Skordis Nicos, Kyriakou Andreas
Paediatric Endocrine Unit, Makarios Hospital, Nicosia 1474, Cyprus.
Pediatr Endocrinol Rev. 2011 Mar;8 Suppl 2:271-7.
Growth failure in thalassaemia major (TM) has been recognised for many years, and has persisted despite major therapeutic advances. The child with TM has a particular growth pattern, which is relatively normal until age 9-10 years; after this age a slowing down of growth velocity and reduced or absent pubertal growth spurt are observed. The pathogenesis of growth failure is multifactorial. The fundamental problem is the free iron and hemosiderosis-induced damage of the endocrine glands. Additional factors may contribute to the aetiology of growth delay including chronic anaemia and hypoxia, chronic liver disease, zinc and folic acid and nutritional deficiencies, intensive use of chelating agents, emotional factors, endocrinopathies (hypogonadism, delayed puberty, hypothyroidism, disturbed calcium homeostasis and bone disease) and last but not least dysregulation of the GH-IGF-1 axis.Three phases of growth disturbances according to age of presentation are well recognised, and have different aetiologies: in the first phase growth disturbance is mainly due to hypoxia, anaemia, ineffective erythropoiesis and nutritional factors. During late childhood (second phase), growth retardation is mainly due to iron overload affecting GH-IGF-1 axis and other potential endocrine complications. Although appropriate iron chelation therapy can improve growth and development, TM children and adolescents treated intensively with desferrioxamine remain short as well, showing body disproportion between the upper and lower body segment. After the age of 10-11 years (third phase), delayed or arrested puberty is an important contributing factor to growth failure in adolescent thalassaemics, who do not exhibit a normal growth spurt. During the last decades therapeutic progress and bone marrow transplantation resulted in a prolonged life expectancy in TM patients. Growth retardation, however, continues to be a significant challenge in these individuals, often affecting their social adjustment and quality of life.
重型地中海贫血(TM)患者生长发育迟缓问题已被认识多年,尽管在治疗方面取得了重大进展,但该问题依然存在。患有TM的儿童具有特殊的生长模式,在9至10岁之前生长相对正常;此后,生长速度开始放缓,青春期生长突增减弱或缺失。生长发育迟缓的发病机制是多因素的。根本问题是游离铁和含铁血黄素沉着症对内分泌腺造成的损害。其他因素可能也导致了生长发育延迟,包括慢性贫血和缺氧、慢性肝病、锌和叶酸及营养缺乏、螯合剂的大量使用、情绪因素、内分泌疾病(性腺功能减退、青春期延迟、甲状腺功能减退、钙稳态紊乱和骨病),以及最后但同样重要的生长激素-胰岛素样生长因子-1(GH-IGF-1)轴失调。根据发病年龄,生长发育障碍可分为三个阶段,病因各不相同:第一阶段生长发育障碍主要是由于缺氧、贫血、无效红细胞生成和营养因素。在儿童晚期(第二阶段),生长发育迟缓主要是由于铁过载影响GH-IGF-1轴及其他潜在的内分泌并发症。尽管适当的铁螯合疗法可以改善生长发育,但接受去铁胺强化治疗的TM儿童和青少年仍然身材矮小,且上下身比例失调。10至11岁之后(第三阶段),青春期延迟或停滞是青少年地中海贫血患者生长发育迟缓的一个重要因素,这些患者没有出现正常的生长突增。在过去几十年中,治疗进展和骨髓移植延长了TM患者的预期寿命。然而,生长发育迟缓仍然是这些患者面临的重大挑战,常常影响他们的社会适应能力和生活质量。