Study on the mothodology of evaluation of striae gravidarum

目的:通过临床评判和仪器检测相结合的方法,对妊娠纹修复的评价方法学进行研究.方法:在32位受试者使用某妊娠纹修复产品前后,用临床评判的方法对妊娠纹的严重程度、颜色、松弛度及靶皮损面积进行评分,并用皮肤扫描仪、皮肤色度仪、皮肤弹性检测仪和扫描图像分析的方法对靶皮损进行客观参数检测.结果:试验前后妊娠纹颜色、面积、松弛度及弹性差异无统计学意义(P ＞ 0.05),临床评判与仪器检测结果一致.靶皮损的临床评估及面积计算结果具有相关性.皮肤扫描结果显示靶皮损的纹理变化参数(VAR)、表面参数(surface)及皮肤粗糙度参数(C-R1)的变化有统计学差异(P < 0.05).结论:临床评判与仪器检测结果一致,皮肤扫描的部分指标可发现临床评判无法察觉的微观变化,并提供各参数的客观依据,二者相结合可为妊娠纹的相关研究提供较为系统的评价方法.     

妊娠纹高危因素和治疗研究进展

妊娠纹常见高危因素包括产妇低龄、有妊娠纹家族史、高基础体重、孕期体重增长较大以及新生儿高体重。强脉冲激光、射频及准分子激光治疗有一定疗效。     

Twisted collagen fibrils in acrocyanosis.

Essential acrocyanosis (EA) present as a dusky discoloration of the hands as the sole symptom without any other abnormal results from laboratory investigation. Previously, the authors have found twisted collagen fibrils (TCF) in the normal skin of an EA patient. This study was intended to evaluate the significance of TCF in EA. Thirteen patients showing dusky discoloration were randomly selected and studied for TCF in normal skin by routine electron microscopy. TCF were found in 10 of 13 patients; 3 patients with only the discoloration (EA), 3 with the mild symptoms which were supposed to be Ehlers-Danlos syndrome (EDS), 1 with definite symptoms of EDS, 1 with Raynaud's disease and 2 with hyperglobulinemia. TCF were the ultrastructural sign for inherited malformation of collagen fibrils. EA was probably elucidated as a vascular disorder in TCF-carrying people. EA could be included in the disease category of EDS but it seems unreasonable to force EA patients into one of the subtypes of EDS. For pathogenesis, the inherited dysfunction in the hypertrophic pericytes of the subpapillary vascular plexus was presumed.     

Decreased expression of collagen and fibronectin genes in striae distensae tissue

Striae distensae are characterized by a thinning of connective tissue stroma to produce linear, atrophic-appearing skin. Excessive adrenocortical activity, genetic factors and inherited defects of connective tissues, etc. are important causative factors in the formation of striae distensae, but the basic aetiology is not known. Total RNA was extracted from skin biopsies of five patients with striae distensae. The expression of genes coding for types I and III procollagen, elastin, fibronectin and β-actin were studied and compared with those of four sex- and age-matched healthy individuals. The percentages of types I and III procollagen mRNA were 9.9 ± 2.9% (mean ± s.d.) and 10.6 ± 1.6%, respectively, of the corresponding controls. The value for fibronectin mRNA in striae distensae was 7.3 ± 1.8% of the control. The steady-state ratio fibronectin/type I procollagen mRNAs was 0.12 ± 0.01 in striae distensae and (MS ± 0.01 in the control. These observations suggest that expression of collagens, elastin and fibronectin genes are apparently decreased, and that there is a marked alteration of fibroblast metabolism, in striae distensae.     

Identification of collagen fibrils in scleroderma skin

Skin from early and late stages of scleroderma has been shown to contain large amounts of thin (30-40 nm diameter) collagen fibrils that may be present in bundles or intermingled with large diameter fibrils (90-120 nm). The nature of these fibrils is unknown. Skin biopsies were obtained from involved areas of nine patients with progressive systemic sclerosis (PSS), one case of generalized morphea, one case of morphea, and six normal controls. Intact skin was analyzed by immunoelectron microscopy (IEM), while extracts were subjected to sodium dodecyl polyacrylamide gel electrophoresis (SDS-PAGE), Western immunoblotting, radioimmunoassay (RIA), and enzyme-linked immunosorbent assay (ELISA). Fine fibrils 20-40 nm in diameter in the mid to lower dermis of scleroderma skin were labeled with antibodies directed against the aminopropeptide (AP) of type III procollagen. Antibodies directed against the AP of type I procollagen labelled fine fibrils in the lower dermis. Larger fibrils (80-120 nm) did not label. pN alpha 1 (III) was found to be present in both normal and scleroderma skin. Extracts of scleroderma skin contained 2.5 times the amount of pN (III) collagen and 3.0 times the amount of fibronectin as did extracts of normal skin. The data indicate that the increase in thin fibrils in scleroderma skin is most likely due to an increase in type III collagen, which retains the AP at its surface.     

