Background  Stretch marks or striae distensae (SD) can be considered a common skin disorder, but their physiopathogenic mechanisms have not been totally clarified. Although it is considered an esthetic complaint, it may have serious psychosocial consequences besides the local and systemic alterations of the conjunctive tissue. This study aims at assessing and quantifying the estrogen, androgen and glucocorticoid receptors in skin samples with striae and comparing with normal skin. Methods  Skin samples for biopsy were obtained from eight patients with SD and eight patients without lesions. The samples were frozen at −80 °C and underwent processing to obtain proteic extract to quantify the estrogen, androgen and glucocorticoid receptors with the Western Blot method. Results  When the estrogen receptor in the skin with SD was compared with healthy skin, it was observed to have increased twice as much (P = 0.00001). The androgen and glucocorticoid receptors in the SD skin had also increased (P = 0.00015 and P = 0.00083, respectively). Conclusions  These findings indicate that under certain conditions there is an increase in hormonal receptor expression, suggesting that regions that undergo greater mechanical stretching of the skin may express greater hormonal receptor activity. This activity may influence the metabolism of the extracellular matrix, causing the formation of SD. Alterations in hormone receptors occur within a well‐defined time period during the formation of SD; however, there are differences in the functionality of hormone receptors during different stages in the development of the lesions. The preliminary results appear to be relevant and represent aninitial step towards an understanding of the pathophysiology of SD.

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Fig. 1b). Interstitial mucins deposition was found in the superficial dermis. Calcification was observed in the deep dermis. A diagnosis of NSF was made. The skin lesions persisted till the patient succumbed to cancer metastasis.Only few cases of NSF were reported in patients who had ARF and never requiring dialysis. 2 Our case is unique because NSF occurred after renal function had returned to normal. The exact cause of NSF remained not clear. However, there was a very strong association between NSF and exposure to gadodiamide (odds ratio, 32.5). 3 The half-life of gadolinium-containing contrast agents was 1.3 h in normal subjects, but was markedly prolonged up to 30-120 h in patients with renal failure. 4 Patients receiving higher doses of gadolinium-containing contrast agents (0.2-0.3 mmol/kg) were more likely to develop NSF than those who had lower dose (0.1 mmol/kg). 1 The medium time from gadodiamide exposure to the first clinical sign of NSF was 25 days. 3 The causal relationship in our case was clear that the patient repeatedly exposed to gadodiamide when his renal function were impaired. NSF occurred one month after last gadodiamide exposure also corroborated with the time sequence. 3 In addition, other possible aetiological factors, including coagulation abnormality, recent vascular surgery, administration of erythropoietin, use of angiotensin-converting enzyme inhibitors, presence of antiphospholipids syndrome, were excluded in our case. 1,5 Taken together, gadodiamide exposure might be the aetiological factor of NSF in our case. In addition, recent studies demonstrated deposition of gadolinium in the dermal vessels, and basal lamina of eccrine glands further provided biological mechanism that link gadolinium to NSF. 6 In sum, we reported a case of NSF resulted from repeated exposures to gadolinium-containing contrast agents during a short period of ARF. NSF developed despite his renal functions had returned to normal. Our case suggested that exposure to gadolinium during a short period of renal insufficiency was sufficient to induce NSF. Therefore, using gadolinium-containing contrast agents in severe renal insufficient patients should be very careful in light of the risk of NSF. 1,5 rare manifestation of this dermatosis. The interesting observation was the rapid development of protruding striae with the transudation of the fluid. It was probably due to a compromised dermal integrity. Some authors suggested that hormonal factors were related to critical changes in the resistance of collagen to stretch. 6 Other authors observed sequential changes of elastolysis accompanied by mast cell degranulation and influx of activated macrophages that enveloped fragmented elastic fibers. 7 The aetiology and pathophysiology of SD are not completely elucidated, and more studies are necessary. We present an exuberant case which demonstrates that despite SD are a very common dermatosis, they can present variations and they are cause of morbidity.RCT Cordeiro,* AM de Moraes

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