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Letter to the Editor
A patient with convulsive syndrome and partial tetrasomy of chromosome 15
Paciente con síndrome convulsivo y tetrasomía parcial del cromosoma 15
G. Gordillo-Gonzáleza,
Corresponding author
giselgordillogonzalez@yahoo.com

Corresponding authors.
, M.P. Hernándezb, M.L. Tamayoa,
, G. Osoriob
a Genética Médica, Instituto de Genética Humana, Facultad de Medicina, Pontificia Universidad Javeriana, Bogotá, Colombia
b Unidad de Citogenética, Instituto de Genética Humana, Facultad de Medicina, Pontificia Universidad Javeriana, Bogotá, Colombia
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Isodicentric chromosome 15 &#40;idic&#91;15&#93;&#41;&#44; also known as inverted duplication 15 &#40;inv dup 15&#41; or partial tetrasomy 15q &#40;OMIM 608636&#41;&#44; is a clearly-defined clinical entity that presents with central hypotonia&#44; developmental delay&#44; intellectual impairment&#44; epilepsy&#44; autistic behaviour&#44; and certain minor phenotypic abnormalities&#46; Its estimated incidence rate is 1 case per 30<span class="elsevierStyleHsp" style=""></span>000 births and it affects both sexes equally&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> From a cytogenetic viewpoint&#44; the disorder is defined as a mirror-image duplication of the piece of chromosome 15 between the end of the short arm and region 12&#8211;13 of the long arm &#40;idic&#91;15&#93;&#91;pter<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>q12&#8211;13&#58;&#58;q12&#8211;13<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>pter&#93;&#41;&#44; including region q11 &#40;q11<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>q13&#41;&#46; This location contains the critical regions for Prader-Willi syndrome &#40;PWS&#41; and Angelman syndrome &#40;AS&#41;&#46; In most of the cases studied to date&#44; the extra chromosome is maternal in origin and related to phenotypic abnormalities and advanced maternal age&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#8211;4</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Chromosomal region 15q1q13 is known for its instability&#44; which is secondary to the presence of repetitive DNA sequences&#46; It is highly susceptible to the formation of clinically relevant DNA rearrangements&#44; such as the formation of supernumerary markers formed by mirror-image duplication of chromosome 15&#46; This phenomenon may result in tetrasomy of the short arm of chromosome 15 &#40;15p&#41; or partial tetrasomy of the long arm of chromosome 15 &#40;15q&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Phenotypic variability in these patients tends to be determined by the specific region involved in each chromosomal rearrangement&#46; We report a case of isodicentric chromosome 15&#44; with multiple physical anomalies and epilepsy&#44; which involves 15q11&#46;2 as a breakpoint&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">A female patient was referred to the genetics department with a working diagnosis of seizures and minor abnormalities&#46; Physical examination revealed oval-shaped face&#44; broad nose&#44; slightly slanting palpebral fissures&#44; prominent ears&#44; moderate midfacial hypoplasia&#44; mild microagnathia&#44; long limbs&#44; and a tendency toward genu valgum and talipes equinovarus&#46; Biochemical testing showed normal amino acid levels&#59; karyotyping confirmed the presence of a minichromosome that could belong to part of either chromosome 14 or 15&#46; Based on phenotypic evidence&#44; it was reported as partial trisomy 15 &#40;15pter<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>15q1&#58;&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46; To confirm the diagnosis&#44; we performed FISH analysis with a centromeric probe for chromosome 15&#46; In both nuclei and in chromosome 15 copies&#44; we observed 4 fluorescent points&#44; one in each normal copy of chromosome 15 and two in the minichromosome&#44; which indicated the presence of dicentric chromosome 15 &#40;<a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#41;&#46; This was interpreted as partial tetrasomy 15q due to inverted duplication of segment 15pter<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>15q11&#46;2&#58; 47&#44;XX&#44;&#43;der&#40;15&#41;&#40;pter&#8594;q1&#58;&#41;&#46;ish invdup&#40;15&#41;&#40;pterq11&#46;2&#41;&#40;D15Z1<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>&#43;&#41; or of 47&#44;XX&#44;&#43;der&#40;15&#41;&#40;pter<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>q1&#58;&#41;&#46;ish