Smouldering Waldenstrom's macroglobulinemia: Factors predicting evolution to symptomatic disease
Clara CesanaSara MiqueleizPatrizia BernuzziElisabetta TresoldiValentina RossiGiovanna D’AvanzoDavide FilippiniEnrica Morra
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Waldenstrom macroglobulinemia (WM) is characterized by the production of serum monoclonal immunoglobulin (Ig) M and by lymphoplasmacytic bone marrow infiltration.[1][1] Upregulation of interleukin 6 (IL6) has been demonstrated in WM,[2][2],[3][3] in accordance with the increased IL6 serum
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Waldenstrom 的 macroglobulinemia/lymphoplasmacytic 淋巴瘤(WM/LPL ) 是低档 B 房间 non-Hodgkin 有一堂懒惰临床的功课的淋巴瘤。高等级的 non-Hodgkin 淋巴瘤(NHL ) 和治疗相关的 myelodysplasia/acute 白血病(t-MDS/AML ) 在以前的研究与 WM/LPL 在病人被报导了。然而，仅仅有 WM/LPL 的二个案例被报导发展到 Hodgkin 淋巴瘤(HL ) 。这里，我们报导 WM/LPL 的第一个案例同时开发了古典 HL 在起始的 nucleoside 以后的 3 年基于类似物的化疗。
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The hazard ratio and median survival time are the routine indicators in survival analysis. We briefly introduced the relationship between hazard ratio and median survival time and the role of proportional hazard assumption. We compared 110 pairs of hazard ratio and median survival time ratio in 58 articles and demonstrated the reasons for the difference by examples. The results showed that the hazard ratio estimated by the Cox regression model is unreasonable and not equivalent to median survival time ratio when the proportional hazard assumption is not met. Therefore, before performing the Cox regression model, the proportional hazard assumption should be tested first. If proportional hazard assumption is met, Cox regression model can be used; if proportional hazard assumption is not met, restricted mean survival times is suggested.风险比（hazard ratio，HR）和中位生存时间是生存分析时的常规分析和报告指标。本文简要介绍了HR和中位生存时间的关系以及比例风险假定在这两者之间的作用，分析了检索出的58篇文献中的110对风险比和中位生存时间比的差异，并通过实例阐明了产生这种差异的原因。结果表明，在不满足比例风险假定时，Cox回归模型计算得到的风险比是不合理的，且与中位生存时间之比不等价。因此，在使用Cox回归模型前，应先进行比例风险假定的检验，只有符合比例风险假定时才能使用该模型；当不符合比例风险假定时，建议使用限制性平均生存时间。.
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Waldenstrom macroglobulinemia is a low-grade B-cell lymphoproliferative disorder of the elderly with characteristic monoclonal IgM-producing neoplastic infiltrates of the bone marrow, lymph node, and spleen. Cutaneous manifestations are usually nonspecific such as purpura, ulcers, and urticarial lesions. These lesions are caused by hyperviscosity of the blood, immune complex-mediated vascular damage, paraprotein deposition, and amyloid deposition. Specific skin lesions occur rarely and generally consist of translucent, flesh-colored papules composed of monoclonal IgM deposits. Rarely, there may be violaceous lesions composed of low-grade lymphoplasmacytic infiltrates characteristic of Waldenstrom macroglobulinemia. Both cutaneous manifestations of the disease, as well as disease transformation to high-grade, large cell lymphoma are rare. We report two very unusual cases of Waldenstrom macroglobulinemia with documented skin disease that demonstrated transformation to high-grade lymphoma. Both patients were elderly men with long-standing Waldenstrom macroglobulinemia involving the bone marrow, who subsequently developed skin involvement by the disease. Waldenstrom macroglobulinemia can rarely manifest as cutaneous disease, sometimes as a high-grade transformation of low-grade Waldenstrom macroglobulinemia elsewhere. Distinction of cases of transformed Waldenstrom macroglobulinemia from de novo cutaneous large cell lymphoma may be important, because the two entities are likely biologically different.
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