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[慢性萎缩性胃炎和贾第虫病继发维生素B12缺乏所致的多发性神经病]

[Polyneuropathy caused by vitamin B12 deficiency secondary to chronic atrophic gastritis and giardiasis].

作者信息

Brieva L, Ara J R, Bertol V, Canellas A, del Agua C

机构信息

Servicio de Neurología, Hospital Miguel Servet, Zaragoza, España.

出版信息

Rev Neurol. 1998 Jun;26(154):1019-20.

PMID:9658486
Abstract

INTRODUCTION

In chronic atrophic gastritis atrophy of the stomach glands leads to intrinsic factor deficit, with consequent failure to absorb vitamin B12 and gastric achylia, which predisposes to Giardia infection which in itself leads to depletion of vitamin B12. We describe the case of a patient with peripheral and central nervous system pathology due to lack of vitamin B12 secondary to the combined effect of these two disorders.

CLINICAL CASE

A 54 year old woman consulted us for paraesthesia and weakness of the legs which had been progressive for the previous two years. She presented with tactile hypoaesthesia, hypoparaesthesia, distal hyperreflexia and dysymmetry of the legs, ataxic-spastic gait and a positive Romberg sign. The investigations carried out showed the serum vitamin B12 level to be 3 pg/ml (N: 180-900), hemoglobin 13 g/dl and MCV 111 fl with MCHC 348/dl; neurophysiological studies: compatible with demyelinating motor polyneuropathy. Schilling test: deficit of absorption of vitamin B12 which was corrected on administration of intrinsic factor; gastroscopy; atrophic gastritis which confirmed the morbid anatomy findings. There was also flora containing Helicobacter and massive Giardia infection. Replacement and antibiotic therapy was followed by complete remission of the clinical picture.

CONCLUSION

We emphasize the excellent clinical response to treatment in spite of the time elapsed since onset of symptoms.

摘要

引言

在慢性萎缩性胃炎中,胃腺萎缩会导致内因子缺乏,进而导致维生素B12吸收障碍和胃酸缺乏,这易引发贾第虫感染,而贾第虫感染本身又会导致维生素B12缺乏。我们描述了一例因这两种疾病共同作用导致维生素B12缺乏而出现周围和中枢神经系统病变的患者病例。

临床病例

一名54岁女性因双腿感觉异常和无力前来就诊,症状在过去两年中逐渐加重。她表现为触觉减退、感觉异常、远端反射亢进和双腿不对称、共济失调 - 痉挛性步态以及Romberg征阳性。检查显示血清维生素B12水平为3 pg/ml(正常范围:180 - 900),血红蛋白13 g/dl,平均红细胞体积111 fl,平均红细胞血红蛋白浓度348/dl;神经生理学研究:符合脱髓鞘性运动性多发性神经病。施林格试验:维生素B12吸收障碍,给予内因子后得以纠正;胃镜检查:萎缩性胃炎,证实了病理解剖学发现。同时还发现有幽门螺杆菌菌群和大量贾第虫感染。经过替代和抗生素治疗后,临床症状完全缓解。

结论

我们强调尽管自症状出现以来已过去一段时间,但治疗仍取得了良好的临床效果。

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Rev Neurol. 1998 Jun;26(154):1019-20.
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