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  • 201. Coenen, Eva A
    et al.
    Raimondi, Susana C
    Harbott, Jochen
    Zimmermann, Martin
    Alonzo, Todd A
    Auvrignon, Anne
    Beverloo, H Berna
    Chang, Myron
    Creutzig, Ursula
    Dworzak, Michael N
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Gibson, Brenda
    Hasle, Henrik
    Harrison, Christine J
    Heerema, Nyla A
    Kaspers, Gertjan J L
    Leszl, Anna
    Litvinko, Nathalia
    Lo Nigro, Luca
    Morimoto, Akira
    Perot, Christine
    Reinhardt, Dirk
    Rubnitz, Jeffrey E
    Smith, Franklin O
    Stary, Jan
    Stasevich, Irina
    Strehl, Sabine
    Taga, Takashi
    Tomizawa, Daisuke
    Webb, David
    Zemanova, Zuzana
    Pieters, Rob
    Zwaan, C Michel
    van den Heuvel-Eibrink, Marry M
    Prognostic significance of additional cytogenetic aberrations in 733 de novo pediatric 11q23/MLL-rearranged AML patients: results of an international study2011Ingår i: Blood, ISSN 0006-4971, E-ISSN 1528-0020, Vol. 117, nr 26, s. 7102-7111Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    We previously demonstrated that outcome of pediatric 11q23/MLL-rearranged AML depends on the translocation partner (TP). In this multicenter international study on 733 children with 11q23/MLL-rearranged AML, we further analyzed which additional cytogenetic aberrations (ACA) had prognostic significance. ACAs occurred in 344 (47%) of 733 and were associated with unfavorable outcome (5-year overall survival [OS] 47% vs 62%, P < .001). Trisomy 8, the most frequent specific ACA (n = 130/344, 38%), independently predicted favorable outcome within the ACAs group (OS 61% vs 39%, P = .003; Cox model for OS hazard ratio (HR) 0.54, P = .03), on the basis of reduced relapse rate (26% vs 49%, P < .001). Trisomy 19 (n = 37/344, 11%) independently predicted poor prognosis in ACAs cases, which was partly caused by refractory disease (remission rate 74% vs 89%, P = .04; OS 24% vs 50%, P < .001; HR 1.77, P = .01). Structural ACAs had independent adverse prognostic value for event-free survival (HR 1.36, P = .01). Complex karyotype, defined as ≥ 3 abnormalities, was present in 26% (n = 192/733) and showed worse outcome than those without complex karyotype (OS 45% vs 59%, P = .003) in univariate analysis only. In conclusion, like TP, specific ACAs have independent prognostic significance in pediatric 11q23/MLL-rearranged AML, and the mechanism underlying these prognostic differences should be studied.

  • 202. Collett-Solberg, Paulo F.
    et al.
    Ambler, Geoffrey
    Backeljauw, Philippe F.
    Bidlingmaier, Martin
    Biller, Beverly M. K.
    Boguszewski, Margaret C. S.
    Cheung, Pik To
    Choong, Catherine Seut Yhoke
    Cohen, Laurie E.
    Cohen, Pinchas
    Dauber, Andrew
    Deal, Cheri L.
    Gong, Chunxiu
    Hasegawa, Yukihiro
    Hoffman, Andrew R.
    Hofman, Paul L.
    Horikawa, Reiko
    Jorge, Alexander A. L.
    Juul, Anders
    Kamenicky, Peter
    Khadilkar, Vaman
    Kopchick, John J.
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Lopes, Maria de Lurdes A.
    Luo, Xiaoping
    Miller, Bradley S.
    Misra, Madhusmita
    Netchine, Irene
    Radovick, Sally
    Ranke, Michael B.
    Rogol, Alan D.
    Rosenfeld, Ron G.
    Saenger, Paul
    Wit, Jan M.
    Woelfle, Joachim
    Diagnosis, Genetics, and Therapy of Short Stature in Children: A Growth Hormone Research Society International Perspective2019Ingår i: Hormone Research in Paediatrics, ISSN 1663-2818, E-ISSN 1663-2826, Vol. 92, nr 1, s. 1-14Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The Growth Hormone Research Society (GRS) convened a Workshop in March 2019 to evaluate the diagnosis and therapy of short stature in children. Forty-six international experts participated at the invitation of GRS including clinicians, basic scientists, and representatives from regulatory agencies and the pharmaceutical industry. Following plenary presentations addressing the current diagnosis and therapy of short stature in children, breakout groups discussed questions produced in advance by the planning committee and reconvened to share the group reports. A writing team assembled one document that was subsequently discussed and revised by participants. Participants from regulatory agencies and pharmaceutical companies were not part of the writing process. Short stature is the most common reason for referral to the pediatric endocrinologist. History, physical examination, and auxology remain the most important methods for understanding the reasons for the short stature. While some long-standing topics of controversy continue to generate debate, including in whom, and how, to perform and interpret growth hormone stimulation tests, new research areas are changing the clinical landscape, such as the genetics of short stature, selection of patients for genetic testing, and interpretation of genetic tests in the clinical setting. What dose of growth hormone to start, how to adjust the dose, and how to identify and manage a suboptimal response are still topics to debate. Additional areas that are expected to transform the growth field include the development of long-acting growth hormone preparations and other new therapeutics and diagnostics that may increase adult height or aid in the diagnosis of growth hormone deficiency.

