儿童双足肿瘤样钙质沉着症1例

肿瘤样钙质沉着症(tumoral calcinosis,TC)是特发性皮肤钙质沉着症的临床亚型之一,临床少见.我科近期收治1例患儿,报道如下.     

皮肤钙质沉着症及治疗

目的:探讨皮肤钙质沉着症的临床特点及治疗方法.方法:回顾性分析2例皮肤钙质沉着症的临床资料.结果:1例头皮皮肤钙质沉着症为外伤性皮肤钙质沉着症,经皮肤扩张及皮瓣转移修复的手术方法治愈;另1 例为特发性阴囊皮肤钙质沉着症,因局部阴囊皮肤修复难度较大而放弃手术治疗.结论:皮肤钙质沉着症为临床少见病,组织病理活检可确诊,手术治疗是有效可靠的治疗方法,切除范围要足够以免复发,一期皮肤扩张器埋植,二期皮瓣转移修复对头皮病灶效果较满意.     

内分泌、代谢、营养障碍性皮肤病

20101520家族性肿瘤样钙沉着症(综述)/晏洪波(广州军区武汉总医院皮肤科),周凌∥国际皮肤性病学杂志.-2010,36(2).-83~85肿瘤样钙沉着症是一种特殊的皮肤异位性钙沉着症,皮损表现为关节周围的肿块,主要是钙磷沉着形成。肿瘤样钙沉着症又可分为原发性和继发性。原发性肿瘤样钙沉着症的30%为家族性肿瘤样钙沉着症(FTC)。FTC是一种常染色体隐性遗传性疾病,对患者的生活质量存在严重的影响。综述FTC的病因和发病机制、临床表现、组织病理特点、影像学改变、诊断和鉴别诊断、治疗等方面的知识和研究进展,指导临床工作中对该病的诊治。参24(樊靖华)20101521中药体膜与水杨酸软膏外用联合     

巨大特发性皮肤钙质沉着症1例

报告1例巨大特发性皮肤钙质沉着症。患者男,因头皮结节、斑块28年就诊,病理检查示：真皮浅中下层密集或散在分布团块状深蓝色钙盐沉积,周围真皮毛细血管扩张,充血,管周少量淋巴细胞、组织细胞浸润。诊断为特发性皮肤钙质沉着症。     

体外冲击波碎石术治疗皮肤钙沉着症

皮肤钙沉着症（calcinosisdeposition）系指不溶性钙盐沉积在皮肤组织。临床主要表现为坚硬的丘疹、结节或肿块,破溃后排出奶酪色油状砂粒样物质。沉积的钙盐主要是无定形的磷酸钙、少量碳酸钙和极少的羟磷灰石。当沉积物为矿物质并形成骨样组织时称皮肤骨瘤或皮肤骨化。根据病因的小同,皮肤钙沉着症分特发性皮肤钙沉着症、转移性皮肤钙沉着症、营养不良性钙沉着症、医源性与创伤性皮肤钙沉着症4种类型。     

内分泌、代谢、营养障碍性皮肤病

20070757 皮肤淀粉样变性皮损中T／B细胞的检测；20070758 维A酸类药物联合苦参素治疗原发性皮肤淀粉样变病22例临床观察；20070759 痒疹样结节型皮肤淀粉样变性1例；20070760 伴抗基膜自身抗体的皮肤异色病样淀粉样变病；20070761 特发性皮肤钙质沉着症1例[编按]     

特发性阴囊钙质沉着症2例报告

例1　男,27岁,工人。阴囊发生黄色结节4～5年,可破溃流出奶油状粘物,无外伤史,其父阴囊有类似皮损。体检:阴囊密布20多个米粒至花生粒大小半球状较软结节,色黄,表面光滑,无压痛,无破溃(照片11)。血钙磷正常。临床诊断:多发性皮脂囊肿。病理活检示复层鳞状上皮,表皮中央变薄,边缘肥厚,基底膜完整,皮下大片浅蓝色钙质团块,边缘有脱落的小钙质团块及大量组织细胞,少量淋巴细胞、纤维母细胞、成纤维细胞浸润,偶见异物巨细胞(照片12)。确诊为阴囊钙质沉着症。例2　男,38岁,工人。阴囊发现肿块1年,无外伤史,无家族史。体检:阴囊可见1个直径1cm大小…     

系统性红斑狼疮并发小腿皮肤广泛钙质沉着症1例

系统性红斑狼疮(SLE)并发皮肤钙质沉着症(calcinosis cutis)临床上少见,文献偶有盘状红斑狼疮并发皮肤钙沉着症的报道[1-2].我们于2008年11月诊治1例SLE并发小腿皮肤广泛钙质沉着致溃疡的患者,现报告如下.     

