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Year : 2005  |  Volume : 71  |  Issue : 5  |  Page : 370-372

Striae distensae

Gurcharan Singh, Lekshmi P Kumar 
 Department of Dermatology and STD, Sri Devaraj Urs Medical College, Tamaka, Kolar, India

Correspondence Address:
Gurcharan Singh
108, A, Jal Vayu Vihar, Kammanahalli, Bangalore-560 043
India




How to cite this article:
Singh G, Kumar LP. Striae distensae.Indian J Dermatol Venereol Leprol 2005;71:370-372


How to cite this URL:
Singh G, Kumar LP. Striae distensae. Indian J Dermatol Venereol Leprol [serial online] 2005 [cited 2019 Oct 21 ];71:370-372
Available from: http://www.ijdvl.com/text.asp?2005/71/5/370/16800


Full Text

Striae distensae or stretch marks were described as a clinical entity hundreds of years ago, and the first histologic descriptions appeared in the medical literature in 1889.[1] They are a common disfiguring cutaneous condition, characterized by linear smooth bands of atrophic appearing skin[2] which occurs in areas of dermal damage produced by stretching.[3]

 Etiopathogenesis



The exact etiology still remains controversial and this is partly due to the variability in the clinical situations in which striae arise.[1] They are the end result of various physiologic states, including pregnancy, adrenocortical excess and changes in body habitus, as seen in rapid weight change. A genetic predisposition is presumed;[4] striae distensae have been reported in monozygotic twins.[5] There is decreased expression of collagen and fibronectin genes in affected tissue.[6] The role of genetic factors is further emphasized by the fact that they are common in inherited defects of connective tissue,[2] as in Marfan's syndrome.[3]

The occurrence of striae correlates closely with obesity.[3] They are highly prevalent in obese adults and children,[3] but the development of striae in adolescents is not related to obesity and rather coincides with the markers of adolescence such as breast development, pubic hair growth and menarche.[4] In a study on skin diseases in children with organ transplants, steroid induced striae distensae were found only in adolescents and not among younger children.[7] Striae are seen in 90% of pregnant women,[8] due to a combination of hormonal factors (e.g. adrenocortical hormones, estrogen, and relaxin) along with increased lateral stress on connective tissue.[8] Young male weightlifters develop striae on their shoulders.[3] Striae also occur frequently in patients with hypercortisolism as in Cushing's syndrome and in those using topical steroids.[3] Edematous striae distensae are uncommon, but can develop due to the combined effects of systemic glucocorticoids and generalized edema.[9]

It has been noted that striae are prevalent in cachetic states, such as tuberculosis, typhoid and after intense slimming diets.[10] They may also be seen in anorexia nervosa.[11] Striae have been reported to occur rarely in human immunodeficiency virus positive patients receiving the protease inhibitor indinavir.[3] A case of idiopathic striae was also reported.[12] Men and women with chronic liver disease may also have striae.[13]

The pathogenesis of striae is unknown but probably relates to changes in the components of extracellular matrix, including fibrillin, elastin and collagen.[14] Arem and Kisher have proposed that striae are a form of dermal scarring in which the dermal collagen ruptures.[1] It has been suggested that they develop more easily in skin which has a critical proportion of rigid cross linked collagen as occurs in early adult life.[3] In a study on early striae distensae, Sheu et al found that sequential changes of elastolysis accompanied by mast cell degeneration occur in the very early stage of striae distensae.[15] Elastic fibre is the primary target of the pathological process and the abnormalities extend as far as 3 cm beyond the lesion into the normal skin.[15]

 Pathology



Inflammatory changes are conspicuous in the early stage, with dermal edema and perivascular lymphocytic cuffing.[3] In later stages, there is epidermal atrophy and loss of rete ridges.[14] In addition, hair follicles and other appendages are absent.[1] The area of striae is sharply demarcated from the surrounding skin by a densely packed area of thin, eosinophilic, collagen bundles, horizontal to the surface in a parallel fashion.[1] There is an increase in the glycosaminoglycan content in striae and furthermore, the number of vertical fibrillin fibres adjacent to the dermal-epidermal junction and the elastin fibres on the papillary dermis are significantly reduced in striae compared to normal skin.[14] On ultrastructural analysis, the dermal matrix of striae was found to be looser and more floccular.[14]

 Clinical features



The natural evolution of striae is for the red to purple, raised wavy lesions (striae rubra) to fade and leave white atrophic lesions with a wrinkly surface (striae alba).[1] Striae are predominantly located on the arms, thighs, abdomen and lumbosacral area, but may involve other regions, including the face, and flexures in case of striae induced by Cushing's syndrome or steroid therapy.[3] In pregnancy, they occur most commonly on abdomen and breasts.[10] In obese patients striae are lighter, with less atrophy, and narrower than those with Cushing's syndrome.[1] Very rarely, severe, extensive striae may ulcerate or tear.[10] Striae distensae like lesions can present as scarring alopecia among children.[16]

 Diagnosis



There are no known laboratory abnormalities unless the patient has Cushing's syndrome, in which case the serum and urinary steroid levels are increased.[10] Striae have been mistakenly reported as child abuse.[4] Linear focal elastosis can be considered in the differential diagnosis of striae, but here the lesions are yellow and palpable unlike striae.[17]

 Treatment



Effective treatment of striae must be instituted during the active stage, well before the scarring process is complete.[1] Various modalities of treatment have been tried. Weight loss by diet alone or a combination of diet and exercise do not change the degree of striae distensae.[18] Topical tretinoin (0.1%) ameliorates striae and the improvement may persist for almost a year after discontinuation of therapy. [1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11],[12],[13],[14],[15],[16],[17],[18],[19], A study comparing topical 20% glycolic acid and 0.05% tretinoin versus 20% glycolic acid and 10% L-ascorbic acid, found that both regimens improved the appearance of striae alba.[20]