  • 203. Cuneo, Bettina
    et al.
    Clur, Sally Ann
    Swan, Heikki
    Ackerman, Michael
    Herberg, Ulrike
    Etheridge, Susan
    Winbo, Annika
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Benson, D. Woodrow
    Schwartz, Peter
    Fetal heart rate and arrhythmia profile predicts long QT syndrome (LQTS) genotype: Results of an 8-center international study2018Ingår i: American Journal of Obstetrics and Gynecology, ISSN 0002-9378, E-ISSN 1097-6868, Vol. 218, nr 1, s. S93-S93Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Objective: 1. Determine if fetal heart rate (FHR) predicts LQTS across gestational ages (GA). 2. Ascertain genotype specific effects on FHR and rhythm.

    Study Design: FHR and rhythm data were ascertained from fetuses with maternal or paternal LQTS1, LQTS2 or LQTS3 genotype at 8 international centers. We reviewed obstetrical history including maternal beta blocker (BB) use. At each obstetrical visit, FHRs were calculated from an average of 3 heart beats (ultrasound) or 3 10-second periods of FHR auscultation (Doppler monitor) measured during fetal quiescence. Postnatal genetic testing was performed by commercial laboratories. We compared FHR in the 1st, 2nd and 3rd trimesters between fetuses with (LQTS+) and without (LQTS-) the family mutation by t-test. Differences in FHR between LQTS genotypes were compared by ANOVA. Log FHR was analyzed by a linear mixed effect model with GA as the continuous variable and adjusting for maternal BB use. The predictive ability of FHR to discriminate LQTS+ from LQTS- was addressed by ROC analysis, evaluating the magnitude of FHR (intercept) and change in FHR (slope) across GA.

    Results: Data were available on 51 LQTS+ and 27 LQTS-. Mean FHR differed between LQTS+ and LQTS- fetuses in 2nd and 3rd but not in the 1st trimesters (Table). The magnitude of FHR change in 2nd and 3rd trimesters discriminated LQTS + from LQTS- (both, p<0.05); with AUC of 0.81. FHR effect was most pronounced for LQTS1 and differed significantly between genotypes. LQTS3 did not exhibit a FHR effect at any GA. Only LQTS2 had signature LQTS arrhythmias (2◦ AV block and/or torsade de pointes). Maternal BB had no significant effect on FHR.

    Conclusion: In this study with a preponderance of LQTS1, FHR discriminated LQTS+ from LQTS- fetuses in the 2nd and 3rd trimesters. LQTS genotype appears to affect the fetal presentation of LQTS. These findings provide insight into the natural history of LQTS before birth and may facilitate early detection of LQTS1 and LQTS2 fetuses.

  • 204. Dahlgren, Jovanna
    et al.
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Niklasson, Aimon
    Nierop, Andreas F M
    Rosberg, Sten
    Albertsson-Wikland, Kerstin
    Models predicting the growth response to growth hormone treatment in short children independent of GH status, birth size and gestational age.2007Ingår i: BMC medical informatics and decision making, ISSN 1472-6947, Vol. 7, s. 40-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: Mathematical models can be used to predict individual growth responses to growth hormone (GH) therapy. The aim of this study was to construct and validate high-precision models to predict the growth response to GH treatment of short children, independent of their GH status, birth size and gestational age. As the GH doses are included, these models can be used to individualize treatment. METHODS: Growth data from 415 short prepubertal children were used to construct models for predicting the growth response during the first years of GH therapy. The performance of the models was validated with data from a separate cohort of 112 children using the same inclusion criteria. RESULTS: Using only auxological data, the model had a standard error of the residuals (SDres), of 0.23 SDS. The model was improved when endocrine data (GHmax profile, IGF-I and leptin) collected before starting GH treatment were included. Inclusion of these data resulted in a decrease of the SDres to 0.15 SDS (corresponding to 1.1 cm in a 3-year-old child and 1.6 cm in a 7-year old). Validation of these models with a separate cohort, showed similar SDres for both types of models. Preterm children were not included in the Model group, but predictions for this group were within the expected range. CONCLUSION: These prediction models can with high accuracy be used to identify short children who will benefit from GH treatment. They are clinically useful as they are constructed using data from short children with a broad range of GH secretory status, birth size and gestational age.

