Low prevalence of patients with mitochondrial disease in the German/Austrian DPV diabetes registry

The aim of this study was to characterize the phenotype and treatment of young patients (manifestation

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Veröffentlicht in:European journal of pediatrics 2016-05, Vol.175 (5), p.613-622
Hauptverfasser: Reinauer, Christina, Meissner, Thomas, Roden, Michael, Thon, Angelika, Holterhus, Paul-Martin, Haberland, Holger, Binder, Elisabeth, Marg, Wolfgang, Bollow, Esther, Holl, Reinhard
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container_issue 5
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container_title European journal of pediatrics
container_volume 175
creator Reinauer, Christina
Meissner, Thomas
Roden, Michael
Thon, Angelika
Holterhus, Paul-Martin
Haberland, Holger
Binder, Elisabeth
Marg, Wolfgang
Bollow, Esther
Holl, Reinhard
description The aim of this study was to characterize the phenotype and treatment of young patients (manifestation
doi_str_mv 10.1007/s00431-015-2675-5
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Only 13 (0.02 %) of all patients with diabetes in this cohort were identified with DMO, mainly due to the Kearns-Sayre ( n  = 5), Pearson ( n  = 3), or mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome ( n  = 2). The onset of DMO (14.2, interquartile range (IQR) 7.1–16 years) was later than diabetes onset in individuals with T1D but earlier than in T2D. At manifestation, patients exhibited a mild elevation of blood glucose concentrations (251, IQR 178–299 mg/dl) without ketoacidosis. They had lower body mass index (BMI) values (−1.39 ± 0.28 kg/m 2 ) than peers with T1D or T2D ( p  &lt; 0.0001) and higher triglycerides (211, IQR 134–574 mg/dl) than in T1D ( p  = 0.04) while there was a high rate of dyslipidemia (86 %). Insulin requirements (0.58, IQR 0.37–0.90 U/kg/d) were between T1D and T2D while glucometabolic control (glycated hemoglobin A1c (HbA1c) 7.4 ± 0.52 %) in DMO was comparable to age-matched T2D and stable over a 5-year follow-up. Conclusion : Primary mitochondrial disorders are a rare cause of juvenile diabetes and likely to be underdiagnosed. As there is clinical overlap with T1D and T2D, dyslipidemia and low body weight may help to identify further DMO cases. What is Known: • In adults diabetes of mitochondrial origin (DMO) is a rare cause of non-autoimmune diabetes, affecting about 0.8 % of diabetes cases. • Common features are a maternal family history of diabetes, hearing loss and neurological abnormalities. What is New: • In our juvenile cohort 0.02 % of diabetes patients (age &lt; 30 years) were affected by DMO, while Kearns Sayre, MELAS and Pearson syndrome were the most frequent entities. • Juvenile DMO patients exhibited dyslipidemia, higher triglycerides and a lower BMI than peers with T1D or T2D, while some patients also showed retinal changes.</description><identifier>ISSN: 0340-6199</identifier><identifier>EISSN: 1432-1076</identifier><identifier>DOI: 10.1007/s00431-015-2675-5</identifier><identifier>PMID: 26670026</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Acidosis ; Adolescent ; Adult ; Age ; Austria - epidemiology ; Body mass index ; Child ; Child, Preschool ; Diabetes ; Diabetes Mellitus - epidemiology ; Diabetes Mellitus - etiology ; Disease ; Endocrinology ; Female ; Follow-Up Studies ; Genotype &amp; phenotype ; Germany - epidemiology ; Hospitals ; Humans ; Male ; Medicine ; Medicine &amp; Public Health ; Metabolic disorders ; Mitochondrial Diseases - complications ; Mitochondrial Diseases - epidemiology ; Mitochondrial DNA ; Mutation ; Neonatal care ; Original Article ; Pediatrics ; Prevalence ; Registries ; Retrospective Studies ; Teenagers ; Triglycerides ; Young Adult</subject><ispartof>European journal of pediatrics, 2016-05, Vol.175 (5), p.613-622</ispartof><rights>Springer-Verlag Berlin Heidelberg 2015</rights><rights>Springer-Verlag Berlin Heidelberg 