Lasers of various types are used in treating striae and seem to be a promising mode of treatment. The 585-nm pulsed dye laser has a moderate beneficial effect in the treatment of striae rubra[21] and the 308-nm excimer laser is effective in treating striae alba.[22] Intense pulsed light is also useful, and has minimal side effects.[23] Short pulsed carbon dioxide laser has been tried as well.[24] Lasers and light sources emitting UVB radiation have been shown to repigment striae distensae.[25]

There is no widely accepted surgical procedure for improving the appearance of striae.[1] Patients should be reassured that striae do fade with time.[3]

References

1Garcia Hidalgo L. Dermatological complications of obesity. Am J Clin Dermatol 2002;3:497-506.
2Viennet C, Bride J, Cohen-Letessier A, Humbert P. Mechanical behavior of fibroblasts included in collagen lattices. J Soc Biol 2001;195:427-30.
3Burrows NP, Lovell CR. Disorders of connective tissue. In: Burns T, Breathnach S, Cox N, Griffith C, editors. Rook's Textbook of dermatology, 7th edn. Oxford: Blackwell Science; 2004. p. 46-7.
4Novak M. Colored striae in adolescent children. J Pediatr 2004;145:645.
5DiLernia V, Bonci A, Cattania M, Bisighini G. Striae distensae in monozygotic twins. Pediatr Dermatol 2001;18:261-2.
6Lee KS, Rho YJ, Jang SI, Suh MH, Song JY. Decreased expression of collagen and fibronectin genes in striae distensae tissue. Clin Exp Dermatol 1994;19:285-8
7Euvrard S, Kanitakis J, Cochat P, Cambazard F, Claudy A. Skin diseases in children with organ transplants. J Am Acad Dermatol 2001;44:932-9.
8Lawley TJ, Yancey KB. Skin changes and diseases in pregnancy. In : Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick's Dermatology in general medicine. 6th edn. New York: McGraw-Hill; 2003. p. 1362.
9Lee JH, Lee EK, Kim TY. A case of edematous striae distensae in lupus nephritis. J Dermatol 1999;26:122-4.
10Sparker MK, Garcia-Gonzalez E, Sanchez LT. Sclerosing and atrophying conditions. In: Schachner LA, Hansen RC, editors. Pediatric dermatology. 2nd edn. New York: Churchill Livingstone; 1996. p. 897.
11Strumia R, Varotti E, Manzato E, Gualandi M. Skin signs in anorexia nervosa. Dermatology 2001;203:314-7.
12Basak P, Dhar S, Kanwar AJ. Involvement of the legs in idiopathic striae distensae - a case report. Indian J Dermatol 1989;34:21-2.
13Johnston GA, Graham-Brown RA. The skin and disorders of the alimentary tract and the hepato biliary system. In: Freedberg IM, Eisen AZ, Wolff K, Austen KF, Goldsmith LA, Katz SI, editors. Fitzpatrick's Dermatology in general medicine. 6th edn. New York: McGraw-Hill; 2003. p. 16-7.
14Watson RE, Parry EJ, Humphries JD, Jones CJ, Polson DW, Kielty CM, et al . Fibrillin microfibrils are reduced in skin exhibiting striae distensae. Br J Dermatol 1998;138:931-7.
15Sheu HM, Yu HS, Chang CH. Mast cell degranulation and elastolysis in the early stage of striae distensae. J Cutan Pathol 1991;18:410-6.
16Sharque KE, Al-Waiz MM, Al-Nuaimy AA. Striae distensae-like lesions. A cause of scarring alopecia among children. Saudi Med J 2002;23:1489-91
17Ming ME. Asymptomatic linear plaque on the neck. Arch Dermatol 2005;141:268.
18Schwingel AC, Shimura Y, Nataka Y, Kazunori O, Tanaka K. Exercise and striae distensae in obese women. Med Sci Sports Exerc 2003;35:33.
19Elson ML. Treatment of striae distensae with topical tretinoin. J Dermatol Surg Oncol 1990;16:267-70
20Ash K, Lord J, Zukowski M, McDaniel DH. Comparison of topical therapy for striae alba (20% glycolic acid/0.05% tretinoin versus 20% glycolic acid/10% L-ascorbic acid). Dermatol Surg 1998;24:849-56.
21Jimeenez GP, Flores F, Berman B, Gunja-Smith Z. Treatment of striae rubra and striae alba with the 585 nm pulsed dye laser. Dermatol Surg 2003;29:362-5.
22Alexiades-Armenakas MR, Bernstein LJ, Friedman PM, Geronemus RG. The safety and efficacy of the 308 nm excimer laser in pigment correction of hypopigmented scars and striae alba. Arch Dermatol 2004;140:955-60.
23Hernandez-Perez E, Colombo-Charrier E, Valencia-Ibiett E. Intense pulsed light in the treatment of striae distensae. Dermatol Surg 2002;28:1124-30.
24Nouri K, Romagosa R, Chartier T, Bowes L, Spencer JM. Comparison of the 585 nm pulsed dye laser and the short-pulsed CO2 laser in the treatment of striae distensae in skin types IV and VI. Dermatol Surg 1999;25:368-70.
25Goldberg DJ, Marmur ES, Schumlts C, Hussain M, Phelps R. Histologic and ultrastuctural analysis of ultraviolet B laser and light source treatment of leukoderma in striae distensae. Dermatol Surg 2005;31:385-7.

 

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