  • 205.
    Dahlquist, G
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Can we slow the rising incidence of childhood-onset autoimmune diabetes? The overload hypothesis.2006Ingår i: Diabetologia, ISSN 0012-186X, Vol. 49, nr 1, s. 20-4Artikel i tidskrift (Övrigt vetenskapligt)
    Abstract [en]

    Overload of the beta cell, mediated by a variety of mechanisms, may sensitise it to immune damage and apoptosis, and thus accelerate ongoing autoimmune processes leading to its destruction. Environmental risk determinants that may exert such overload effects include insulin resistance due to excess fat cell accumulation, and increased insulin requirement due to a high growth rate, physical stress (infection, inflammation) or psychological stress. The increasing incidence of childhood diabetes, and the shift to younger age at onset, is unlikely to be driven by environmental risk factors that have been associated with initiation of autoimmunity, e.g. virus infections or early infant feeding. Risk factors that may accelerate beta cell destruction have shown a steady increase in the population, and are more plausible causes of such a pattern of change. Child growth, weight and birthweight are well-established estimates of community wealth and increase in most countries of Europe. Overfeeding of children early in life leads to both accelerated growth and weight, and even a moderate excess of child growth, not necessarily associated with obesity, is associated with risk of type 1 diabetes. New, safe and effective immune-modulating drugs for possible arrest of the autoimmune process may become available in time, but in the interim these accelerating factors may be targeted. Public health programmes for pregnant mothers and young families, aiming at changing overfeeding and the sedentary lifestyle of the children would be preferable to other alternatives. Interventions such as these would be safe and could potentially influence future risks of type 1 and type 2 diabetes and other major threats to adult health.

  • 206.
    Dahlquist, G G
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Primary and secondary prevention strategies of pre-type 1 diabetes. Potentials and pitfalls.1999Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 22 Suppl 2, s. B4-6Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Over the past decade, a large part of type 1 diabetes research has focused on the possibility of preventing the disease. The objective of this article is to analyze which potential and pitfalls different preventive strategies may involve from the individual, epidemiological, and ethical perspectives. Two potential prevention strategies are considered: l) to try to arrest or delay an already ongoing immune destruction of the beta-cells, and 2) to try to intervene with exposures that may initiate this process. In addition to the potential effects of immune modulation, this prevention strategy depends on screening for risk markers. There are inherent ethical problems with screening because of the introduction of awareness of risk in healthy individuals and also because false positivity, the rate of which differs tremendously in high- and low-risk groups. Because of these latter circumstances, the most promising low-risk preventive treatments presently used in trials, i.e., nicotinamide and insulin, will probably only be feasible in high-risk groups, such as family members, though this group covers only 10-15% of potential cases. The second strategy aiming at eradicating environmental initiators of the beta-cell destruction will avoid the problem of screening and approach a total population at risk. Potential risk factors, such as food components (cow's milk proteins, gliadin or nitroso products) or different viruses, are indicated by animal and epidemiological studies. So far, however, no single environmental risk factor has been proven to be necessary and certainly not sufficient for the disease causation, and the etiological fractions estimated in population-based studies are low. It is concluded that more basic research is warranted before effective and safe prevention can be introduced for type 1 diabetes. Most probably, different preventive strategies must be applied to different groups and populations and in different phases of the beta-cell destruction.

  • 207.
    Dahlquist, G G
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Boman, J E
    Juto, P
    Enteroviral RNA and IgM antibodies in early pregnancy and risk for childhood-onset IDDM in offspring.1999Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 22, nr 2, s. 364-5Artikel i tidskrift (Refereegranskat)
  • 208.
    Dahlquist, G G
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Patterson, C
    Soltesz, G
    Perinatal risk factors for childhood type 1 diabetes in Europe. The EURODIAB Substudy 2 Study Group.1999Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 22, nr 10, s. 1698-702Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Different perinatal events are associated with an increased risk of type 1 diabetes. The effect of maternal-child blood group incompatibility is strong and indicates a true effect that must be further explored.

