Recent cases have discussed patients’ responses to various therapies [40, 52], most commonly laser phototherapy. Although treatment is not required in UNTS because the lesions are generally asymptomatic, patients may request therapy for cosmetic reasons. Pulsed-dye laser therapy of the involved areas may be used with good cosmetic outcome [40, 52, 56]. However, the lesions frequently recur [40].

The differential diagnosis of UNTS includes other cutaneous vascular lesions such as hemangioma, angioma serpiginosum, and rarely nevus flammeus. The dermatomal nevoid telangiectasias of UNTS should be clinically discernable from those of a typical hemangioma. Histologically, hemangioma also shows a more distinct vascular proliferation compared to the sparse papillary dermal telangiectatic vessels of UNTS. Angioma serpiginosum is characterized by a distinct distribution (usually lower extremities) of multiple punctate red or purple lesions, typically arranged in a serpiginous pattern. Angioma serpiginosum is composed of thick-walled, dilated capillaries in the superficial or mid-dermis [61]. This distribution and appearance is typical and would not often be confused with UNTS. Nevus flammeus has a more macular clinical appearance compared UNTS. Nevus flammeus presents at birth and should be considered in cases of suspected congenital UNTS.

In summary, UNTS, although still an uncommon condition, is not as rare as previously reported. It is characterized by aymptomatic superficial dermal telangiectasias that occur unilaterally (or much more rarely bilaterally) in a dermatomal distribution and commonly involve the trigeminal nerve divisions as well as cervical and upper thoracic nerve distributions (C3-T2). A 2:1 female:male predominance is noted and many patients present at the onset of puberty and during pregnancy, which implicates hyperestrogenic states as an underlying pathophysiologic cause of the syndrome. However, there is no documented evidence to support this hypothesis to date. As such, UNTS remains somewhat of a mystery, and its physiologic characteristics are still unknown. Further studies are needed to better understand this unique condition.


1. Blaschko A. Telangiektasien Versammlungen BerlingerDermatologische Gesellschaft. Monatsschr Prakt Dermat 1899; 28:451.

2. Pautrier L, Ullmo A. Télangiectasies stellaires acquises chez une femme enceinte, localisées au membre supérieur droit, su le territoire du plexus cervical. Bull Soc Fr Derm Syph 1931; 38:309-316.

3. Bowen EJ. Neo-Eruptive Microangiomatosis Tardive Systematized (Microtelangiectasis Essential Progressive Unilateral), Tommasi? Arch Dermatol 1964; 89:615-6. [PubMed]

4. Selmanowitz VJ. Unilateral nevoid telangiectasia. Ann Intern Med 1970; 73:87-90. [PubMed]

5. Aram H, Solomon LM. Linear telangiectasia. Acta Derm Venereol 1970; 50:302-8. [PubMed]

6. Cunliffe WJ, Dodman B, Butterworth MJ. Unilateral spider naevi. Br J Dermatol 1972; 87:51-2. [PubMed]

7. Koopmans-van Dorp B. [Unilateral telangiectasis during pregnancy]. Ned Tijdschr Geneeskd 1972; 116:691-2. [PubMed]

8. Wilkin JK. Unilateral dermatomal superficial telangiectasia. Dermatologica 1978; 157:33-41. [PubMed]

9. Zeisler E. Telangiectasia associated with syphilis and pregnancy. Archives of Dermatology and Syphilology 1922; 5:781.

10. Tommasi L. Giornale Italiano Della Malatie Veneree I Della Pelle 1923; 64:275.

11. Billings FT, Jr. Unusual Distribution of Vascular Spiders in Pregnancy. Arch Intern Med 1963; 112:835-9. [PubMed]

12. Mirrer E, Cipriano A, McGuire J. Unilateral nevoid telangiectasia. Arch Dermatol 1971; 103:320-3. [PubMed]

13. Frankel EB. Letter: Unilateral nevoid telangiectasia. Arch Dermatol 1974; 110:638. [PubMed]

14. Greer KE. Letter: Unilateral nevoid telangiectasia. Arch Dermatol 1974; 109:100-1. [PubMed]

15. Anderton RL, Smith JG, Jr. Unilateral nevoid telangiectasia with gastric involvement. Arch Dermatol 1975; 111:617-21. [PubMed]

