Blanche S, Tardieu M, Duliege A, Rouzioux C, Le Deist F, Fukunaga K, Caniglia M, Jacomet C, Messiah A, Griscelli C
Immunology Unit, INSERM U 132, Paris, France.
Am J Dis Child. 1990 Nov;144(11):1210-5. doi: 10.1001/archpedi.1990.02150350042021.
To better define the clinical and biological evolution of infants after vertical human immunodeficiency virus type 1 infection, we analyzed 94 consecutive infected patients followed up after their first clinical symptoms. The expression of clinical symptoms and biological abnormalities followed a bimodal distribution, some patients having an early and severe disease and the others having a slowly progressive one. One third of our patients suffered from early onset of opportunistic infection (OI). These patients had a significantly higher incidence of severe encephalopathy compared with patients without OI. The rate of survival at 3 years was 48% +/- 24%. In contrast, the patients without early OI or severe encephalopathy had a probability of survival at 3 years of 97% +/- 3%. This probability was not modified by the occurrence of bacterial infection or lymphoid interstitial pneumonitis. Lymphoid interstitial pneumonitis occurred at a mean age of 29 months, significantly later than OI or severe encephalopathy. Laboratory results at initial examination were correlated with clinical symptoms. Thus, when the number of CD4 lymphocytes was less than 500/mm3, children suffered more frequently from life-threatening symptoms (OI and severe encephalopathy): 15 of 22 vs 14 of 69. The same was true when the lymphocytes did not proliferate after antigenic stimulation, when anti-p18 and/or anti-p25 antibodies were absent in the serum, and when p24 antigen was detected in serum. Finally, severe encephalopathy was associated with low anti-human immunodeficiency virus cerebrospinal fluid antibody titer, whereas 88% of patients with moderate or no encephalopathy had signs of intrathecal anti-human immunodeficiency virus antibody synthesis. In conclusion, a subgroup of patients expressed very early signs of severe immunodeficiency and encephalopathy, whereas the majority of patients had a longer survival and less severe clinical symptoms during their first years of life than previously thought.
为了更好地明确1型人类免疫缺陷病毒垂直感染后婴儿的临床及生物学演变情况，我们分析了94例首次出现临床症状后接受随访的连续感染患者。临床症状和生物学异常的表现呈双峰分布，一些患者患有早期严重疾病，另一些患者则病情进展缓慢。我们三分之一的患者出现机会性感染（OI）的早期发作。与未发生OI的患者相比，这些患者严重脑病的发生率显著更高。3年生存率为48%±24%。相比之下，未发生早期OI或严重脑病的患者3年生存概率为97%±3%。这一概率不受细菌感染或淋巴样间质性肺炎发生情况的影响。淋巴样间质性肺炎的平均发病年龄为29个月，明显晚于OI或严重脑病。初检时的实验室结果与临床症状相关。因此，当CD4淋巴细胞数量少于500/mm³时，儿童更常出现危及生命的症状（OI和严重脑病）：22例中有15例，而69例中有14例。当淋巴细胞在抗原刺激后不增殖、血清中不存在抗p18和/或抗p25抗体以及血清中检测到p24抗原时，情况也是如此。最后，严重脑病与脑脊液抗人类免疫缺陷病毒抗体滴度低相关，而88%有中度或无脑病的患者有鞘内抗人类免疫缺陷病毒抗体合成的迹象。总之，一部分患者表现出严重免疫缺陷和脑病的非常早期迹象，而大多数患者在生命的头几年存活时间更长，临床症状也不如之前认为的严重。