  • 209.
    Dahlquist, G G
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Pundziūte-Lyckå, A
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Nyström, L
    Birthweight and risk of type 1 diabetes in children and young adults: a population-based register study.2005Ingår i: Diabetologia, ISSN 0012-186X, Vol. 48, nr 6, s. 1114-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AIMS/HYPOTHESIS: We investigated the association between type 1 diabetes and birthweight by age at disease onset. METHODS: This population-based case-referent study used data from two nationwide case registers that are linked to the Swedish Medical Birth Registry and cover incident cases of type 1 diabetes in the 0- to 14-year (since 1 July 1977) and 15- to 34-year age groups (since 1 January 1983). Of the cases linked to the Medical Birth Registry, a total of 9,283 cases with onset before 15 years of age was recorded before 1 January 2003, and 1,610 cases were recorded with onset before 30 years of age and born after 1973 (together 95% of eligible cases). Multiple births and babies of diabetic mothers were excluded. Sex-specific birthweight by gestational week is expressed as multiples of the standard deviation (SDS) and adjusted for year of birth, maternal age and parity. RESULTS: Cases with onset before 10 years of age (n = 5,792) showed a significant linear trend in odds ratio (OR) by SDS of adjusted birthweight (OR by SDS: 0.062; 95% CI: 0.037-0.086; p < 0.0001), while cases with onset at the age of 10-29 years showed no significant trend (OR by SDS: 0.004; 95% CI: -0.007 to 0.0014; p = 0.22). CONCLUSIONS/INTERPRETATION: The association between type 1 diabetes risk and birthweight seems to be limited to cases with disease onset in younger years.

  • 210.
    Dahlquist, G
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Källén, B
    School marks for Swedish children whose mothers had diabetes during pregnancy: a population-based study.2007Ingår i: Diabetologia, ISSN 0012-186X, Vol. 50, nr 9, s. 1826-31Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AIMS/HYPOTHESIS: To study, at a population level, school performance when leaving compulsory school of Swedish children whose mothers had diabetes during pregnancy compared with a reference population. METHODS: We linked the Swedish Medical Birth Register with the Swedish School Mark Register, which contains school marks for all children in Sweden when leaving compulsory school. A total of 6,397 children were identified whose mothers had a diagnosis of diabetes during pregnancy in the years 1973 to 1986. Data on these children were compared with 1,300,683 children whose mothers had no diagnosis of diabetes during pregnancy. Risks were estimated as odd ratios (ORs) after adjustment for year of birth, maternal age, parity and educational level of the mother. RESULTS: The children's average numerical school marks (for children leaving school between 1988 and 1997) were statistically significantly lower among children born to mothers with diabetes in pregnancy compared with reference children (3.13 +/- 0.01 vs 3.23, p < 0.001). The effect was similar among boys and girls. There was also an effect of maternal diabetes during pregnancy on the risk of the child not completing compulsory school (OR 1.25; 95% CI 1.10-1.43, and after exclusion of infants with certain perinatal characteristics an OR of 1.25; 95% CI 1.02-1.53). When sports and the core subjects mathematics, English and Swedish were studied, there were increased risks of having scores below pass level and decreased probabilities of having scores above pass level for children of mothers with diabetes during pregnancy. CONCLUSIONS/INTERPRETATION: Children of mothers with diabetes during pregnancy performed slightly but significantly less well than reference children when leaving compulsory school at about 16 years old; this was also seen after adjustment for some putative perinatal and social confounders.

  • 211.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    [A high standard of living can contribute to the increase of childhood diabetes. Rapid growth and weight gain are risk factors].2002Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 99, nr 10, s. 1046-50Artikel i tidskrift (Refereegranskat)
    Abstract [sv]

    According to records kept by The Swedish Child Diabetes Register the incidence of childhood diabetes type I before 15 years of age has increased. The increase is most noticeable in children before the age of 5. The genetic basis of this disease is complex and the different risk genes have a low penetrance, thus indicating non-genetic factors to have a great impact. One risk factor for type I diabetes is rapid growth, measured either as weight or as height gain. As a high standard of living favours rapid growth in children this may contribute to the onset of the disease.