2016</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-f8fa35e4494f31379a09dcbf59a424b92b0dd7b1545e10a517fede3089a8fd0d3</citedby><cites>FETCH-LOGICAL-c372t-f8fa35e4494f31379a09dcbf59a424b92b0dd7b1545e10a517fede3089a8fd0d3</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/s00431-015-2675-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00431-015-2675-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27922,27923,41486,42555,51317</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26670026$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reinauer, Christina</creatorcontrib><creatorcontrib>Meissner, Thomas</creatorcontrib><creatorcontrib>Roden, Michael</creatorcontrib><creatorcontrib>Thon, Angelika</creatorcontrib><creatorcontrib>Holterhus, Paul-Martin</creatorcontrib><creatorcontrib>Haberland, Holger</creatorcontrib><creatorcontrib>Binder, Elisabeth</creatorcontrib><creatorcontrib>Marg, Wolfgang</creatorcontrib><creatorcontrib>Bollow, Esther</creatorcontrib><creatorcontrib>Holl, Reinhard</creatorcontrib><title>Low prevalence of patients with mitochondrial disease in the German/Austrian DPV diabetes registry</title><title>European journal of pediatrics</title><addtitle>Eur J Pediatr</addtitle><addtitle>Eur J Pediatr</addtitle><description>The aim of this study was to characterize the phenotype and treatment of young patients (manifestation &lt;30 years) with diabetes of mitochondrial origin (DMO), based on the German/Austrian DPV (Diabetes Patienten Verlaufsdokumentation) registry. Only 13 (0.02 %) of all patients with diabetes in this cohort were identified with DMO, mainly due to the Kearns-Sayre ( n  = 5), Pearson ( n  = 3), or mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome ( n  = 2). The onset of DMO (14.2, interquartile range (IQR) 7.1–16 years) was later than diabetes onset in individuals with T1D but earlier than in T2D. At manifestation, patients exhibited a mild elevation of blood glucose concentrations (251, IQR 178–299 mg/dl) without ketoacidosis. They had lower body mass index (BMI) values (−1.39 ± 0.28 kg/m 2 ) than peers with T1D or T2D ( p  &lt; 0.0001) and higher triglycerides (211, IQR 134–574 mg/dl) than in T1D ( p  = 0.04) while there was a high rate of dyslipidemia (86 %). Insulin requirements (0.58, IQR 0.37–0.90 U/kg/d) were between T1D and T2D while glucometabolic control (glycated hemoglobin A1c (HbA1c) 7.4 ± 0.52 %) in DMO was comparable to age-matched T2D and stable over a 5-year follow-up. Conclusion : Primary mitochondrial disorders are a rare cause of juvenile diabetes and likely to be underdiagnosed. As there is clinical overlap with T1D and T2D, dyslipidemia and low body weight may help to identify further DMO cases. What is Known: • In adults diabetes of mitochondrial origin (DMO) is a rare cause of non-autoimmune diabetes, affecting about 0.8 % of diabetes cases. • Common features are a maternal family history of diabetes, hearing loss and neurological abnormalities. What is New: • In our juvenile cohort 0.02 % of diabetes patients (age &lt; 30 years) were affected by DMO, while Kearns Sayre, MELAS and Pearson syndrome were the most frequent entities. • Juvenile DMO patients exhibited dyslipidemia, higher triglycerides and a lower BMI than peers with T1D or T2D, while some patients also showed retinal changes.</description><subject>Acidosis</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Age</subject><subject>Austria - epidemiology</subject><subject>Body mass index</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Diabetes</subject><subject>Diabetes Mellitus - epidemiology</subject><subject>Diabetes Mellitus - etiology</subject><subject>Disease</subject><subject>Endocrinology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Genotype &amp; phenotype</subject><subject>Germany - epidemiology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Metabolic disorders</subject><subject>Mitochondrial Diseases - complications</subject><subject>Mitochondrial Diseases - epidemiology</subject><subject>Mitochondrial DNA</subject><subject>Mutation</subject><subject>Neonatal care</subject><subject>Original Article</subject><subject>Pediatrics</subject><subject>Prevalence</subject><subject>Registries</subject><subject>Retrospective