Graft versus host reaction and lichen planus‐like eruption in man
Graft versus host reaction and lichen planus‐like eruption in man
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人类移植物抗宿主反应和扁平苔藓样皮疹
DOI：
10.1111/j.1365-2133.1975.tb03131.x
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发表时间：
1975
影响因子：
10.3
通讯作者：
A. Bussel
中科院分区：
文献类型：
--
作者：
J. Saurat;L. Didier;E. Gluckman;A. Bussel
扁平苔藓样皮疹可见于多种情况，但在骨髓移植患者中发生的移植物抗宿主反应(GVHR)从未被报道为病因。扁平苔藓(LP)的组织学事件序列似乎包括最初的表皮基底细胞损伤(Pinkus，1973)。这种损害的机制尚不清楚(Black，1972)。人类GVHR的皮肤损伤似乎主要与基底细胞损伤有关(Slavin&Santos 1973)。由于LP和GVHR的初始皮损相似，GVHR可能会出现苔藓样皮疹。然而，临床上从未报道过GVHR皮疹是苔藓样斑疹或干性鳞屑猩红样疹，甚至在GVHR急性期出现毒性表皮坏死松解(Peck，Herzig&Elias，1972)，或在静止期出现萎缩和色素沉着(Slavin&Santos，1973)。Slavin&Santos(1973)首先注意到扁平苔藓和GVHR的组织学上的相似性，这种相似性主要是在GVHR的第二阶段观察到的，作者称之为“侵袭性淋巴细胞破坏性损伤的花期”。以下是一例患者的病史，其急性GVHR皮疹最初为斑丘性皮疹，随后发展为慢性皮疹，临床和组织学特征为广泛的扁平苔藓样皮疹。这名13岁的男孩因肝炎后再生障碍性贫血入院。移植手术是用他匹配的姐姐的骨髓进行的。在第7天，观察到了植入的第一个迹象，立即的过程很顺利。在第11天，他出现了弥漫性斑丘疹。两天后出现高峰热、腹泻和SGOT升高。第11天的皮肤活检显示H级GVHR，没有任何淋巴组织浸润物。从第18天到第52天，他接受了280 mg/kg的抗胸腺细胞球蛋白。62天SGOT正常，75天腹泻和食欲不振消失。皮损持续结垢和色素沉着。第二次皮肤活检，在第56天，显示持续的II-HI GVHR，只有稀疏的淋巴样细胞。第59天，诊断为巨细胞病毒(CMV)间质性肺炎合并病毒血症。停止所有免疫抑制治疗，给予抗CMV血浆、丙种球蛋白和转移因子治疗。当时存在严重的免疫缺陷(无丙种球蛋白血症、淋巴细胞对植物血凝素或同种异体淋巴细胞的免疫反应)。临床症状逐渐改善，但皮损持续和改变。出现典型的丘疹状扁平苔藓样病变。它们首先在四肢上被观察到，然后逐渐蔓延到全身。口腔黏膜和指甲也受累。第90天的皮肤活检显示扁平苔藓的特征性病变：基底表皮细胞损害，有胶体，以及
Lichen planus-like eruptions can be seen in various circumstances, but graft versus host reactions (GVHR) occurring in bone marrow transplanted patients have never been reported as an aetiological factor. The sequence of histological events in lichen planus (LP) seems to include initial epidermal basal cell damage (Pinkus, 1973). The mechanism of this damage is unknown (Black, 1972). Skin lesions of GVHR in man appear to be related mainly to basal cell damage (Slavin & Santos 1973). Because of the similarity of the initial lesions in LP and in GVHR, lichenoid eruptions in GVHR could be expected. Nevertheless, GVHR skin eruptions have never been reported to be clinically lichenoid j maculopapular or dry scaling scarlatiniform rashes and even toxic epidermal necrolysis (Peck, Herzig & Elias, 1972) have been noted in the acute stage of GVHR, or atrophy and pigmentation in the 'quiescent phase' (Slavin & Santos, 1973). Slavin & Santos (1973) first drew attention to the similarity between the histology of lichen planus and of GVHR j this similarity was observed mainly during a secondary phase of GVHR called by these authors: 'florid phase of aggressor lymphocytes destructive lesion'. The following is the history of a patient whose acute GVHR skin eruption was initially maculopapular and subsequently became chronic with clinical and histological features of an extensive lichen planus-like eruption. This 13-year-old boy was admitted for post-hepatitis aplastic anaemia. Transplantation was performed with the marrow of his matched sister. On day 7, the first signs of engraftment were observed and the immediate course was uneventful. On day 11, he developed a diffuse maculopapular rash. Two days later, high spiking fever, diarrhoea and a rise of SGOT appeared. A skin biopsy on day 11 showed a grade H GVHR without any lymphoid infiltrate. From day 18 to day 52 he received a total dose of 280 mg IgG/kg of anti-thymocyte globulin. The SGOT was normal by day 62, and diarrhoea and anorexia disappeared on day 75. The skin lesions persisted with scaling and pigmentation. A second skin biopsy, on day 56, showed persisting grade II-HI GVHR, only sparse lymphoid cells were seen. On day 59, a cytomegalovirus (CMV) interstitial pneumonitis with viraemia was diagnosed. All immuno-suppressive therapy was discontinued and treatment with anti-CMV plasma, gammaglobulin and transfer factor was given. At that time there was a severe immunodeficiency (agammaglobulinaemia, vinresponsiveness of lymphocytes to phytohaemagglutin or to allogeneic lymphocytes). The clinical status improved progressively but skin lesions persisted and changed. Typical papular lichen planuslike lesions appeared. They were first observed on the extremities and progressively spread to the whole body. The buccal mucous membrane and nails were also involved. A skin biopsy, on day 90, demonstrated the characteristic lesions of lichen planus: basal epidermal cell damage with colloid bodies, and