The Retina
The Retina
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DOI：
10.1136/jnnp.51.11.1472-a
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
MD Sanders
中科院分区：
文献类型：
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作者：
MD Sanders
这本书，虽然在thecover上声明已由凯利，凯尔和拉托夫编辑，实际上是由这三个人写的，他们都积极参与了这一领域的最新进展。因此，他们能够以权威的方式写作。在讨论了浆细胞恶液质和相关神经病变的定义和流行病学之后，作者调查了周围神经的相关生物化学和免疫学。然后，他们回顾了目前关于与Waldenstr 6 m巨球蛋白血症、良性单克隆IgM副蛋白血症和单克隆IgM冷球蛋白血症相关的神经病变的知识。与具有抗髓鞘相关糖蛋白（MAG）活性的单克隆副蛋白相关的神经病特别重要，震颤和共济失调的发生是突出的临床特征。其他有趣的变体正在出现，如单克隆IgM副蛋白，其具有针对GM和GDlb神经节苷脂共享的表位的活性;这些与多灶性运动神经病相关。另一种是IgM副蛋白，具有抗硫酸异黄酮的活性，其临床特征为轴突感觉运动性多发性神经病和表皮病的发生。与IgG和伊加单克隆副蛋白相关的神经病变与伴随的IgM副蛋白分离，并被认为与慢性炎性脱髓鞘性多发性神经病相似，这一观点需要验证。伴随骨髓瘤的神经病变被认识的时间要长得多，可能有多种机制，包括神经内淀粉样蛋白沉积。鉴于神经病变和这种罕见的骨髓瘤之间的特殊联系，骨质疏松性骨髓瘤被单独列为一章。本文指出POEMS综合征（多发性神经病、器官肿大、水肿、M带、皮肤改变）虽然有一个醒目的首字母缩写，但可能以不完全形式与这种类型的骨髓瘤相关。该综合征也可能与非恶性IgG和伊加副蛋白血症有关。与免疫源性淀粉样蛋白相关的神经病变（AL淀粉样蛋白）包括考虑的最终条件。在鉴别诊断中提出的遗传性淀粉样神经病的讨论并不是很及时。在这些章节中，描述了临床特征，并附有说明性的病例史，随后是调查结果的说明，基础书回顾了病理学以及关于病理发生和治疗的已知知识。这些神经病变的发病机制在很大程度上仍不清楚。有证据表明，抗MAG的IgM副蛋白直接导致脱髓鞘，但淀粉样蛋白在神经中沉积的原因和神经纤维损伤的机制尚不清楚。
This book, although stated on thecover to have been edited by Kelly, Kyle and Latov, is actually written by these three individuals, all of whom have been actively involved in the recent advances in this area. They are therefore in a position to write with authority. After discussing definitions and the epidemiology of plasma cell dyscrasias and associated neuropathies, the authors survey the relevant biochemistry and immunology of peripheral nerve. They then review current knowledge concerning neuropathy associated with Waldenstr6m's macro-globulinaemia, benign monoclonal IgM paraproteinaemias and monoclonal IgM cryoglobulinaemia. Those neuropathies related to monoclonal paraproteins with activity against myelin-associated glycoprotein (MAG) are of particular impor-tance, the occurrence of tremor and ataxia being a prominent clinical feature. Other intriguing variants are emerging such as monoclonal IgM paraproteins with activity against an epitope shared by GM, and GDlb gangliosides; these are associated with a multifocal motor neuropathy. Another is an IgM paraprotein with activity against chondriotin sulphate, characterised clinically by the occurrence of an axonal sensorimotor polyneuropathy and epidermolysis. Neuropathies associated with IgG and IgA monoclonal paraproteins are separated off from those accompanying IgM paraproteins and are considered to be similar to chronic inflammatory demyelinating polyneuropathy, a view that requires validation. Neuropathy accompanying myeloma has been recognised for a substantially longer period and probably has a variety of mechanisms, including the intraneural deposition of amyloid. Osteosclerotic myeloma is given a separate chapter in view of the particular association between neuropathy and this rare form of myeloma. It is pointed out that the POEMS (polyneuropathy, organomegaly, oedema, M band, skin changes) syndrome, although identified by an eye-catching acronym, may be present in an incomplete form in asso-ciation with this type of myeloma. The syndrome can also be associated with non-malignant IgG and IgA paraproteinaemia. Neuropathy related to amyloid of im-munological origin (AL amyloid) comprises the final condition that is considered. The discussion of the hereditary amyloid neuropathies, brought up in the differential diagnosis, is not very contempory. Throughout these chapters, a description of the clinical features, with illustrative case histories, is followed by accounts of the findings on investigation, the underlyingBook reviews pathology and what is known about patho-genesis, and treatment. The pathogenesis of these neuropathies is still largely obscure. There is some evidence that IgM paraproteins active against MAG directly lead to demyelination, but the reason for amyloid deposition in nerve and the mechanism of nerve fibre damage is uncer-tain.