16. Engebretsen T. [Unilateral teleangiectases during pregnancy]. Tidsskr Nor Laegeforen 1975; 95:1577, 1593, 1602. [PubMed]

17. Wilkin JK. Unilateral nevoid telangiectasia: three new cases and the role of estrogen. Arch Dermatol 1977; 113:486-8. [PubMed]

18. Grupper C, Bermejo D, Bouyx P, Belperron P, Verret JL, Schnitzler L. [Congenital or acquired unilateral nevoid stellar telangiectasias. About 5 cases (author's transl)]. Ann Dermatol Venereol 1978; 105:691-7. [PubMed]

19. Ortonne JP, Guillet G, Perrot H. Unilateral nevoid telangiectasia. Arch Dermatol 1978; 114:446-7. [PubMed]

20. Jucas JJ, Rietschel RL, Lewis CW. Unilateral nevoid telangiectasia. Arch Dermatol 1979; 115:359-60. [PubMed]

21. Person JR, Ossi MJ, Mundra R. Unilateral nevoid telangiectasia. Arch Dermatol 1979; 115:1034. [PubMed]

22. Reymond JL, Stoebner P, Amblard P. [Acquired nevoid telangiectasia (author's transl)]. Dermatologica 1979; 159:489-94. [PubMed]

23. Capron JP, Kantor G, Dupas JL, Degott C, Locquet MC. Unilateral nevoid telangiectasia and chronic liver disease. Report of a case and review of the literature. Am J Gastroenterol 1981; 76:47-51. [PubMed]

24. Christensen OB. Unilateral nevoid telangiectasia. Arch Dermatol 1981; 117:63. [PubMed]

25. Raff M, Bardach HG. [Unilateral nevoid telangiectatic syndrome]. Hautarzt 1982; 33:148-51. [PubMed]

26. Duong MH, Raymond GP. Unilateral dermatomal superficial telangiectasia. Can Med Assoc J 1983; 129:1117-8. [PubMed]

27. Uhlin SR, McCarty KS, Jr. Unilateral nevoid telangiectatic syndrome. The role of estrogen and progesterone receptors. Arch Dermatol 1983; 119:226-8. [PubMed]

28. 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 1983; 8:468-77. [PubMed]

29. Colver GB, Shrank AB, Ryan TJ. Unilateral dermatomal superficial telangiectasia. Clin Exp Dermatol 1985; 10:455-8. [PubMed]

30. Labohm EB, Misere JF, Veen C. [Unilateral nevoid telangiectasis syndrome]. Hautarzt 1985; 36:107-8. [PubMed]

31. Vestey JP, Buxton PK, Hawkins RA. Unilateral naevoid telangiectatic syndrome--a study of two cases. Clin Exp Dermatol 1985; 10:288-91. [PubMed]

32. Wagner RF, Jr., Grande DJ, Bhawan J, Hellerstein MK, Longcope C. Unilateral dermatomal superficial telangiectasia overlapping Becker's melanosis. Int J Dermatol 1989; 28:595-6. [PubMed]

33. Beacham BE, Kurgansky D. Unilateral naevoid telangiectasia syndrome associated with metastatic carcinoid tumour. Br J Dermatol 1991; 124:86-8. [PubMed]

34. Trueb RM, Burg G. [Unilateral "nevoid" spider nevi]. Vasa 1993; 22:82-5. [PubMed]

35. Tok J, Berberian BJ, Sulica VI. Unilateral nevoid telangiectasia syndrome. Cutis 1994; 53:53-4. [PubMed]

36. Woollons A, Darley CR. Unilateral naevoid telangiectasia syndrome in pregnancy. Clin Exp Dermatol 1996; 21:459-60. [PubMed]

37. Esteve E, Georgescu V, Kalis B. [A case for diagnosis: unilateral nevoid telangiectasia]. Ann Dermatol Venereol 1997; 124:407-8. [PubMed]

38. Hynes LR, Shenefelt PD. Unilateral nevoid telangiectasia: occurrence in two patients with hepatitis C. J Am Acad Dermatol 1997; 36:819-22. [PubMed]

39. Taskapan O, Harmanyeri Y, Sener O, Aksu A. Acquired unilateral nevoid telangiectasia syndrome. Acta Derm Venereol 1997; 77:62-3. [PubMed