Studies</subject><subject>Teenagers</subject><subject>Triglycerides</subject><subject>Young Adult</subject><issn>0340-6199</issn><issn>1432-1076</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kU9v1DAQxS0EokvhA3BBlrhwCR3_i-NjVaAgrUQPhavlxOOuq8RZ7ISq3x6vtiBUqaeRZn7vzWgeIW8ZfGQA-qwASMEaYKrhrVaNekY2TAreMNDtc7IBIaFpmTEn5FUpt1A1hnUvyQlvWw3A2w3pt_Md3Wf87UZMA9I50L1bIqal0Lu47OgUl3nYzcnn6EbqY0FXkMZElx3SS8yTS2fna1nqONFPVz8r4npcsNCMN7H271-TF8GNBd881FPy48vn64uvzfb75beL820zCM2XJnTBCYVSGhkEE9o4MH7ogzJOctkb3oP3umdKKmTgFNMBPQrojOuCBy9OyYej7z7Pv1Ysi51iGXAcXcJ5LZbpThimW9ZV9P0j9HZec6rXHSheMQFtpdiRGvJcSsZg9zlOLt9bBvYQgD0GYGsA9hCAVVXz7sF57Sf0_xR_P14BfgRKHaUbzP-tftL1D71VkKI</recordid><startdate>20160501</startdate><enddate>20160501</enddate><creator>Reinauer, Christina</creator><creator>Meissner, Thomas</creator><creator>Roden, Michael</creator><creator>Thon, Angelika</creator><creator>Holterhus, Paul-Martin</creator><creator>Haberland, Holger</creator><creator>Binder, Elisabeth</creator><creator>Marg, Wolfgang</creator><creator>Bollow, Esther</creator><creator>Holl, Reinhard</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20160501</creationdate><title>Low prevalence of patients with mitochondrial disease in the German/Austrian DPV diabetes registry</title><author>Reinauer, Christina ; 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Only 13 (0.02 %) of all patients with diabetes in this cohort were identified with DMO, mainly due to the Kearns-Sayre ( n  = 5), Pearson ( n  = 3), or mitochondrial myopathy, encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome ( n  = 2). The onset of DMO (14.2, interquartile range (IQR) 7.1–16 years) was later than diabetes onset in individuals with T1D but earlier than in T2D. At manifestation, patients exhibited a mild elevation of blood glucose concentrations (251, IQR 178–299 mg/dl) without ketoacidosis. They had lower body mass index (BMI) values (−1.39 ± 0.28 kg/m 2 ) than peers with T1D or T2D ( p  &lt; 0.0001) and higher triglycerides (211, IQR 134–574 mg/dl) than in T1D ( p  = 0.04) while there was a high rate of dyslipidemia (86 %). Insulin requirements (0.58, IQR 0.37–0.90 U/kg/d) were between T1D and T2D while glucometabolic control (glycated hemoglobin A1c (HbA1c) 7.4 ± 0.52 %) in DMO was comparable to age-matched T2D and stable over a 5-year follow-up. Conclusion : Primary mitochondrial disorders are a rare cause of juvenile diabetes and likely to be underdiagnosed. As there is clinical overlap with T1D and T2D, dyslipidemia and low body weight may help to identify further DMO cases. What is Known: • In adults diabetes of mitochondrial origin (DMO) is a rare cause of non-autoimmune diabetes, affecting about 0.8 % of diabetes cases. • Common features are a maternal family history of diabetes, hearing loss and neurological abnormalities. What is New: • In our juvenile cohort 0.02 % of diabetes patients (age &lt; 30 years) were affected by DMO, while Kearns Sayre, MELAS and Pearson syndrome were the most frequent entities. • Juvenile DMO patients exhibited dyslipidemia, higher triglycerides and a lower BMI than peers with T1D or T2D, while some patients also showed retinal changes.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>26670026</pmid><doi>10.1007/s00431-015-2675-5</doi><tpages>10</tpages></addata></record>
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subjects Acidosis
Adolescent
Adult
Age
Austria - epidemiology
Body mass index
Child
Child, Preschool
Diabetes
Diabetes Mellitus - epidemiology
Diabetes Mellitus - etiology
Disease
Endocrinology
Female
Follow-Up Studies
Genotype & phenotype
Germany - epidemiology
Hospitals
Humans
Male
Medicine
Medicine & Public Health
Metabolic disorders
Mitochondrial Diseases - complications
Mitochondrial Diseases - epidemiology
Mitochondrial DNA
Mutation
Neonatal care
Original Article
Pediatrics
Prevalence
Registries
Retrospective Studies
Teenagers
Triglycerides
Young Adult
title Low prevalence of patients with mitochondrial disease in the German/Austrian DPV diabetes registry
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