% 187260

TELANGIECTASIA, HEREDITARY BENIGN


Alternative titles; symbols

HBT
TELANGIECTASIA, GENERALIZED ESSENTIAL


Cytogenetic location: 5q14   Genomic coordinates (GRCh38) : 5:77,600,001-93,000,000


Gene-Phenotype Relationships
Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
5q14 Telangiectasia, hereditary benign 187260 AD 2
Clinical Synopsis
 

INHERITANCE
- Autosomal dominant
SKIN, NAILS, & HAIR
Skin
- Telangiectases, random body distribution
- Small, red lesion, may increase in size with age
- Lesions become soft and paler with age
- Size variation (1 x 1 to 6 x 4 cm)
- Variable number of lesions (1 to greater than 10)
- No hemorrhage
- No systemic vascular lesions
Skin Histology
- Dilatation of the small vessels in the upper part of the dermis
- Usually venules, but can also be capillaries and arterioles
MISCELLANEOUS
- Onset usually in early childhood
- More frequent in females

TEXT

Clinical Features

Ryan and Wells (1971) described 7 kindreds in each of which several persons had widespread telangiectases. The areas affected were predominantly the face, upper limbs, and upper trunk. The telangiectases were venular and associated with upper dermal atrophy. Wells and Dowling (1981) reported 3 affected families with an autosomal dominant pattern. Person and Longcope (1985) described a 21-year-old man with hereditary benign telangiectasia whose mother and 1 of his 2 sisters were similarly affected. No mucosal lesions or history of hemorrhagic problems were elicited. The authors noted that the disorder, also known as generalized essential telangiectasia, occurs more frequently in women. Person and Longcope (1985) could not demonstrate estrogen or progesterone receptors in the skin lesions of their proband. They were prompted to look for receptors because of the finding of a considerable increase in such receptors in the lesion of unilateral nevoid telangiectasia (Uhlin and McCarty, 1983), a segmental disorder seen in women at puberty, during pregnancy, or while taking contraceptives, but also observed in men with hepatic cirrhosis.

Brancati et al. (2003) reported a large family from northern Italy in which 13 members over 3 generations had autosomal dominant hereditary benign telangiectasia. Age at onset could not always be determined, but some parents noted macular telangiectases in their sons during the first months of life. There was a large variability in size (1 x 1 to 6 x 4 cm) and number (1 to greater than 10) of telangiectases observed among affected family members, but lesions invariably became paler with increasing age. Histologic examination showed normal epidermis and dilatation of the smallest blood vessels of the upper part of the dermis.


Mapping

In a large family with HBT from northern Italy, Brancati et al. (2003) found linkage to a 7-Mb region on chromosome 5q14 (maximum lod score of 5.27 at marker D5S641). The authors noted that the linked interval in this family coincided with the CMC1 locus (163000), suggesting that HBT and capillary malformations may be variable clinical presentations of the same disorder.


REFERENCES

  1. Brancati, F., Valente, E. M., Tadini, G., Caputo, V., Di Benedetto, A., Gelmetti, C., Dallapiccola, B. Autosomal dominant hereditary benign telangiectasia maps to the CMC1 locus for capillary malformation on chromosome 5q14. J. Med. Genet. 40: 849-853, 2003. [PubMed: 14627680, related citations] [Full Text]

  2. Person, J. R., Longcope, C. Estrogen and progesterone receptors are not increased in generalized essential telangiectasia. (Letter) Arch. Derm. 121: 836-837, 1985. [PubMed: 4015128, related citations]

  3. Ryan, T. J., Wells, R. S. Hereditary benign telangiectasia. Trans. St. John's Hosp. Derm. Soc. 57: 148-156, 1971.

  4. Uhlin, S. R., McCarty, K. S. Unilateral nevoid telangiectasia syndrome: the role of estrogen and progesterone receptors. Arch. Derm. 119: 226-228, 1983. [PubMed: 6824361, related citations] [Full Text]

  5. Wells, R. S., Dowling, G. B. Hereditary benign telangiectasia. Brit. J. Derm. 84: 93-94, 1981.


Contributors:
Cassandra L. Kniffin - updated : 1/6/2004
Creation Date:
Victor A. McKusick : 6/2/1986
mgross : 03/18/2004
tkritzer : 1/13/2004
ckniffin : 1/6/2004
mimadm : 5/10/1995
supermim : 3/16/1992
supermim : 3/20/1990
ddp : 10/27/1989
marie : 3/25/1988
reenie : 6/2/1986

