Deutsche medizinische Wochenschrift (1946) · 2001
[Schonlein-Henoch purpura associated with hepatitis B in a patient with HIV infection].
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Braun S, Ramaker J, Dippel E, Zouboulis C C
Аннотация
HISTORY AND CLINICAL FINDINGS: 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.
INVESTIGATIONS: 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.
TREATMENT AND COURSE: 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.
CONCLUSION: It is likely that the hepatitis B may have been the trigger for the Schönlein-Hennoch-purpura.
INVESTIGATIONS: 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.
TREATMENT AND COURSE: 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.
CONCLUSION: It is likely that the hepatitis B may have been the trigger for the Schönlein-Hennoch-purpura.