Severe Combined Immunodeficiency in Serbia and Montenegro Between Years 1986 and 2010: A Single-Center Experience
Severe combined immunodeficiency (SCID), including the ‘variant’ Omenn syndrome (OS), represent a heterogeneous group of monogenic disorders characterized by defect in differentiation of T- and/or B lymphocytes and susceptibility to infections since birth. In the period of 25 years, between January...
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creator | Pasic, Srdjan Vujic, Dragana Veljković, Dobrila Slavkovic, Bojana Mostarica-Stojkovic, Marija Minic, Predrag Minic, Aleksandra Ristic, Goran Giliani, Silvia Villa, Anna Sobacchi, Cristina Lilić, Desa Abinun, Mario |
description | Severe combined immunodeficiency (SCID), including the ‘variant’ Omenn syndrome (OS), represent a heterogeneous group of monogenic disorders characterized by defect in differentiation of T- and/or B lymphocytes and susceptibility to infections since birth. In the period of 25 years, between January 1986 and December 2010, a total of 21 patients (15 SCID, 6 OS) were diagnosed in Mother & Child Health Institute of Serbia, a tertiary-care teaching University hospital and a national referral center for patients affected with primary immunodeficiency (PID). The diagnoses were based on anamnestic data, clinical findings, and immunological and genetic analysis. The median age at the onset of the first infection was the 2nd month of life. Seven (33 %) patients had positive family history for SCID. Out of five male infants with T-B+NK- SCID phenotype, mutation analysis revealed interleukin-2 (common) gamma-chain receptor (IL2RG) mutations in 3 with positive X-linked family history, and Janus-kinase (
JAK
)-3 gene defects in the other two. Six patients had T-B-NK+ SCID phenotype and further 6 features of OS, 11 of which had recombinase-activating gene (
RAG1
or
RAG2
) and 1 Artemis gene mutations. One child with T+B+NK+ SCID phenotype as well had proven RAG mutation. One child each with T-B+NK+ SCID phenotype, CD8 lymphopenia and unknown phenotype remained without known underlying genetic defect. Of the eight patients who underwent hematopoetic stem cell transplant (HSCT) 5 survived, the other 13 died between 2 days and 12 months after diagnosis was made. Early diagnosis of SCID, before onset of severe infections, offers possibility for HSCT and cure. Education of primary-care pediatricians, in particular including awareness of the risk of using live vaccines and non-irradiated blood products, should improve prognosis of SCID in our setting. |
doi_str_mv | 10.1007/s10875-014-9991-9 |
format | Article |
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JAK
)-3 gene defects in the other two. Six patients had T-B-NK+ SCID phenotype and further 6 features of OS, 11 of which had recombinase-activating gene (
RAG1
or
RAG2
) and 1 Artemis gene mutations. One child with T+B+NK+ SCID phenotype as well had proven RAG mutation. One child each with T-B+NK+ SCID phenotype, CD8 lymphopenia and unknown phenotype remained without known underlying genetic defect. Of the eight patients who underwent hematopoetic stem cell transplant (HSCT) 5 survived, the other 13 died between 2 days and 12 months after diagnosis was made. Early diagnosis of SCID, before onset of severe infections, offers possibility for HSCT and cure. Education of primary-care pediatricians, in particular including awareness of the risk of using live vaccines and non-irradiated blood products, should improve prognosis of SCID in our setting.</description><identifier>ISSN: 0271-9142</identifier><identifier>EISSN: 1573-2592</identifier><identifier>DOI: 10.1007/s10875-014-9991-9</identifier><identifier>PMID: 24481607</identifier><identifier>CODEN: JCIMDO</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Age of Onset ; Biomedical and Life Sciences ; Biomedicine ; Delayed Diagnosis ; Hematopoietic Stem Cell Transplantation ; Humans ; Immunology ; Infant ; Infant, Newborn ; Infectious Diseases ; Internal Medicine ; Medical Microbiology ; Montenegro - epidemiology ; Neonatal Screening ; Original Research ; Prenatal Diagnosis ; Retrospective Studies ; Serbia - epidemiology ; Severe Combined Immunodeficiency - diagnosis ; Severe Combined Immunodeficiency - epidemiology ; Severe Combined Immunodeficiency - therapy ; Treatment Outcome</subject><ispartof>Journal of clinical immunology, 