Abraham Suneetha Susan Cleave, Barney Anitha, Mohan Sony, Joy Praisy, Ganesan Paramasivam, Das Sweta, Cherupanakkal Cleetus, Jose Arun, A Rekha, Zatkova Andrea, Danda Sumita
Department of Clinical Genetics, Christian Medical College, Vellore, Tamil Nadu, India.
Department of Biochemistry, Believers Church Medical College and Hospital, Thiruvalla, Kerala, India.
Indian J Med Res. 2024 Nov;160(5):448-456. doi: 10.25259/ijmr_1900_23.
Background & objectives Alkaptonuria (AKU) is an autosomal recessive disease wherein biallelic pathogenic variants in the homogentisate 1,2- dioxygenase (HGD) gene encoding the enzyme homogentisate 1,2 dioxygenase cause high levels of homogentisic acid (HGA) to circulate within the body leading to its deposition in connective tissues and excretion in urine. A homozygous splice donor variant (c.87+1G>A) has been identified to be the founder variant causing alkaptonuria among Narikuravars, a group of gypsies settled in Tamil Nadu. Methods Blood and urine samples of 30 homozygous splice site donor variant individuals (2 groups aged 7-20 and 21-83 yr, with 9 and 21 individuals, respectively), carriers and 30 wild-type individuals from the Narikuravars were collected during field visits after obtaining informed consent. Clinical evaluation and genetic counselling were done. The plasma and urine HGA levels were estimated by high-performance liquid chromatography. RNA was extracted from the peripheral blood and reverse transcribed. Sanger sequencing was done to check the consequence of the splice donor variant. Relative quantification of the cDNA in the three groups was done by real-time qPCR (RT-qPCR) studies using reference genes followed by Pearson's correlation analysis. Results In our cohort, among the affected alkaptonuria individuals, the minimum age for eye pigmentation detected was 23 yr. Similarly, the minimum age for back pain and any joint pain was 30 yr and 38 yr, respectively. Sequencing of the cDNA confirmed exon 2 skipping in affected individuals. In comparison to the normal individuals, the affected individuals showed reduced HGD expression. HGD relative expression showed a significant correlation (P<0.05) with mean plasma HGA levels in the younger (≤22 yr) age group but not in the older one. There was also a significant correlation (P<0.05) of reduced HGD expression with back pain in the 21-37 yr age group. Increasing age showed a positive correlation with circulating mean plasma HGA levels and a negative correlation with excreted HGA. Interpretation & conclusions As per the authors' knowledge, this is the first study to confirm the functional effect by RT-PCR of this highly prevalent founder HGD variant causing alkaptonuria in the Narikuravar community. Both plasma and urinary HGA levels correlated well with the gene expression of this variant and could serve as potential markers of AKU severity for those with this variant.
背景与目的 黑尿症(AKU)是一种常染色体隐性疾病,其中编码尿黑酸1,2-双加氧酶的尿黑酸1,2-双加氧酶(HGD)基因的双等位基因致病变异导致体内高水平的尿黑酸(HGA)循环,从而使其沉积在结缔组织中并随尿液排出。已确定一种纯合剪接供体变异(c.87+1G>A)是导致定居在泰米尔纳德邦的一群吉普赛人——纳里库拉瓦尔人中黑尿症的始祖变异。方法 在获得知情同意后,于实地考察期间收集了30名纯合剪接位点供体变异个体(2组,年龄分别为7至20岁和21至83岁,分别有9名和21名个体)、携带者以及30名来自纳里库拉瓦尔人的野生型个体的血液和尿液样本。进行了临床评估和遗传咨询。通过高效液相色谱法测定血浆和尿液中的HGA水平。从外周血中提取RNA并进行逆转录。采用桑格测序法检查剪接供体变异的后果。使用参考基因通过实时定量PCR(RT-qPCR)研究对三组中的cDNA进行相对定量,随后进行皮尔逊相关性分析。结果 在我们的队列中,在受影响的黑尿症个体中,检测到眼睛色素沉着的最小年龄为23岁。同样,背痛和任何关节痛的最小年龄分别为30岁和38岁。对cDNA的测序证实了受影响个体中存在外显子2跳跃。与正常个体相比,受影响个体的HGD表达降低。在较年轻(≤22岁)年龄组中HGD相对表达与平均血浆HGA水平呈显著相关性(P<0.05),而在较年长组中则无此相关性。在21至37岁年龄组中,HGD表达降低与背痛也存在显著相关性(P<0.05)。年龄增长与循环平均血浆HGA水平呈正相关,与排泄的HGA呈负相关。解读与结论 据作者所知,这是第一项通过RT-PCR证实这种在纳里库拉瓦尔社区中导致黑尿症的高度流行的始祖HGD变异的功能效应的研究。血浆和尿液中的HGA水平均与该变异的基因表达密切相关,对于携带该变异的个体而言,可作为黑尿症严重程度的潜在标志物。