投稿者：大日輝記

リンパ球主体の血管炎です。好酸球も見られます。付属器への侵襲は目立ちません。鑑別として lymphomatoid papulosis が挙がると思いますが、もっと浸潤が密になるのではと思い上記としました。

角質は軽度ながらparakeratosis、mildな表皮肥厚からsubacute程度の経過を伺わせます。病変の主体はやはり真皮上層〜中層までに留まり、中小静脈周囲のリンパ球主体とした浸潤、血管壁膨化＋好酸性物質による塞栓像、周囲にはごく軽度な好酸球＋extravasating RBCを認める一方、真皮線維系の反応に乏しい所見と読みました。以上より、�@livedo vasculitis with thrombophlebitis、�A陳旧化しつつあるsuperficial allergic vasculitis (Ruiter)などを考えます。

４月から勉強させて頂きますので、ご教授よろしくお願い致します。

Perivascular polymorphous infiltrates consist of neutrophils, eosinophils and mononuclear cells. Nuclear dusts can sparsely be observed. Erythrocyte diapedesis suggests the lesion is purpuric. Whereas fibrinous deposits in the vessel wall seem to be minimal, fibrinous aggregates occlude the inflamed small vessels. The nature of these aggregates could be either fibrin thrombi or pseudothrombi, the latter of which reminds me either mixed cryoglobulinemic vasculitis or localized cryoprecipitate reaction caused by insect bites. If the precipitates are the true fibrin thrombi, then I must think a number of thrombotic small vessel vasculitides, both systemic and localized. Thrombophilic conditions such as antiphospholipid antibody (APA) syndrome and thrombotic microangiopathy are unlikely, because of its vasculitic rather than thrombopathic nature. DIC is also unlikely, but septic vasculitis remains in consideration. Livedoid vasculitis is hard to be realized by the lacking parietal hyalinization and the existing substantial inflammation. It is noteworthy that livedoid vasculitides merge with high incidence of APA and low plasminogen activity, suggesting their coagulopathic rather than vasculitic etiology. If one assumes this lesion to be primary lymphocytic vasculitis, then PPPD and atrophic papulosis must be included in the differentiation. In conclusion, I prefer to think the time-elapsing leukocytoclastic vasculitis with thrombosis in this case, if it is not cryoprecipitated vasculitis. Looking forward to convincing answer, I remain.

This lesion is a single plaque on the left lower leg from 59-year-old male suffering from Hepatitis C for a long time.
Te clinical diagnosis was Eczema. The laboratory data told us that the patient had Cryoglobulinemia(the clinician did not know the nature of criyoglobulin) and the SGOT was 170, SGPT 230, LDH 300 and ZTT 30.
The possible histopathological diagnosis includes A. Cryoglobulinemia: 1. Monoclonal cryoglobulinamia(type 1), 2. Mixed cyroglobulinemia(Type 2), or 3. polyclonal crioglobulinamia(tyoe 3) and B: Cryoprecipitates scondary to tick-bite reaction.
Our initial histopathological diagnosis was Livedo vasculitis. Now we know it is a skin manifestation of Cryoglobulinemia, type 3(probably), due to Hepatitis C.
The patient is free from skin lesion these days.

Thank you very much for answering my request. My initial impression was mixed cryoglobulinemic vasculitis rather than livedoid vasculitis in this case, because of its vasculitic rather than thrombopathic nature. I feel happy if you give me your opinion concerning the etiology of livedoid vascultis. Thank you again.

You will see the diagnosis of this case on the website.
In advance
Cryoglobulinemia, probably type 3, in patient with Hepatitis C,
manifested as intravascular cryoprecipitate housed in small blood vessels with the features of Leukocytoclastic vasculitis (Neutrophils, nuclear dusts, extravasated erythrocytes but fibrin deposit in the vessel wall).