2014-04, Vol.34 (3), p.304-308</ispartof><rights>Springer Science+Business Media New York 2014</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-5ddb8b620ac4665010020ba68edbabab47a923d84d08c4874d8dbe4b3ad0f68f3</citedby><cites>FETCH-LOGICAL-c471t-5ddb8b620ac4665010020ba68edbabab47a923d84d08c4874d8dbe4b3ad0f68f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10875-014-9991-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10875-014-9991-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24481607$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pasic, Srdjan</creatorcontrib><creatorcontrib>Vujic, Dragana</creatorcontrib><creatorcontrib>Veljković, Dobrila</creatorcontrib><creatorcontrib>Slavkovic, Bojana</creatorcontrib><creatorcontrib>Mostarica-Stojkovic, Marija</creatorcontrib><creatorcontrib>Minic, Predrag</creatorcontrib><creatorcontrib>Minic, Aleksandra</creatorcontrib><creatorcontrib>Ristic, Goran</creatorcontrib><creatorcontrib>Giliani, Silvia</creatorcontrib><creatorcontrib>Villa, Anna</creatorcontrib><creatorcontrib>Sobacchi, Cristina</creatorcontrib><creatorcontrib>Lilić, Desa</creatorcontrib><creatorcontrib>Abinun, Mario</creatorcontrib><title>Severe Combined Immunodeficiency in Serbia and Montenegro Between Years 1986 and 2010: A Single-Center Experience</title><title>Journal of clinical immunology</title><addtitle>J Clin Immunol</addtitle><addtitle>J Clin Immunol</addtitle><description>Severe combined immunodeficiency (SCID), including the ‘variant’ Omenn syndrome (OS), represent a heterogeneous group of monogenic disorders characterized by defect in differentiation of T- and/or B lymphocytes and susceptibility to infections since birth. In the period of 25 years, between January 1986 and December 2010, a total of 21 patients (15 SCID, 6 OS) were diagnosed in Mother & Child Health Institute of Serbia, a tertiary-care teaching University hospital and a national referral center for patients affected with primary immunodeficiency (PID). The diagnoses were based on anamnestic data, clinical findings, and immunological and genetic analysis. The median age at the onset of the first infection was the 2nd month of life. Seven (33 %) patients had positive family history for SCID. Out of five male infants with T-B+NK- SCID phenotype, mutation analysis revealed interleukin-2 (common) gamma-chain receptor (IL2RG) mutations in 3 with positive X-linked family history, and Janus-kinase (
JAK
)-3 gene defects in the other two. Six patients had T-B-NK+ SCID phenotype and further 6 features of OS, 11 of which had recombinase-activating gene (
RAG1
or
RAG2
) and 1 Artemis gene mutations. One child with T+B+NK+ SCID phenotype as well had proven RAG mutation. One child each with T-B+NK+ SCID phenotype, CD8 lymphopenia and unknown phenotype remained without known underlying genetic defect. Of the eight patients who underwent hematopoetic stem cell transplant (HSCT) 5 survived, the other 13 died between 2 days and 12 months after diagnosis was made. Early diagnosis of SCID, before onset of severe infections, offers possibility for HSCT and cure. Education of primary-care pediatricians, in particular including awareness of the risk of using live vaccines and non-irradiated blood products, should improve prognosis of SCID in our setting.</description><subject>Age of Onset</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Delayed Diagnosis</subject><subject>Hematopoietic Stem Cell Transplantation</subject><subject>Humans</subject><subject>Immunology</subject><subject>Infant</subject><subject>Infant, Newborn</subject><subject>Infectious Diseases</subject><subject>Internal Medicine</subject><subject>Medical Microbiology</subject><subject>Montenegro - epidemiology</subject><subject>Neonatal Screening</subject><subject>Original Research</subject><subject>Prenatal Diagnosis</subject><subject>Retrospective Studies</subject><subject>Serbia - epidemiology</subject><subject>Severe Combined Immunodeficiency - diagnosis</subject><subject>Severe Combined Immunodeficiency - epidemiology</subject><subject>Severe Combined Immunodeficiency - 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epidemiology</topic><topic>Neonatal Screening</topic><topic>Original Research</topic><topic>Prenatal Diagnosis</topic><topic>Retrospective Studies</topic><topic>Serbia - epidemiology</topic><topic>Severe Combined Immunodeficiency - diagnosis</topic><topic>Severe Combined Immunodeficiency - epidemiology</topic><topic>Severe Combined Immunodeficiency - therapy</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pasic, Srdjan</creatorcontrib><creatorcontrib>Vujic, Dragana</creatorcontrib><creatorcontrib>Veljković, Dobrila</creatorcontrib><creatorcontrib>Slavkovic, Bojana</creatorcontrib><creatorcontrib>Mostarica-Stojkovic, Marija</creatorcontrib><creatorcontrib>Minic, Predrag</creatorcontrib><creatorcontrib>Minic, Aleksandra</creatorcontrib><creatorcontrib>Ristic, Goran</creatorcontrib><creatorcontrib>Giliani, Silvia</creatorcontrib><creatorcontrib>Villa, Anna</creatorcontrib><creatorcontrib>Sobacchi, Cristina</creatorcontrib><creatorcontrib>Lilić, Desa</creatorcontrib><creatorcontrib>Abinun, Mario</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pasic, Srdjan</au><au>Vujic, Dragana</au><au>Veljković, Dobrila</au><au>Slavkovic, Bojana</au><au>Mostarica-Stojkovic, Marija</au><au>Minic, Predrag</au><au>Minic, Aleksandra</au><au>Ristic, Goran</au><au>Giliani, Silvia</au><au>Villa, Anna</au><au>Sobacchi, Cristina</au><au>Lilić, Desa</au><au>Abinun, Mario</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Severe Combined Immunodeficiency in Serbia and Montenegro Between Years 1986 and 2010: A Single-Center Experience</atitle><jtitle>Journal of clinical immunology</jtitle><stitle>J Clin Immunol</stitle><addtitle>J Clin Immunol</addtitle><date>2014-04-01</date><risdate>2014</risdate><volume>34</volume><issue>3</issue><spage>304</spage><epage>308</epage><pages>304-308</pages><issn>0271-9142</issn><eissn>1573-2592</eissn><coden>JCIMDO</coden><abstract>Severe combined immunodeficiency (SCID), including the ‘variant’ Omenn syndrome (OS), represent a heterogeneous group of monogenic disorders characterized by defect in differentiation of T- and/or B lymphocytes and susceptibility to infections since birth. In the period of 25 years, between January 1986 and December 2010, a total of 21 patients (15 SCID, 6 OS) were diagnosed in Mother & Child Health Institute of Serbia, a tertiary-care teaching University hospital and a national referral center for patients affected with primary immunodeficiency (PID). The diagnoses were based on anamnestic data, clinical findings, and immunological and genetic analysis. The median age at the onset of the first infection was the 2nd month of life. Seven (33 %) patients had positive family history for SCID. Out of five male infants with T-B+NK- SCID phenotype, mutation analysis revealed interleukin-2 (common) gamma-chain receptor (IL2RG) mutations in 3 with positive X-linked family history, and Janus-kinase (
JAK
)-3 gene defects in the other two. Six patients had T-B-NK+ SCID phenotype and further 6 features of OS, 11 of which had recombinase-activating gene (
RAG1
or
RAG2
) and 1 Artemis gene mutations. One child with T+B+NK+ SCID phenotype as well had proven RAG mutation. One child each with T-B+NK+ SCID phenotype, CD8 lymphopenia and unknown phenotype remained without known underlying genetic defect. Of the eight patients who underwent hematopoetic stem cell transplant (HSCT) 5 survived, the other 13 died between 2 days and 12 months after diagnosis was made. Early diagnosis of SCID, before onset of severe infections, offers possibility for HSCT and cure. Education of primary-care pediatricians, in particular including awareness of the risk of using live vaccines and non-irradiated blood products, should improve prognosis of SCID in our setting.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24481607</pmid><doi>10.1007/s10875-014-9991-9</doi><tpages>5</tpages></addata></record> |
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subjects | Age of Onset Biomedical and Life Sciences Biomedicine Delayed Diagnosis Hematopoietic Stem Cell Transplantation Humans Immunology Infant Infant, Newborn Infectious Diseases Internal Medicine Medical Microbiology Montenegro - epidemiology Neonatal Screening Original Research Prenatal Diagnosis Retrospective Studies Serbia - epidemiology Severe Combined Immunodeficiency - diagnosis Severe Combined Immunodeficiency - epidemiology Severe Combined Immunodeficiency - therapy Treatment Outcome |
title | Severe Combined Immunodeficiency in Serbia and Montenegro Between Years 1986 and 2010: A Single-Center Experience |
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