Miró O, Pedrol E, Cebrián M, Masanés F, Casademont J, Mallolas J, Grau J M
Department of Internal Medicine, Hospital Clinic i Provincial, Universitat de Barcelona, Spain.
J Neurol Sci. 1997 Sep 10;150(2):153-9. doi: 10.1016/s0022-510x(97)00079-8.
Previous reports have suggested that HIV-related wasting syndrome may be considered as a form of myopathy. The aim of the present study was to investigate histopathological muscle changes in HIV-related wasting syndrome in order to know if there is a common substrate and whether muscle plays a primary or secondary role in its development. Patients with wasting syndrome diagnosed by Centers for Disease Control (CDC) criteria were prospectively evaluated. Clinical, analytical, nutritional, anthropometrical and muscular data were recorded. The patients were subdivided into two groups: group A was constituted by patients in whom wasting syndrome was the AIDS-defining illness, and group B by patients in whom AIDS diagnosis was previously made. In all cases muscle biopsy was performed and processed for conventional stainings and histochemical reactions. Thirty patients were included (group A, 12; group B, 18). Clinical, analytical, nutritional and anthropometrical data did not essentially differ between the two groups. All patients were malnourished with respect to controls. Histopathological findings in muscle biopsy were heterogeneous and similar in both groups, except for HIV-related myopathies, which were more frequently seen in the patients from group A (P=0.05). In five cases (17%) an unsuspected and potentially treatable myopathy was diagnosed. Patients with polyarteritis nodosa (two) or polymyositis (one) were treated with prednisone, which improved their wasting syndrome. By contrast, patients with AZT-myopathy (two) did not improve when the drug was discontinued. We conclude that in most cases the wasting syndrome cannot be considered as a true myopathy, and probably metabolic and/or nutritional factors may account for wasting development. However, in a subset of patients muscle biopsy allows the diagnosis of a treatable myopathy leading to the improvement of wasting syndrome.
先前的报告表明,与HIV相关的消瘦综合征可能被视为一种肌病形式。本研究的目的是调查与HIV相关的消瘦综合征的组织病理学肌肉变化,以了解是否存在共同的病理基础,以及肌肉在其发展中是起主要还是次要作用。对符合疾病控制中心(CDC)标准诊断的消瘦综合征患者进行前瞻性评估。记录临床、分析、营养、人体测量和肌肉数据。患者被分为两组:A组由以消瘦综合征为艾滋病界定疾病的患者组成,B组由先前已确诊艾滋病的患者组成。在所有病例中均进行了肌肉活检,并进行常规染色和组织化学反应处理。共纳入30例患者(A组12例;B组18例)。两组的临床、分析、营养和人体测量数据基本无差异。与对照组相比,所有患者均存在营养不良。肌肉活检的组织病理学结果在两组中是异质性的且相似,但与HIV相关的肌病在A组患者中更常见(P = 0.05)。在5例(17%)患者中诊断出一种未被怀疑且可能可治疗的肌病。结节性多动脉炎患者(2例)或多发性肌炎患者(1例)接受泼尼松治疗后,消瘦综合征有所改善。相比之下,AZT相关性肌病患者(2例)在停药后并未改善。我们得出结论,在大多数情况下,消瘦综合征不能被视为真正的肌病,代谢和/或营养因素可能是消瘦发展的原因。然而,在一部分患者中,肌肉活检可诊断出可治疗的肌病,从而使消瘦综合征得到改善。