invdup&#40;15&#41;&#40;pter<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>q11&#46;2&#58;&#58;q11&#46;2<span class="elsevierStyleHsp" style=""></span>&#8594;<span class="elsevierStyleHsp" style=""></span>pter&#41;&#40;D15Z1<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>&#43;&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0020" class="elsevierStylePara elsevierViewall">In general&#44; patients with isodicentric 15 present developmental delays and begin sitting up between 10 and 20 months and walking between 2 and 3 years&#46; They also display cognitive deficit in the areas of comprehension and expressive language &#40;some exhibit echolalia&#41;&#46; Their behaviour is frequently referred to as autistic or autistic-like&#46; Epilepsy characteristics vary&#44; and no specific type predominates except for Lennox-Gastaut syndrome&#44; which Battaglia described in 4 patients in 1997&#46; These patients presented tonic-atonic&#44; tonic&#8211;clonic&#44; and absence seizures&#46; Other types of seizures include partial complex seizures&#44; generalised myoclonic seizures with adult onset&#44; generalised tonic&#8211;clonic seizures&#44; and benign epilepsy with centrotemporal spikes&#46; Patient age at seizure onset varied from 6 months to 9 years&#46; It has been suggested that the degree of intellectual impairment and psychomotor delay could be correlated with the severity and intractability of convulsions&#46; However&#44; few studies have specifically addressed this subject&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> In general&#44; patients&#8217; facial appearance is normal&#46; Non-specific features may be present&#44; including downward-slanting palpebral fissure&#44; epicanthic fold&#44; deep-set eyes&#44; low-set ears with or without backwards rotation&#44; high palate&#44; broad nose&#44; anteverted nostrils&#44; clinodactyly of the fifth digit of the hand and partial sindactyly of the second and third digits of the feet&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Our patient did not present any of the neurological changes reported except for convulsions and minor physical anomalies&#44; plus a few more significant features including talipes equinovarus&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Chromosome 15&#44; and more specifically&#44; the 15q11&#8211;q13 locus&#44; is a cluster of genes whose genetic imprint is essential for normal neural development in mammals&#46; As mentioned previously&#44; this locus is extremely unstable&#44; especially at the 5 common breakpoints &#40;from BP1 to BP5&#41;&#44; which may give rise to genomic rearrangements including deletions and duplications&#46; One of the suggested mechanisms for idic&#40;15&#41; involves U-type recombination between homologous chromosomes&#44; followed by the disjunction and inactivation of one of the centromeres&#46; The most common form of idic&#40;15&#41; is characterised by an asymmetric recombination event between BP4 and BP5&#46; This produces tetrasomy of the region between the centromere and BP4 and trisomy of the region between BP4 and BP5&#46;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> Maternal-origin interstitial duplications and supernumerary isodicentric chromosomes produce various types of neurodevelopmental disorders which sometimes present with autistic traits&#46; This duplication is the main cytogenetic cause of autism&#44; and responsible for 1&#37; to 3&#37; of all cases&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In the same way&#44; we are aware of the environmental and genetic factors that contribute to the characteristics of each clinical case&#46; This is also true for most behavioural syndromes which have been related to a wide array of infectious diseases&#44; such as embryopathy induced by rubella or encephalitis&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> It should be noted that the second leading cause of isodicentric 15 is intrachromosomal triplication&#46; This type of anomaly may arise in response to a 2-step process taking place during meiosis&#46; First&#44; a U-type exchange occurs &#40;rather than a normal&#44; X-type exchange&#41;&#44; resulting in an inverted dicentric duplication which subsequently recombines with a normal copy of chromosome 15 to form the triplication&#46; The anomaly may also form as the result of a U-type exchange between 3 chromatids in a single step&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The large majority of chromosome 15 duplications &#40;dup&#91;15&#93;&#41; and SMC&#40;15&#41; containing the critical region for PWS&#47;AS