  • 212.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    [Acceleration of diabetes among children in Europe]2008Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 105, nr 26-27, s. 1917-Artikel i tidskrift (Refereegranskat)
  • 213.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Celiac disease and insulin-dependent diabetes mellitus - no proof for a causal association1995Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 84, nr 12, s. 1337-1338Artikel i tidskrift (Refereegranskat)
  • 214.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    [Cloning of children--a step toward anti-humanism and racial hygiene].2003Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 100, nr 6, s. 442-4Artikel i tidskrift (Refereegranskat)
  • 215.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    [Fetal virus infection a risk factor of diabetes mellitus type 1 in children].2000Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 97, nr 4, s. 313-5Artikel i tidskrift (Refereegranskat)
    Abstract [sv]

    The incidence of type-1 diabetes mellitus is high and increasing in Sweden. The etiology of IDDM is complex: several genes appear to interact with each other and with various nongenetic risk factors to induce and complete the autoimmune destruction of beta-cells. IDDM has its onset most often in childhood, and during the past decade incidence is increasing specifically among children under the age of five. Factors initiating the process should thus be sought in early life. A number of recent studies have identified perinatal events as risk determinants; among these, fetal viral infections may be causally related to the disease and may become targets for intervention and prevention.

  • 216.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Hippokrates i vår tid2011Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 108, nr 47, s. 2438-2440Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Hippocrates, the controversial but outstanding innovator both of our views on clinical medicine and of our role as doctors is an important idol also in our time. The interests of the weakest groups must be defended in medical research as well as in clinical medicine and ethics must have a self- evident place in everyday patient care as well as in education and research. We as doctors must keep up the debate between us but also with the stake holders to communicate insights about the needs of the weakest. We must help others to see those who cannot themselves maintain their rights to equality in health care in our dynamic time.

  • 217.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Obesity consultation for children and adolescents. Be realistic about childhood obesity. Interview by Kerstin Danielsson1991Ingår i: Nordisk Medicin, ISSN 0029-1420, Vol. 106, nr 6-7, s. 194-195Artikel i tidskrift (Refereegranskat)
  • 218.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    [Pediatric research is necessary. The children must be guaranteed with a complete protection]2004Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 101, nr 26-27, s. 2238-9Artikel i tidskrift (Refereegranskat)
  • 219.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Potentials and pitfalls in neonatal screening for type 1 diabetes.1999Ingår i: Acta Paediatrica. Supplement, ISSN 0803-5326, Vol. 88, nr 432, s. 80-2Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Childhood-onset diabetes is increasing all over the western world. Only 20-30% of monozygotic twin pairs are concordant for the disease. So far, more than 20 different risk genes have been identified on different chromosomes. The dominating risk genes differ with different age at onset and also in different populations. Thus, the aetiology of the disease is complex, with interactions between different risk genes and environmental risk factors. Several pathogenetic models have been proposed, most of which include autoimmune destruction mechanisms. Screening for genetic markers for diseases with such complex aetiology encounters pitfalls due to the low predictive value of each single marker in the general population. To overcome such problems combinations of markers and decision-tree analysis are necessary. The identification of several immune markers for the disease has provided potential for screening for secondary prevention. When increasing the number of markers to increase the predictive value, sensitivity will be lost. A Swedish population-based study found the best combined positive predictive value in the general population to be 20%, whereas the sensitivity was only 34%. Type 1 diabetes still needs more precise risk markers in addition to a very safe prevention strategy before neonatal screening programmes may be instituted.

  • 220.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    The aetiology of type 1 diabetes: an epidemiological perspective.1998Ingår i: Acta Paediatrica. Supplement, ISSN 0803-5326, Vol. 425, s. 5-10Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Type 1 diabetes is increasing rapidly in many parts of the Western world, most evidently in Scandinavia. A low concordance rate of insulin-dependent diabetes mellitus among monozygotic twins clearly indicates that genetic risk factors may be necessary, but are not sufficient for the disease to occur. The strongest genetic risk markers are located in the HLA region of chromosome 6, but these DNA specificities differ in different populations. Risk genes are indicated in other chromosomes of the human genome, suggesting a complex interaction between genes and environment as the cause of the disease. The pathogenesis of the disease is proposed to be autoimmune in nature and environmental risk factors may either initiate autoimmunity or accelerate an already ongoing beta-cell destruction. Risk factors disclosed by epidemiological studies that may accelerate the pathogenetic process are: a cold environment, a high growth rate, infections and stressful life events. Risk factors that may initiate the autoimmune process include early exposure to cow's milk proteins, nitrosamines or early foetal events such as blood group incompatibility or foetal viral infections. In conclusion, population-based epidemiological studies have helped to confirm proposed aetiological models that have arisen from experimental research. These epidemiological studies have also introduced important new findings that may reveal the complex aetiology of the disease and advance understanding closer to the ultimate goal of primary prevention.

