Ling Catriona M, Sheferaw Tewabu F, Denno Donna M, Chasweka Dennis, Kamiza Steve B, Ordi Jaume, Moxon Christopher A, Kats Kim, Khoswe Stanley, Mbale Emmie, Ziwoya Frank, Tembo Abel, Attipa Charalampos, Potani Isabel, Kim Peter K, Berkley James A, Walson Judd L, Voskuijl Wieger P, Bandsma Robert H J
Department of Nutritional Sciences, University of Toronto, Toronto, Canada.
Translational Medicine, The Hospital for Sick Children, Toronto, Canada.
Glob Pediatr. 2024 Sep;9:None. doi: 10.1016/j.gpeds.2024.100199.
To describe and compare liver mitochondrial and peroxisomal histopathology by nutritional status in children who died following hospitalization for acute illness in Malawi.
Liver tissue was collected using Minimally Invasive Tissue Sampling from eleven children under-five years old who died during hospitalization and were either non-wasted ( = 4), severely wasted ( = 4) or had edematous malnutrition ( = 3). Histology was assessed on hematoxylin and eosin stained slides. Mitochondrial and peroxisomal ultrastructural features were characterized using electron microscopy (EM) and immunofluorescence (IF).
Hepatic steatosis was present in 50 % of non-wasted and severely wasted children and all children with edematous malnutrition. Edematous malnutrition was associated with 56 % and 45 % fewer mitochondria than severe wasting ( < 0.001) and no wasting ( = 0.006), respectively, and abnormal mitochondrial morphology compared to severe wasting ( = 0.002) and no wasting ( = 0.035). Peroxisomal abundance was reduced in edematous malnutrition compared to severe wasting ( = 0.005), but did not differ from no-wasting.
Edematous malnutrition is associated with reduced abundance and altered morphology of hepatic mitochondria and peroxisomes. Interventions targeting improvements in hepatic metabolic function may be beneficial in improving metabolism and reducing mortality in children with severe malnutrition, particularly in those with nutritional edema.
描述并比较马拉维因急性疾病住院后死亡儿童的肝脏线粒体和过氧化物酶体组织病理学与营养状况之间的关系。
采用微创组织采样法,从11名五岁以下住院期间死亡的儿童身上采集肝脏组织,这些儿童分别为非消瘦型(n = 4)、重度消瘦型(n = 4)或水肿型营养不良(n = 3)。对苏木精和伊红染色的玻片进行组织学评估。使用电子显微镜(EM)和免疫荧光(IF)对线粒体和过氧化物酶体的超微结构特征进行表征。
50%的非消瘦型和重度消瘦型儿童以及所有水肿型营养不良儿童均存在肝脂肪变性。与重度消瘦(p < 0.001)和非消瘦(p = 0.006)相比,水肿型营养不良儿童的线粒体数量分别减少了56%和45%,且与重度消瘦(p = 0.002)和非消瘦(p = 0.035)相比,线粒体形态异常。与重度消瘦相比,水肿型营养不良儿童的过氧化物酶体丰度降低(p = 0.005),但与非消瘦儿童无差异。
水肿型营养不良与肝脏线粒体和过氧化物酶体的丰度降低及形态改变有关。针对改善肝脏代谢功能的干预措施可能有助于改善重度营养不良儿童的代谢并降低死亡率,特别是对那些患有营养性水肿的儿童。