Graft versus host reaction and lichen planus
Graft versus host reaction and lichen planus
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移植物抗宿主反应和扁平苔藓
DOI：
10.1111/j.1365-2133.1975.tb03130.x
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发表时间：
1975
影响因子：
10.3
通讯作者：
P. Mannoni
中科院分区：
文献类型：
--
作者：
R. Touraine;J. Revuz;B. Dreyfus;H. Rochant;P. Mannoni
在移植物抗宿主反应（GVHR）中发生扁平地衣样的爆发以前没有报道。1973年4月，我们观察到一名患者在接受其姐姐的组织相容性骨髓移植治疗肝炎后再生障碍性贫血22天后发生严重的GVHR （IV级）。根据Slavin & Santos（1973）的标准，皮肤、肝脏和肠道病变在1周内改善，患者进入GVHR的静息期，没有严重的皮肤后遗症。移植后第102天，患者出现典型的扁平苔藓粘膜和皮肤病变。颊部及甲部病变为糜烂型。手掌病变的组织学检查证实为扁平苔藓。肝脏和小肠未受影响。皮肤病变在3个月内缓慢改善，导致皮损变浅。一年后，皮肤后遗症非常严重，包括皮肤硬化、表皮萎缩、瘢痕性脱发、网状色素沉着、角化过度和无愈合倾向的广泛溃疡。尽管血液学结果很好，而且没有肝脏或肠道疾病，但皮肤并发症现在已经危及生命。Slavin和Santos描述了GVHR与扁平地衣的组织学相似性；上皮基底层局灶性坏死和真皮淋巴细胞浸润是这两种疾病的显著特征。然而，早期皮肤GVHR的淋巴细胞浸润通常是稀疏的，并且GVHR的临床表现从未报道过地衣样细胞。我们的病例报告似乎很重要，因为两个原因：这是第一个临床和组织学证实的扁平苔藓发生在严重的GVHR愈合后。这种联系似乎不是偶然的，在这期杂志上报道了第二个病例（Saurat et al., 1975）。这类病例的稀少可以解释为严重GVHR患者通常生存时间较短。这种扁平地衣之后是严重的皮肤变化。这类病变以前发生在严重GVHR （Storb，个人交流）之后。也许GVHR后的扁平地衣是最初的事件。在我们的病例中，扁平苔藓的意义并不明显。它可能是一种仅位于皮肤上的持续慢性GVHR: GVHR后的扁平苔藓可能是细胞介导的自身免疫性疾病的模型。另一种假设是，地衣样物质的爆发，无论其背景如何，都是细胞对基底细胞坏死（各种病因）的一种反应（免疫或非免疫），正如Pinkus（1973）和Black（1972）所提出的那样。这些假设并非相互排斥。皮肤科医生必须注意慢性GVHR。进一步研究皮肤GVHR可为了解扁平苔藓的发病机制提供新的思路。
The occurrence of a lichen planus like eruption during a graft versus host reaction (GVHR) has not been reported previously. In April 1973 we observed a patient undergoing a severe GVHR (grade IV) 22 days after being treated for post-hepatitis aplastic anaemia by a histocompatible bone marrow transplantation from his sister. The cutaneous as well as liver and intestinal lesions improved within i rrionth and the patient entered the quiescent stage of GVHR, according to Slavin & Santos' (1973) criteria, without severe cutaneous sequelae. On day 102 after grafting, he presented mucous membrane and cutaneous lesions typical of lichen planus. Buccal and nail lesions were of the erosive variety. Histological examination of a palmar lesion confirmed lichen planus. The liver and small bowel remained unaffected. The cutaneous lesions improved very slowly over 3 months leading to a poikilodermatous state. One year later, the cutaneous sequelae are extremely severe, with dermal sclerosis, epidermal atrophy, cicatricial alopecia, reticulate pigmentation, hyperkeratosis, and widespread ulceration showing no tendency to healing. The skin complications are now life threatening in spite of a very good haematological result and of the absence of liver or bowel disease. Histological similarities between GVHR and lichen planus have been described by Slavin and Santos; focal necrosis of the epithelial basal layer and dermal infiltration by lymphocytes are prominent features of both diseases. However, the lymphocytic infiltrate is usually sparse in early cutaneous GVHR and the clinical aspect of GVHR has never been reported to be lichenoid. Our case report seems to be important for two reasons: it is the first clinically and histologically verified lichen planus occurring after a severe GVHR has healed. This association does not seem to be fortuitous, and a second case is reported in this issue (Saurat et al., 1975). The scarcity of such cases can be explained by the usually short survival of patients with severe GVHR. This lichen planus was followed by severe skin changes. Such lesions have occurred previously after severe GVHR (Storb, personal communication). Maybe lichen planus following GVHR was the initial event. The significance of lichen planus in our cases is not obvious. It could be a persisting chronic GVHR exclusively located on the skin: lichen planus following GVHR would be a model of cell mediated autoimmune disease. Another hypothesis is that a lichenoid eruption, whatever its background, is a way of cellular reaction (immune or not) to a necrosis (from various aetiology) of the basal cells, as suggested by Pinkus (1973) and Black (1972). These hypotheses are not mutually exclusive. Dermatologists have to pay attention to chronic GVHR. Further research into cutaneous GVHR could give a new insight into the pathogenesis of lichen planus.