  • 221.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Utvärdering av processekonomi ger otillräckligt underlag för vårdpolitiska beslut1995Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 92, nr 21, s. 2211-Artikel i tidskrift (Refereegranskat)
  • 222.
    Dahlquist, Gisela
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Vem ska besluta om avslutande av livshuppehållande behandling av barn?2009Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 106, nr 14, s. 985-Artikel i tidskrift (Refereegranskat)
    Abstract [sv]

    Att ge upp professionens ansvar för att sträva efter objektiva beslut just i livets slutskede och lämna denna del av vården till föräldrar och anhöriga vore en katastrofal utveckling, etiskt och humanitärt. Viktigare än ytterligare riktlinjer från Socialstyrelsen vore att skapa resurser för forskning inom detta område.

  • 223.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Bergström, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Gebre-Medhin, M
    Häger, A
    Kihlstedt-Odeen, A C
    Marcus, C
    [What can we do for overweight children and adolescents? The prognosis is mostly good; attitudes often dubious].1995Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 92, nr 34, s. 3022-5Artikel i tidskrift (Refereegranskat)
  • 224.
    Dahlquist, Gisela G
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Forsberg, Jenny
    Hagenfeldt, Lars
    Boman, Jens
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Juto, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi, Virologi.
    Increased prevalence of enteroviral RNA in blood spots from newborn children who later developed type 1 diabetes: a population-based case-control study.2004Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 27, nr 1, s. 285-6Artikel i tidskrift (Refereegranskat)
  • 225.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Gothefors, Leif
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    The cumulative incidence of childhood diabetes mellitus in Sweden unaffected by BCG-vaccination.1995Ingår i: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 38, nr 7, s. 873-4Artikel i tidskrift (Refereegranskat)
  • 226.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Janson, Staffan
    Barn och ungdomar: sårbara »osynliga« anhöriga2013Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, nr 45, s. 2003-Artikel i tidskrift (Övrig (populärvetenskap, debatt, mm))
  • 227.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Janson, Staffan
    Örebro universitet.
    Kräv vetenskaplig evidens för surrogatmoderskap2013Ingår i: Läkartidningen, ISSN 0023-7205, E-ISSN 1652-7518, Vol. 110, nr 25-26, s. 1200-1201Artikel i tidskrift (Övrig (populärvetenskap, debatt, mm))
  • 228.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Kallen, Bengt
    Indications that phototherapy is a risk factor for insulin-dependent diabetes.2003Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 26, nr 1, s. 247-8Artikel i tidskrift (Refereegranskat)
  • 229.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Källén, B
    Early neonatal events and the disease incidence in nonobese diabetic mice.1997Ingår i: Pediatric Research, ISSN 0031-3998, E-ISSN 1530-0447, Vol. 42, nr 4, s. 489-91Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Epidemiologic studies have shown that perinatal events are associated with an increased risk for type 1 (insulin-dependent) diabetes in childhood. We used nonobese diabetic mice to examine whether neonatal separation from the mother with or without phototherapy would affect the incidence of diabetes in this genetically susceptible mouse model. The newborn pups were taken from their mothers for two 4-h periods during each of five successive days. One group of animals was just taken from their mothers and were left lying in daylight in the cage, whereas another group was exposed to identical light as used for treatment of neonatal jaundice in infants. Treatment resulted in a 30% death rate. For animals surviving more than 3 mo the incidence of diabetes was significantly higher in both treatment groups compared with control animals, allowed to stay with their mother. The odds ratio for treatment versus control, stratifying for sex, was 3.42 (95% confidence interval, 1.57-7.74). Histologic insulitis did not differ between treated and untreated animals when examined either at clinical diabetes onset or at 8 mo of age. Blood glucose values at 8 mo of age (in animals without clinical diabetes) did not differ between-treated and untreated animals. It is concluded that neonatal separation of the nonobese diabetic mice from their mothers will lead to a significantly increased risk for diabetes. This increase in risk seems to be associated with the induction of metabolic alterations leading to increased peripheral insulin need rather than with an increased rate of beta cell destruction.

  • 230.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Källén, B
    School performance in children with type 1 diabetes: a population-based register study2007Ingår i: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 50, nr 5, s. 957-964Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AIMS/HYPOTHESIS: We examined the school marks of diabetic children in Sweden at the time of leaving compulsory education. Marks were examined in comparison with non-diabetic children and with special regard to age at onset of diabetes.

    SUBJECTS AND METHODS: The study involved 5,159 children who developed diabetes between 1 July 1977 and 1 July 2000, and 1,330,968 non-diabetic children. We linked the nationwide Swedish Childhood Diabetes Register to the Swedish School-Mark Register, which contains school marks for all children in Sweden at the time of leaving compulsory education (usually at 16 years old). Adjustment was made for potential confounders such as year of birth, maternal age, parity and educational level.

