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Year : 1990  |  Volume : 56  |  Issue : 2  |  Page : 125-126

17-ketosteroid levels in striae cutis distensae

Correspondence Address:
K Pramod Nigam

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Eighteen patients with striae cutis distensae were studied. The, most common site of the lesion was shoulder. Acne vugaris was e,d in 27.7% cases. History (if weight l athletics or attaining rapid growth was presenters 94% of patients. The 24-hour urinary 17-ketosteroid excretion was normal in all he patients.

Keywords: Striae cutis distensae, 17-ketosteroids

How to cite this article:
Nigam K P, Ramesh V, Mishra R S. 17-ketosteroid levels in striae cutis distensae. Indian J Dermatol Venereol Leprol 1990;56:125-6

How to cite this URL:
Nigam K P, Ramesh V, Mishra R S. 17-ketosteroid levels in striae cutis distensae. Indian J Dermatol Venereol Leprol [serial online] 1990 [cited 2020 Dec 5];56:125-6. Available from:

Striae cutis distensae (SCD) are a cosme­tically undesirable and aetiopathogenetically ill-understood clinical entity. The lesions are frequently located on the thighs, lower back, buttocks, shoulders and breasts. Striae are seen more commonly during the pubertal growth spurt and association of striae with acne, genital and breast development, pubic hairs and menarche has been observed.[1] Due to their frequent association with a rapid increase or decrease in body weight,[2] obesity,[1] Cushing's syndrome,[3] prolonged systemic corticosteroid therapy[4] and topical corticosteroid applications especially under occlusion,[5] a role of adreno­corticotrophic hormones on mechanically heavily strained tissues has been proposed. Increased serum levels of corticosteroid hor­mones[6] as well as their metabolites[5],[6] have been demonstrated, while others[7],[8] have found no clinical or laboratory evidence of significant hyper-adrenocoiticism in patients with striae.

  Materials and Methods Top

Eighteen patients with SCD, (15 males and 3 females), without having any overt endocrino­logical or renal complaint and with normal serum creatinine levels were investigated. The patients had not used any systemic or topical corticosteroids in the past. The height, weight and occupation of the patients along with the age of onset, duration and distribution of striae were recorded. Obesity was diagnosed when patients were 20% over weight according to the standard height and weight tables. The patients were asked to collect 24-hour urine and the 17-ketosteroid (KS) levels were estimated by chloroform extraction followed by Zimmerman reaction technique' in mg/24 hours taking the normal range of 24-hour urinary 17-KS excre­tion for men and women over 12 years of age as 8-22 mg and 5-15 mg respectively.

  Results Top

The age of the patients ranged from 16 years to 28 years. The age at onset of SCD ranged from 15 years to 28 years (mean age 19.38+ 3.36 years). The duration of the lesions was from 3 months to 18 months (mean 8.44+3.86 months). The sites involved were shoulder in 12, lower back in 6, thighs in 6, buttocks in 3 and breasts in one patient. Ten (55%) patients were either athletes or weight lifters and 7 (39%) patients had a history of rapid increase in height and/or weight. Four patients were over-weight and 1 patient was obese. Five patients had moderate acne. A family history of SCD was not present in any of the cases. The routine blood, urine and stools examinations were normal. The 24-hour urinary 17-KS levels ranged from 6.98 mg to 23.01 mg (mean 15.73 +­4.41 mg; 24 hour) for males and from 11.9 mg to 16.43 mg (mean 14.72 + 2.16 mg/24 hour) for females.

  Comments Top

Increased urinary excretion of corticoste­roids was observed in patients with SCD and it was suggested that striae are due to hyperactivity of the adrenal cortex.[5] Others have however, observed normal levels of urinary 17-KS in patients with SCD.[10] The mean urinary 17-KS levels were normal in our patients also. Stress rupture of the connective tissue framework as results from stretching of the skin in rapid weight gain or mechanical stress as in weight lifting is another explana­tion for striall and 94% of our patients had a history of increased mechanical stress to the body in the form of weight lifting, athletics, physical exercises or attaining rapid growth. Besides mechanical effects, other factors such as an inherent defect in the dermal elastic tissues, as seen in Marfan's syndrome, [13] may also be participating in the production of striae. It is also hypothesized that there is a very early inflammatory stage in the formation of striae which leads to destruction of the collagen and elastin, followed by regeneration of new collagen and elastin, this time oriented in the direction of the stress.

  References Top

1.Sisson WR : Coloured striae in adolescent children, J Paediat, 1954; 45 : 520-531.  Back to cited text no. 1    
2.Arem AJ and Kisher CW : Analysis of striae, Plast Reconst Surg, 1980; 65 : 22-29.  Back to cited text no. 2    
3.Pinkus H, Krech MK and Mehregan AH: Histopa­thology of striae distensae with special reference to striae and wound healing in the Marfan's syndrome, J Invest Dermatol, 1966; 46 : 283-289.  Back to cited text no. 3    
4.Behl PN, Sehgal VK and Sood NK : Striae atro­phicae: a clinicopathological study, Ind J Derma­to] Venereol Leprol, 1974; 40 : 236-239.  Back to cited text no. 4    
5.Simkin B and Arce R : Steroid excretion in obese patients with coloured abdominal striae, New Eng J Mcd, 1962; 266 : 1031-1035.  Back to cited text no. 5    
6.Shirai Y : Studies in striae cutis at puberty, Hiroshima J Med Sci, 1966; 8 : 215-222.  Back to cited text no. 6    
7.Carr RD and Hamilton JF : Transverse striae of the back, Arch Dermatol, 1969; 99 : 26-30.  Back to cited text no. 7    
8.Shuster S : The cause of striae distensae, Acta Dermato-Venereol, 1985; 65 : 161-169.  Back to cited text no. 8    
9.Varley H : Hormones, in : Practical Clinical Biochemistry, Arnold-Heinemann, New Delhi, 1976; p 667.  Back to cited text no. 9    
10.Gogate AN and Prunty FIG : Adrenalcortical functions in obesity with pink striae in the young adults, J Clin Endocrinol Metabol, 1963; 23 747-751.  Back to cited text no. 10    
11.Moretti G, Rebora A and Guarrera M : Striae distensae : how and why they are formed, in Striae Distensae, Editors, Moretti G and Rebora A : Brocades, Milan, 1976; p 9.  Back to cited text no. 11    
12.Zheng P, Lavker RM and Kligman AM : Anatomy of striae, Brit J Dermatol, 1985; 112 : 185-193.  Back to cited text no. 12    
13.Loveman AB, Gordon AM and Fliegelman MT Marfan's syndrome : some cutaneous aspects, Arch Dermatol, 1963: 87 : 428-435.  Back to cited text no. 13    


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