% 187260

TELANGIECTASIA, HEREDITARY BENIGN


Alternative titles; symbols

HBT
TELANGIECTASIA, GENERALIZED ESSENTIAL


SNOMEDCT: 238763007, 238764001;   MONDO: 0008534;  


Cytogenetic location: 5q14   Genomic coordinates (GRCh38) : 5:77,600,001-93,000,000


Gene-Phenotype Relationships

Location Phenotype Phenotype
MIM number
Inheritance Phenotype
mapping key
5q14 Telangiectasia, hereditary benign 187260 Autosomal dominant 2

TEXT

Clinical Features

Ryan and Wells (1971) described 7 kindreds in each of which several persons had widespread telangiectases. The areas affected were predominantly the face, upper limbs, and upper trunk. The telangiectases were venular and associated with upper dermal atrophy. Wells and Dowling (1981) reported 3 affected families with an autosomal dominant pattern. Person and Longcope (1985) described a 21-year-old man with hereditary benign telangiectasia whose mother and 1 of his 2 sisters were similarly affected. No mucosal lesions or history of hemorrhagic problems were elicited. The authors noted that the disorder, also known as generalized essential telangiectasia, occurs more frequently in women. Person and Longcope (1985) could not demonstrate estrogen or progesterone receptors in the skin lesions of their proband. They were prompted to look for receptors because of the finding of a considerable increase in such receptors in the lesion of unilateral nevoid telangiectasia (Uhlin and McCarty, 1983), a segmental disorder seen in women at puberty, during pregnancy, or while taking contraceptives, but also observed in men with hepatic cirrhosis.

Brancati et al. (2003) reported a large family from northern Italy in which 13 members over 3 generations had autosomal dominant hereditary benign telangiectasia. Age at onset could not always be determined, but some parents noted macular telangiectases in their sons during the first months of life. There was a large variability in size (1 x 1 to 6 x 4 cm) and number (1 to greater than 10) of telangiectases observed among affected family members, but lesions invariably became paler with increasing age. Histologic examination showed normal epidermis and dilatation of the smallest blood vessels of the upper part of the dermis.


Mapping

In a large family with HBT from northern Italy, Brancati et al. (2003) found linkage to a 7-Mb region on chromosome 5q14 (maximum lod score of 5.27 at marker D5S641). The authors noted that the linked interval in this family coincided with the CMC1 locus (163000), suggesting that HBT and capillary malformations may be variable clinical presentations of the same disorder.


REFERENCES

  1. Brancati, F., Valente, E. M., Tadini, G., Caputo, V., Di Benedetto, A., Gelmetti, C., Dallapiccola, B. Autosomal dominant hereditary benign telangiectasia maps to the CMC1 locus for capillary malformation on chromosome 5q14. J. Med. Genet. 40: 849-853, 2003. [PubMed: 14627680] [Full Text: https://doi.org/10.1136/jmg.40.11.849]

  2. Person, J. R., Longcope, C. Estrogen and progesterone receptors are not increased in generalized essential telangiectasia. (Letter) Arch. Derm. 121: 836-837, 1985. [PubMed: 4015128]

  3. Ryan, T. J., Wells, R. S. Hereditary benign telangiectasia. Trans. St. John's Hosp. Derm. Soc. 57: 148-156, 1971.

  4. Uhlin, S. R., McCarty, K. S. Unilateral nevoid telangiectasia syndrome: the role of estrogen and progesterone receptors. Arch. Derm. 119: 226-228, 1983. [PubMed: 6824361] [Full Text: https://doi.org/10.1001/archderm.119.3.226]

  5. Wells, R. S., Dowling, G. B. Hereditary benign telangiectasia. Brit. J. Derm. 84: 93-94, 1981.


Contributors:
Cassandra L. Kniffin - updated : 1/6/2004

Creation Date:
Victor A. McKusick : 6/2/1986

Edit History:
mgross : 03/18/2004
tkritzer : 1/13/2004
ckniffin : 1/6/2004
mimadm : 5/10/1995
supermim : 3/16/1992
supermim : 3/20/1990
ddp : 10/27/1989
marie : 3/25/1988
reenie : 6/2/1986