皮肤钙质沉着症1例

报告1例皮肤钙质沉着症。患者男性，40岁。左侧臀部肌注青霉素后，注射部位陆续出现黄豆大小淡白色丘诊和结节，自行破溃流出白色石灰样物，逐渐形成凹凸不平的硬性斑块33年。组织病理检查示真皮深部组织可见大小不等团状钙化物沉积，呈均质性或钙化球，HE染色呈深蓝色。     

阴囊特发性皮肤钙质沉着症1例

1临床资料患者男,33岁。阴囊多发性结节8年。8年前无明显诱因阴囊皮肤出现数个肉色绿豆大丘疹,无自觉症状,丘疹逐渐增多、变大、变硬,形成多个结节。搔抓挤压后可有白色乳酪样物质排出。既往体健,家族中无类似患者。体检:系统检查无异常,外生殖器发育正常。皮肤科情况:阴囊上可见9余枚结节,直径0.4~3 cm,质硬,无压痛,表面光滑,无破溃及分泌物(图1,见封3)。双侧睾丸及附睾无异常。实验室检查:血、尿常规,肝、肾功能,血清钙、磷水平均正常。诊断:阴囊特发性皮肤钙质沉着症。在局麻下行阴囊结节切除术。切除物组织病理示:真皮内可见大量团块状蓝色物质沉积,阴囊皮下多发性钙化伴肉芽肿反应(图2,见封3)。结     

Tumoral Calcinosis: Report of a Case and Brief Review of the Literature

A patient with a 32-year history of tumoral calcinosis is described. The calcified lesions involved the soft tissues in the hips, shoulders, and ankles. Periodically, a chalky semifluid material extruded through several cutaneous sinuses. Laboratory tests including serum calcium concentration were normal, except for slight elevation of serum phosphorous levels. Ophthalmologic examination revealed the interesting finding of subretinal angioid streaks. The dental radiograms disclosed pathognomonic short bulbous roots and partial obliteration of pulp cavities, while the radiological evaluation of the tumoral masses revealed typical features of tumoral calcinosis.     

Nanobacteria and calcinosis cutis

BACKGROUND: The nanobacteria are a recently characterized group of extremely small bacteria capable of precipitating calcium salts implicated in the pathogenesis of urinary calculi and calcific atherosclerosis. The pathogenesis of calcinosis cutis and its significance in conjunction with a variety of unrelated scarring and pre-existing cutaneous entities are incompletely understood. METHODS: A series of cases, including basal cell carcinoma with dystrophic calcification, subepidermal calcified nodule, pilomatricoma, and tumoral calcinosis, were ultrastructurally examined for the presence of Nanobacteria sp. RESULTS: All cases, including three basal cell carcinomas, two subepidermal calcified nodules, three cases of pilomatricoma, and two cases of tumoral calcinosis, were negative for Nanobacteria. CONCLUSIONS: The dystrophic calcification that occurs in conjunction with the above entities does not likely involve a bacterial-induced etiology. The cause of these entities remains unknown.     

PROPOSAL FOR A PATHOGENESIS-BASED CLASSIFICATION OF TUMORAL CALCINOSIS

Background. Deposition of calcium in skin is currently categorized into a group of disorders referred to as calcinosis cutis. Divisions between types and subtypes within this confusing classification are predominantly based on morphologic differences in the calcification and serve to obscure pathogenesis. This is especially evident in a subtype of calcinosis cutis, known as tumoral calcinosis. Calcifications in cases of tumoral calcinosis share the following characteristics, but without evidence of a common pathogenesis: large size, juxtaarticular location, progressive enlargement over time, a tendency to recur after surgical removal, and an ability to encase adjacent normal structures. The goal of this study was to formulate a pathogenesis-based classification for cases of tumoral calcinosis. Methods. In a literature review 121 cases of tumoral calcinosis were identified. These cases, along with a case evaluated in our clinic, were reviewed retrospectively, and their features compared. Results. Analysis suggests three pathogenetically distinct subtypes of tumoral calcinosis: (1) Primary normophosphatemic tumoral calcinosis: patients have normal serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; (2) primary hyperphosphatemic tumoral calcinosis: patients have elevated serum phosphate, normal serum calcium, and no evidence of disorders previously associated with soft tissue calcification; and (3) secondary tumoral calcinosis: patients have a concurrent disease capable of causing soft tissue calcification. Justification for this classification is based on the presence or absence of disorders known to promote soft tissue calcification and statistically significant differences in family history, mean calcification number, mean serum phosphate level, and calcification recurrence after excision. Conclusions. A classification for tumoral calcinosis is devised that outlines potential pathogenetic mechanisms and predicts response to therapy and prognosis. Analysis of other forms of calcinosis cutis may reveal definable pathogenetic differences that suggest a coherent classification for all cutaneous calcinoses.     