    RESULTS: The mean of all numerical school marks for diabetic children was slightly but statistically significantly lower than those of the referent children (3.15 +/- 0.01 [mean + SD] vs 3.23, p < 0.001). The lowest mean score was among children with diabetes diagnosis before the age of 2 years (2.97 +/- 0.09 vs 3.08-3.17 in the older age groups, p = 0.10). When individual subjects were studied (sports, mathematics, English and Swedish), a more complex picture emerged. In four subjects (mathematics, English, Swedish and sports) the risk of a diabetic child not getting a school mark or not passing was increased; in sports and English the diabetic children had significantly reduced odds of getting a high mark.

    CONCLUSIONS/INTERPRETATION: Despite a well-developed diabetes care system, we have not succeeded in preventing the disease from affecting school achievements. Among children with a young age at onset and therefore longer duration, the negative effects tend to be greater.

  • 231.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Källén, Bengt
    Mortality in childhood-onset type 1 diabetes: a population-based study.2005Ingår i: Diabetes Care, ISSN 0149-5992, Vol. 28, nr 10, s. 2384-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: To describe the age- and sex-specific mortality in a cohort of young type 1 diabetic patients and to analyze the causes of death with special focus on suicide, accidents, and unexplained deaths. RESEARCH DESIGN AND METHODS: A population-based incident childhood diabetes register, covering onset cases since 1 July 1977, was linked to the Swedish Cause of Death Register up to 31 December 2000. The official Swedish population register was used to calculate age- and sex-standardized mortality rates (SMRs), excluding neonatal deaths. To analyze excess risks for specific diagnoses, case subjects were compared with five nondiabetic control subjects, matched by age, sex, and year of death. Death certificates were collected for all case and control subjects. For case subjects with an unclear diagnosis, hospital records and/or forensic autopsy reports were obtained. RESULTS: Mean age- and sex-SMR was 2.15 (95% CI 1.70-2.68) and tended to be higher among females (2.65 vs. 1.93, P = 0.045). Mean age at death was 15.2 years (range 1.2-27.3) and mean duration 8.2 years (0-20.7). Twenty-three deaths were clearly related to diabetes; 20 died of diabetic ketoacidosis. Only two case subjects died with late diabetes complications (acute coronary infarction). Thirty-three case subjects died with a diagnosis not directly related to diabetes; 7 of them committed suicide, and 14 died from accidents. There was no significant difference in traffic accidents (odds ratio 1.02 [95% CI 0.40-2.37]). Obvious suicide tended to be increased but not statistically significantly so (1.55 [0.54-3.89]). Seventeen diabetic case subjects were found deceased in bed without any cause of death found at forensic autopsy. Only two of the control subjects died of similar unexplained deaths. CONCLUSIONS: In a well-developed health care system, there is still a significant excess mortality in young type 1 diabetic patients. We confirm a very large proportion of unexplained deaths in bed, which should be further studied. There is no clear excess death rate caused by suicide or traffic accidents among young diabetic subjects.

  • 232.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Mustonen, L
    Analysis of 20 years of prospective registration of childhood onset diabetes time trends and birth cohort effects. Swedish Childhood Diabetes Study Group.2000Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 89, nr 10, s. 1231-7Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The Swedish Childhood Diabetes Registry has been recording all cases of childhood onset diabetes nationwide, with a high level of ascertainment, since 1 July 1977. The present report describes and analyses the 8358 childhood onset cases occurring between 1 January 1978 and 31 December 1997. The mean annual incidence was 26.4/100,000 children per year (1978: 21.1 and 1997: 31.9). There was a significant log-linear increase over time, with a mean annual increase of 1.7%. The steepest mean increase was seen among the young onset cases (2.5%) and the steepest yearly increase (6.3%) was seen in this age group during the last 10-y period. A shift towards a younger age at onset was clearly indicated, as the age at onset was less during the last compared with the first 10-y period of observation. The increase over time was similar between the sexes and during winter and summer. When analysing the six full birth cohorts covered, we found no clear-cut shift in the trend. Birth cohorts (1978-82) up to 5 y of onset showed a time variability but no clear trend over time. Ecological analyses associating cumulative incidence by birth cohort to breastfeeding frequency showed no significant association. A statistically significant log-linear association was found to the official estimate of gross domestic product adjusted for similar price levels (p = 0.002). CONCLUSION: The incidence of childhood onset diabetes is rapidly increasing in Sweden, with a shift towards the younger age groups but with no trend in birth cohorts. Precipitating rather than initiating environmental risk factors are suggested, and the correlation to gross domestic product may suggest risk factors associated with wealth-such as a high growth rate, a known risk factor for childhood diabetes.