非剥脱点阵激光治疗妊娠纹的疗效观察

目的 评估非剥脱1 565 nm铒玻璃点阵激光治疗妊娠纹的有效性和安全性。方法 简单随机化方法将30例妊娠纹受试者腹部左右侧妊娠纹分为治疗侧和对照侧,治疗侧接受3次1 565 nm非剥脱铒玻璃点阵激光治疗,治疗间隔4周;对照侧不予治疗。在基线、第4周、第8周和第12周随访并拍照,测定皮肤弹性和妊娠纹宽度;在末次治疗后第4周由被设盲医师根据临床照片和3D照片评估临床改善情况,对受试者行疗效满意度调查,并取3例受试者治疗侧和对照侧妊娠纹处皮肤行病理检查。末次治疗后4个月电话随访受试者复发及不良反应情况。结果 27例受试者完成整个试验。末次治疗后4周,医生判定25例（92.6%）治疗有效;21例（77.8%）受试者认为治疗有效。经过3次治疗,治疗侧妊娠纹最大宽度从4.852 mm降至3.296 mm（P < 0.001）,皮肤弹性从0.803上升至0.878（P < 0.001）。组织学上,非治疗侧表皮明显萎缩,真皮胶原蛋白和弹性蛋白明显减少;治疗侧平均表皮厚度增加,表皮突延长,真皮变厚,胶原纤维和弹性纤维均有明显增加,并规则排列。治疗过程中的即刻不良反应包括红斑、水肿,其他不良反应包括微结痂、瘙痒感和炎症后色素沉着。炎症后色素沉着在末次治疗后4个月随访时较末次治疗后4周好转。结论 非剥脱1 565 nm铒玻璃点阵激光可以显著改善妊娠纹的宽度和外观,提高治疗区域的皮肤弹性。     

Abnormality of dermal collagen fibrils in Ehlers Danlos syndrome. Anticipation of the abnormality for the inherited hypermobile disorders

The abnormality of dermal collagen fibrils is the ultrastructural criterion of Ehlers-Danlos syndrome (EDS). This study evaluates the clinical significance of the abnormality. Besides 348 lax patients presenting the stigmata of EDS, skin specimens from 12 normal members in the pedigree of EDS, 98 randomly selected normal individuals, 7 Marfan syndrome and 4 osteogenesis inperfecta type I, were studied by electron microscopy. The abnormality was defined by thickness, array and shape of collagen fibrils. Of 348 lax patients, 115 patients showed Beighton's score higher than 6 and constantly the abnormality (EDS). Variable numbers of the patients with scores 1 to 5 displayed the abnormality (forme fruste). The abnormality did not correspond with variation of laxity. Marfan syndrome and osteogenesis imperfecta were indistinguishable from EDS by the abnormality. Some of the normal persons in the EDS pedigree and some controls also showed the abnormality. The abnormality expressed the disposition for heritably defected collagen fibril formation.     

Intracellular collagen fibrils in cultured human skin.

During cultivation, the collagen fibrils of skin explants are broken down. The cells of the explants participate in this resorption. The ultrastructure of the intracellular degradation of collagen fibrils of cultured human skin has been examined. Intracellular collagen fibrils occur in fibroblasts, macrophages, smooth muscle cells and unidentifiable cells. Normal collagen fibrils are engulfed and appear within membrane-bounded tubes of the cytoplasm. Primary lysosomes fuse with the tubes. Degraded intracellular collagen fibrils are frequently present in secondary lysosomes and show decreasing diameters, filamentous splitting, loss of axial periodicity, variable stainability and cross-banded filamentous aggregates. The changes in the intracellular collagen fibrils are identical with those seen in the extracellular space. The present study demonstrates that various cell types in dermis are involved in collagen fibril degradation and that the lysosomes play an important part in the intracellular resorption.     

Contractile forces generated by striae distensae fibroblasts embedded in collagen lattices

Striae distensae are characterized by linear, smooth bands of atrophic-appearing skin that are reddish at first and finally white. They are due to stretching of the skin, as in rapid weight gain, or mechanical stress, as in weight lifting. The pathogenesis of striae distensae is unknown but probably relates to changes in the fibroblast phenotype. In order to characterize striae distensae fibroblasts, alpha-smooth muscle actin expression and contractile forces were studied. Five healthy women with early erythematous striae and five healthy women with older striae were selected. Paired biopsies were taken from the center of lesional striae and adjacent normal skin. Fibroblasts were obtained by an explant technique and expanded in vitro in Dulbecco’s modified Eagle‘s medium. Contractile forces generated by fibroblasts in collagen lattices were measured with the Glasbox device developed in our laboratory. Alpha-smooth muscle actin expression was studied by immunofluorescence labeling of cells and by flow cytometry. Fibroblasts from early striae distensae were the richest cells in alpha-smooth muscle actin filaments and generated the highest contractile forces. Their peak contractile force was 26% greater than normal fibroblasts. There was a 150% higher level of alpha-smooth muscle actin content in fibroblasts from early striae distensae compared with fibroblasts from normal skin. In contrast, there was no significant difference in force generation between old striae fibroblasts and normal fibroblasts with cells expressing no alpha-smooth muscle actin. The contractile properties of fibroblasts from striae distensae varies depending on the stage of the disease. In early striae distensae, fibroblasts acquire a more contractile phenotype, corresponding to that of myofibroblasts.     

Characterization of dermal collagen in systemic sclerosis

The amount of dermal collagen is increased in systemic sclerosis. However, unlike certain inflammatory conditions, the relative proportions of Type I and Type III collagens are closely similar to those found in normal adult dermis. Similarly, no change in the distribution of the collagen types could be detected by immunofluorescent staining, although a considerable thickening of the epidermis was clearly evident in all the sclerotic lesions examined.     

Mast cell degranulation and elastolysis in the early stage of striae distensae

The lesions of nine patients with early striae distensae (SD) during puberty were examined by light and electron microscopy. Specific changes were seen in very early stage SD, and in clinically uninvolved skin 0.5 to 3 cm remote from the edge of the long axis of the SD lesions. Sequential changes of elastolysis accompanied by mast cell degranulation appeared first, followed by an influx of activated macrophages that enveloped fragmented elastic fibers. The relationships among elastic fibers, mast cells, and macrophages seen in the present work suggest their critical roles in the process of SD formation, especially in the early stage. Our results also indicate that the elastic fiber is the primary target of the pathological process, and the abnormalities extend as far as 3 cm beyond the lesion into normal skin.