Tumoral calcinosis

Tumoral calcinosis is a distinct entity, which is rarely seen in Europe and North America but much more common in black Africans. Typical symptoms are calcified nodules, which grow while remaining asymptomatic and are found in the tissues adjacent to the large joints of the body. Histologically there is collagen necrobiosis initially, which results in aggregates of densely calcified material. The aetiology is unknown, but the condition is probably a form of dystrophic calcification caused by mechanical injury. A patient with tumoral calcinosis is presented, and the clinical and histological findings are described.     

Metastatic calcinosis cutis

Calcinosis cutis may be associated with metastatic calcification, dystrophic calcification, tumoral calcinosis, or may be deemed idiopathic. The association of cutaneous calcification with metastatic or tumoral calcinosis is quite rare. A case of metastatic calcinosis cutis in a woman with chronic renal failure and secondary hyperparathyroidism is presented. Other causes of calcinosis cutis are discussed briefly.     

家族性肿瘤样钙沉着症

家族性肿瘤样钙沉着症是一种常染色体隐性遗传性疾病,其发病与基因突变有关.家族性肿瘤样钙沉着症分为两型,高磷酸血症型和正常磷酸水平型.临床主要表现为皮肤及皮下组织、近关节软组织和(或)内脏组织的钙盐沉着,正常磷酸水平型患者具有高磷酸血症型所没有的炎症表现.特殊的临床表现结合病理活检和影像学检查可确立诊断.此病治疗药物和手术切除均可选择,但疗效欠佳.     

家族性肿瘤样钙沉着症

家族性肿瘤样钙沉着症是一种常染色体隐性遗传性疾病,其发病与基因突变有关。家族性肿瘤样钙沉着症分为两型,高磷酸血症型和正常磷酸水平型。临床主要表现为皮肤及皮下组织、近关节软组织和（或）内脏组织的钙盐沉着,正常磷酸水平型患者具有高磷酸血症型所没有的炎症表现。特殊的临床表现结合病理活检和影像学检查可确立诊断。此病治疗药物和手术切除均可选择,但疗效欠佳。     

Cutaneous manifestations of tumoral calcinosis.

We have followed up a large family in which seven members have tumoral calcinosis. One girl had the skin lesions of localized calcinosis cutis apart from the typical subcutaneous deposits of calcium. Like most persons with tumoral calcinosis, our patient had normal serum calcium concentrations; however, the serum phosphorus levels were greatly elevated. The familial occurrence and elevated serum phosphorus levels suggest the possibility of some as yet undefined, heritable metabolic defect as the underlying cause. The occurrence of tumoral calcinosis with localized calcinosis cutis is a rare association, and there has been only one other reported case to our knowledge. This report describes our patient and offers a brief discussion of tumoral calcinosis. The therapeutic response to the phosphate depletion regimen and topical steroids was disappointing in our case.     

Tumoral calcinosis in scleroderma

A 36-year-old female patient with scleroderma/Sjögren's syndrome developed multiple cystic tumors on the dorsal aspect of her left hand, right elbow, and left shoulder joint two years after the onset of scleroderma. Histologically, amorphous eosinophilic substances located in subcutaneous tissue showed a strong positive reaction to PTAH and rosindole stain, and focal positive reaction to Von Kossa stain. Rheumatoid rice body like substances with chalky fluid were discharged from tumoral lesions. From these results, this case was diagnosed as tumoral calcinosis secondary to connective tissue degeneration due to the pathogenetic mechanism underlying scleroderma/Sjögren's syndrome.     

Spontaneous regression of multiple tumoral calcinosis in a child

We report a case of multiple tumoral calcinosis on the head and back of a one-year-old boy who had no renal diseases. After an excisional biopsy of one of the tumors from the occipital region, all of the tumors spontaneously regressed without any further surgical or medical treatment. Although he had neonatal hepatitis, his liver function improved as well as the course of the spontaneous regression of the tumoral calcinosis. There has been only one case of a child with this condition in the literature.