Braun S, Ramaker J, Dippel E, Zouboulis C C
Klinik und Poliklinik für Dermatologie, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Berlin.
Dtsch Med Wochenschr. 2001 Feb 2;126(5):103-7. doi: 10.1055/s-2001-10866.
A 23-year-old man with HIV-infection and recently diagnosed hepatitis B infection developed painful swelling and palpable purpura in the limbs. In addition, relapsing diarrhoea, arthralgia and pain at the level of the right kidney were noted. The liver, the palpable lymph nodes and the tonsils were enlarged.
The following laboratory parameters were abnormal: sedimentation rate 64/70 mmHg, CD4+ cells 462/ml, CD4/CD8 ratio 0.3, serum CRP 16 mg/l, antistreptolysin titre 542 kU/l, complement C3 < 0.1 g/l, GPT 37 U/l, albumin 49.5% and gamma-globulin 28.5%, in urine, leukocytes 25/microliter and protein 0.25 g/l. Hepatitis serology: anti-HBc, HBs-Ag and HBe-Ag positive, anti-HBs and anti-HBe negative, hepatitis A-Ab (IgG) positive, hepatitis A-Ab (IgM) negative, hepatitis C-Ab negative. Pharyngial swab: beta-haemolytic streptococci of group A. Stool examination: amoeba cysts, corona virus and fungi 10(4)-10(5)/ml (control specimen negative). Abdominal sonography showed minor hepatomegaly, splenomegaly and two 0.8 cm-large lymph nodes near the liver entrance. The histology of a skin lesion revealed a florid leukocytoclastic vasculitis at the upper and middle dermal vessels. The immunohistological examination detected IgA, IgM and C3 deposits.
The multiple bacterial infections had initially been considered as triggering the Schönlein-Henoch purpura. However despite successful treatment of these infections severe relapses of both the skin lesions and the systemic manifestations occurred. A drug reaction, autoimmune diseases and tumours were excluded. Only after treatment of hepatitis B infection with recombinant interferon alpha together with administration of zidovudine (treatment of choice at that time) the lesions quickly disappeared without further relapses. During the 5-year-follow-up, recurrent bacterial infections did not induce relapses of the disease, whereas the hepatitis B infection was seroconverted.
It is likely that the hepatitis B may have been the trigger for the Schönlein-Hennoch-purpura.
一名23岁男性，感染HIV且近期诊断为乙型肝炎感染，出现四肢疼痛性肿胀及可触及的紫癜。此外，还发现有复发性腹泻、关节痛及右肾区疼痛。肝脏、可触及的淋巴结及扁桃体肿大。
以下实验室参数异常：血沉64/70 mmHg，CD4+细胞462/ml，CD4/CD8比值0.3，血清CRP 16 mg/l，抗链球菌溶血素滴度542 kU/l，补体C3<0.1 g/l，谷丙转氨酶37 U/l，白蛋白49.5%，γ球蛋白28.5%，尿中白细胞25/微升，蛋白0.25 g/l。肝炎血清学检查：抗-HBc、HBs-Ag及HBe-Ag阳性，抗-HBs及抗-HBe阴性，甲型肝炎抗体（IgG）阳性，甲型肝炎抗体（IgM）阴性，丙型肝炎抗体阴性。咽拭子检查：A组β溶血性链球菌。粪便检查：阿米巴囊肿、冠状病毒及真菌10(4)-10(5)/ml（对照标本阴性）。腹部超声显示轻度肝肿大、脾肿大及肝门附近两个0.8 cm大的淋巴结。皮肤病变组织学检查显示真皮上部和中部血管有明显的白细胞破碎性血管炎。免疫组织学检查检测到IgA、IgM及C3沉积。
多种细菌感染最初被认为是引发过敏性紫癜的原因。然而，尽管这些感染得到了成功治疗，但皮肤病变和全身表现仍严重复发。排除了药物反应、自身免疫性疾病及肿瘤。仅在用重组干扰素α治疗乙型肝炎感染并同时给予齐多夫定（当时的首选治疗药物）后，病变迅速消失且未再复发。在5年的随访期间，复发性细菌感染未诱发疾病复发，而乙型肝炎感染发生了血清学转换。
乙型肝炎很可能是过敏性紫癜的触发因素。
