Whyte Michael P, Hughes Anne E
Center for Metabolic Bone Disease and Molecular Research, Shriners Hospitals for Children, St. Louis, Missouri 63131, USA.
J Bone Miner Res. 2002 Jan;17(1):26-9. doi: 10.1359/jbmr.2002.17.1.26.
Expansile skeletal hyperphosphatasia (ESH) is a singular disorder characterized in the year 2000 in a mother and daughter with early-onset deafness, premature loss of teeth, progressive hyperostotic widening of long bones causing painful phalanges in the hands, accelerated bone remodeling, and episodic hypercalcemia likely inherited as a highly penetrant, autosomal dominant trait. Absence of large osteolytic lesions with cortical thinning in major long bones, together with bouts of hypercalcemia, indicated that ESH is not a variant of familial expansile osteolysis (FEO). Here, we investigated the molecular basis of ESH after three families with FEO were reported to have an identical 18-base pair tandem duplication (84dup18) in the signal peptide sequence of the TNFRSF11A gene that encodes receptor activator of nuclear factor-kappaB (RANK). We find that ESH is caused by a remarkably similar 15-base pair tandem duplication (84dup15) in TNFRSF11A. Hence, ESH and FEO are allelic diseases and ESH, like FEO, probably reflects increased activity in the skeleton of the RANK target, nuclear factor-kappaB (NF-kappaB).
膨胀性骨高磷酸酶血症(ESH)是一种独特的疾病,于2000年在一对母女中被发现,她们患有早发性耳聋、牙齿过早脱落、长骨进行性骨质增生增宽导致手部指骨疼痛、骨重塑加速以及间歇性高钙血症,可能作为一种高外显率的常染色体显性性状遗传。主要长骨无伴有皮质变薄的大溶骨性病变,以及间歇性高钙血症,表明ESH不是家族性膨胀性骨质溶解症(FEO)的一种变体。在此,在报道了三个FEO家族在编码核因子κB受体激活剂(RANK)的TNFRSF11A基因的信号肽序列中存在相同的18个碱基对串联重复(84dup18)之后,我们对ESH的分子基础进行了研究。我们发现ESH是由TNFRSF11A中一个非常相似的15个碱基对串联重复(84dup15)引起的。因此,ESH和FEO是等位基因疾病,并且ESH与FEO一样,可能反映了RANK靶点核因子κB(NF-κB)在骨骼中的活性增加。