Iran J Pediatr. 2021 August; 31(4):e111431.
Published online 2021 August 30.
doi: 10.5812/ijp.111431.
Case Report
Frameshift Mutation in Polar Rich Domain (PRD) of PQBP1 Gene
Associated with Asymmetric Cerebellar Hemispheres: A Case Report
of Renpenning Syndrome
Dejan Aleksic
1, *
, Milan Borkovic
2
, Jelena Krivacic
3
, Igor Petrusic
4
and Vedrana Milic Rasic
5
1
Department of Neurology, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia
2
Clinic for Neurology and Psychiatry for Children and Youth, Belgrade, Serbia
3
Institute for Psychophysiological Disorders and Speech Pathology "Prof. Dr Cvetko Brajovic", Belgrade, Serbia
4
Laboratory for Advanced Analysis of Neuroimages, Faculty of Physical Chemistry, University of Belgrade, Belgrade, Serbia
5
Clinic for Neurology and Psychiatry for Children and Youth, School of Medicine, University of Belgrade, Belgrade, Serbia
*
Corresponding author: Department of Neurology, Faculty of Medical Sciences, University of Kragujevac, Kragujevac, Serbia. Email: drdeal1987@gmail.com
Received 2020 November 21; Revised 2021 June 18; Accepted 2021 July 27.
Abstract
Introduction: In 1962, Renpenning et al. published an article with 20 male patients from three generations with mental retar-
dation. Scientists suggested that the syndrome with mutation mapped to the locus Xp11.2-p11.4 should be called Renpenning syn-
drome. The deletion/duplication of an AG dinucleotide on proximal Xp in the polyglutamine tract-binding protein 1 (PQBP1) gene
causing frameshift in the fourth coding exon was identified as the most frequent mutation in this syndrome. Renpenning syndrome
with asymmetric cerebellar hemispheres has not been reported previously.
Case Presentation: In this case report, we presented an 11-year-old male with mild developmental delay and mild intellectual dis-
ability, microcephaly, dysmorphic face, short stature, and seizures. The following morphological abnormalities were detected: a
wide nasal bridge, midfacial hypoplasia, short philtrum, low-set ears, low hanging columella, high palate, and narrow face. Neuro-
logical examination showed upper and lower extremities hypotonia with joint hypermobility. The patient had his first seizure at the
age of seven, and he experienced a total of 10 seizures by the age 11. A systolic murmur of intensity 2/6 was present, and echocardiog-
raphy showed chordae tendineae abnormalities in the left ventricle. Brain magnetic resonance imaging (MRI) showed asymmetric
cerebellar hemispheres (mild right cerebellar hemisphere hypoplasia). A frameshift mutation in the polar reach domain (PRD) of
the PQBP1 gene (c.459-462 delAGAG) was detected by exome sequencing.
Conclusions: We showed the first case of genetically confirmed Renpenning syndrome in Serbia. Our patient had classical clinical
manifestations for Renpenning syndrome as a consequence of frameshift mutation in the PRD of the PQBP1 gene. To the best of our
knowledge, according to the literature, this is the first patient with Renpenning syndrome with asymmetric cerebellar hemispheres
(mild right cerebellar hemisphere hypoplasia).
Keywords: PQBP1 Gene, Polar Rich Domain, Cerebellar Hypoplasia, Renpenning Syndrome, Seizures
1. Introduction
Renpenning et al. (1) published an article in 1962 with
20 male patients from three generations with mental re-
tardation (MR), which were associated with microcephaly,
prominent ears, cataracts, congenital ocular coloboma,
and seizures. Turner et al. (2), from a group of 148 males
with intellectual disability (ID), analyzed 17 who were con-
sidered to have that same syndrome because of the same
pattern of inheritance. Scientists mapped the locus to
Xp11.2-p11.4 and suggested that the syndrome with this mu-
tation should be called Renpenning syndrome (3). In five of
29 families with X-linked mental retardation (XLMR), the
deletion/duplication of an AG dinucleotide on proximal
Xp in the polyglutamine tract-binding protein 1 (PQBP1)
gene was identified, causing frameshift in the fourth cod-
ing exon (4). Stevenson et al. (5) identified a 4-bp deletion
in exon 4 of the PQBP1 gene denoted by the mutation as
459-462delAGAG. It was then proposed that all mutations
in the PQBP1 gene whose clinical manifestations over time
received different names in the literature were unified un-
der the same name: Renpenning syndrome (5). Also, this
mutation in the PQBP1 gene (the fourth coding exon) has
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