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

41. Creamer D, Clement M, McGregor JM, Hawk JL. Polymorphic light eruption occurring solely on an area of naevoid telangiectasia. Clin Exp Dermatol 1999; 24:202-3. [PubMed]

42. Sardana K, Sarkar R, Busu S, Sharma RC, Koranne RV. Unilateral nevoid telangiectasia syndrome. J Dermatol 2001; 28:453-4. [PubMed]

43. Mazereeuw-Hautier J, Thibaut I, Bonafe JL. Pyogenic granuloma within unilateral dermatomal superficial telangiectasia. Br J Dermatol 2003; 148:823-4. [PubMed]

44. Ramírez-Andreo A G-AP, Tercedor J, Fernández-Vilariño E, Morales E, García-López C, García-Mellado V. Telangiectasia nevoide unilateral. Actas Dermosifiliogr 2003; 94:258-9.

45. Karakas M, Durdu M, Sonmezoglu S, Akman A, Gumurdulu D. Unilateral nevoid telangiectasia. J Dermatol 2004; 31:109-12. [PubMed]

46. Kavak A, Kutluay L. Unilateral nevoid telangiectasia and hyperthyroidism: a new association or coincidence? J Dermatol 2004; 31:411-4. [PubMed]

47. Kreft B, Marsch WC, Wohlrab J. Unilateral nevoid telangiectasia syndrome. Dermatology 2004; 209:215-7. [PubMed]

48. Tang SJ, Faughnan ME, Marcon NE. Bilateral nevoid telangiectasia syndrome. Gastrointest Endosc 2004; 60:468-71. [PubMed]

49. Grimaldi M, Pranteda G, Talerico C, Pranteda G, Di Napoli A. Acquired unilateral naevoid telangiectasia in a healthy boy. Acta Derm Venereol 2006; 86:469-70. [PubMed]

50. Karabudak O, Dogan B, Taskapan O, Harmanyeri Y. Acquired unilateral nevoid telangiectasia syndrome. J Dermatol 2006; 33:825-6. [PubMed]

51. Rodriguez-Martin M, Saez M, Carnerero A, et al. Unilateral naevoid telangiectasia in a young man after chemotherapy: a simple coincidence or a new clinical association? J Eur Acad Dermatol Venereol 2006; 20:1001-2. [PubMed]

52. Sharma VK, Khandpur S. Unilateral nevoid telangiectasia--response to pulsed dye laser. Int J Dermatol 2006; 45:960-4. [PubMed]

53. Afsar FS, Ortac R, Diniz G. Unilateral nevoid telangiectasia with no estrogen and progesterone receptors in a pediatric patient. Indian J Dermatol Venereol Leprol 2008; 74:163-4. [PubMed]

54. Dadlani C, Kamino H, Walters RF, Rosenman K, Pomeranz MK. Unilateral nevoid telangiectasia. Dermatol Online J 2008; 14:3. [PubMed]

55. Derrow AE, Adams BB, Timani S, Mutasim DF. Acquired unilateral nevoid telangiectasia in a 51-year-old female. Int J Dermatol 2008; 47:1331-3. [PubMed]

56. Senel E, Gulec AT. Congenital unilateral naevoid telangiectasia with a wide dermatomal distribution. Clin Exp Dermatol 2008; 33:663-4. [PubMed]

57. Almazan-Fernandez FM, Guiote MV, Burkhardt P, Naranjo R. [Unilateral nevoid telangiectasis in a patient with chronic hepatitis B virus infection]. Actas Dermosifiliogr 2009; 100:82-3. [PubMed]

58. Blaise S, Kherat N, Seinturier C, Beani JC. [Circumscribed telangiectasic lesions of the upper limb: unilateral nevoid telangiectasia syndrome?]. J Mal Vasc 2009; 34:272-4. [PubMed]

59. Kawakami T, Kimura S, Soma Y. Unilateral nevoid telangiectasia on the lower extremity of a pediatric patient. J Am Acad Dermatol 2010; 62:528-30. [PubMed]

60. Kumar V, Abbas AK, Fausto N, Aster JC. Robbins and Cotran: Pathologic Basis of Disease. China: Saunders Elsevier, 2010.

61. McKee PH, Calonje E, Granter SR. Pathology of the Skin with Clinical Correlations. China: Elsevier Mosby, 2005.

© 2011 Dermatology Online Journal