are maternal in origin&#46; This fact implies that paternal-origin duplication is either uncommon and lethal&#44; meaning that the fetus would rarely be brought to term&#44; or else not capable of causing phenotypic effects&#44; meaning that the duplication would go undetected&#46; However&#44; we cannot rule out the possibility that apparent lack of a phenotype could be secondary to a position effect that would lead to the inactivation of the transcriptionally active gene or genes near the breakpoint in 15q&#46;<a class="elsevierStyleCrossRefs" href="#bib0050"><span class="elsevierStyleSup">10&#44;11</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">Modern basic and molecular cytogenetic techniques have allowed us to establish a correlation between the size of the duplicated fragment and the resulting phenotype&#46; Small duplications in regions that are very close to the centromere produce no effects&#44; whereas duplications affecting more extensive areas&#44; with breakpoints in q12 and q13&#44; give rise to intellectual impairment&#44; autism&#44; or seizures&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> In this particular case&#44; the affected region&#44; 15q11&#46;2&#44; includes genes that may potentially contribute to epilepsy&#44; such as genes encoding gamma-aminobutyric acid &#40;GABA&#41; receptor subunits&#46; GABA is known as the main inhibitory neurotransmitter in mammal brains&#59; however&#44; it also displays an excitatory effect in mature neurons of the hypothalamic suprachiasmatic nucleus&#46; This dual activity may be regulated by diurnal oscillations in intracellular chloride concentrations&#46; Therefore&#44; excessive duplication and expression of these neurotransmitter receptors may contribute to the induction of disease&#44; or the development of hyperactivity and aggressive behaviour&#44; as has been observed in adults with epilepsy and idic&#40;15&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0025"><span class="elsevierStyleSup">5&#44;11&#44;12</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Since physical examination of these patients reveals no dysmorphic features or minor anomalies in most cases&#44; chromosome analysis may never be carried out&#46; As a result&#44; the underlying chromosomal anomaly is not diagnosed in many such patients&#46; For that reason&#44; high-resolution karyotyping and molecular cytogenetic analysis are recommended for all patients with developmental delays&#44; epilepsy &#40;especially drug-resistant epilepsy&#41; and autism&#44; whether or not they present dysmorphic features&#44; in order to rule out chromosomal alterations&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">This case report was written for academic and pedagogical purposes in light of the low incidence rate of this disease &#40;1&#58;30<span class="elsevierStyleHsp" style=""></span>000 live births&#41; and the importance of the complementary study performed on this patient&#46; That study enabled doctors to assign a final diagnosis and thus offer appropriate genetic counselling to the patients&#8217; parents&#46;</p></span>"
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        "etiqueta" => "&#9734;"
        "nota" => "<p class="elsevierStyleNotepara">Please cite this article as&#58; Gordillo-Gonz&#225;lez G&#44; et al&#46; Paciente con s&#237;ndrome convulsivo y tetrasom&#237;a parcial del cromosoma 15&#46; Neurolog&#237;a&#46; 2013&#59;28&#58;191&#8211;3&#46;</p>"
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        "nota" => "<p class="elsevierStyleNotepara">This article was presented in poster format at the 11th Colombian Congress on Human Genetics&#44; Medell&#237;n&#44; October 2010&#46;</p>"
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          "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">&#40;A&#41; G-banding karyotype showing an extra chromosome derived from chromosome 15 &#40;arrow&#41;&#46; &#40;B&#41; Ideogram of the extra chromosome&#44; identifying breakpoints&#46;</p>"
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          "en" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">FISH image with centromeric probe specific to chromosome 15 and nuclei in metaphase&#46; Note the 2 green signals on the derived chromosome&#44; plus one in each centromere of the normal copies of chromosome 15&#46;</p>"
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Article information
ISSN: 21735808
Original language: English
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es en pt

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