  • 233.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Möllsten, Anna
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Källén, B
    Hospitalization for vascular complications in childhood onset type 1 diabetes--effects of gender and age at onset.2008Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 97, nr 4, s. 483-8Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    AIMS: To study the cumulative incidence of hospitalization for severe diabetic vascular complications in childhood onset type 1 diabetes patients with special regards to age at onset and gender. METHODS: The Swedish Childhood Diabetes Register (SCDR) was linked to the Swedish Hospital Discharge Register up to 31 December 2004. The following diagnoses were traced: diabetic kidney disease, myocardial infarction, stroke, lower limb arterial disease and diabetes with multiple complications. Cox proportional hazards survival method was applied with the following covariates: maternal age, birthweight deviation from gestational week standard, age at onset and gender. RESULTS: Until 31 December 9974 children had been followed for at least 10 years corresponding to 141 839 person years at risk and 103 (7.3 per 1000 person years) had been hospitalized at least once at the maximum duration of follow-up of 26 years. Diabetic kidney disease was the most common cause of hospitalization and 63 patients had more than one diabetic complication. Female gender (RR=2.02, 95% CI=1.05-3.89) and age at onset of diabetes (RR=1.37, 95% CI=1.20-1.56) were significant risk factors for severe complication. CONCLUSIONS: Hospitalization for severe diabetic complications at a maximum follow-up of 26 years is rather low in Sweden. There is a higher hospitalization rate among females than among males, and also among patients diagnosed with diabetes after 10 years of age than among patients diagnosed before the age of 10 years.

  • 234.
    Dahlquist, Gisela
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Nyström, Lennarth
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och global hälsa.
    Patterson, Christopher C.
    Centre for Public Health, Queen’s University, Belfast, Northern Ireland .
    Incidence of Type 1 Diabetes in Sweden Among Individuals Aged 0-34 Years, 1983-2007: An analysis of time trends2011Ingår i: Diabetes Care, ISSN 0149-5992, E-ISSN 1935-5548, Vol. 34, nr 8, s. 1754-1759Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Objective: To clarify whether the increase in childhood type 1 diabetes is mirrored by a decrease in older age-groups, resulting in younger age at diagnosis.

    Research design and methods: We used data from two prospective research registers, the Swedish Childhood Diabetes Register, which included case subjects aged 0–14.9 years at diagnosis, and the Diabetes in Sweden Study, which included case subjects aged 15–34.9 years at diagnosis, covering birth cohorts between 1948 and 2007. The total database included 20,249 individuals with diabetes diagnosed between 1983 and 2007. Incidence rates over time were analyzed using Poisson regression models.

    Results: The overall yearly incidence rose to a peak of 42.3 per 100,000 person-years in male subjects aged 10–14 years and to a peak of 37.1 per 100,000 person-years in female subjects aged 5–9 years and decreased thereafter. There was a significant increase by calendar year in both sexes in the three age-groups <15 years; however, there were significant decreases in the older age-groups (25- to 29-years and 30- to 34-years age-groups). Poisson regression analyses showed that a cohort effect seemed to dominate over a time-period effect.

    Conclusions: Twenty-five years of prospective nationwide incidence registration demonstrates a clear shift to younger age at onset rather than a uniform increase in incidence rates across all age-groups. The dominance of cohort effects over period effects suggests that exposures affecting young children may be responsible for the increasing incidence in the younger age-groups.

     

  • 235. Dalin, Frida
    et al.
    Nordling Eriksson, Gabriel
    Dahlqvist, Per
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Medicin.
    Hallgren, Åsa
    Wahlberg, Jeanette
    Ekwall, Olov
    Söderberg, Stefan
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Kardiologi.
    Rönnelid, Johan
    Olcén, Per
    Winqvist, Ola
    Catrina, Sergiu-Bogdan
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Laudius, Maria
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Avdelningen för medicin.
    Isaksson, Magnus
    Halldin Stenlid, Maria
    Gustafsson, Jan
    Gebre-Medhin, Gennet
    Björnsdottir, Sigridur
    Janson, Annika
    Åkerman, Anna-Karin
    Åman, Jan
    Duchen, Karel
    Bergthorsdottir, Ragnhildur
    Johannsson, Gudmundur
    Lindskog, Emma
    Landin-Olsson, Mona
    Elfving, Maria
    Waldenström, Erik
    Hulting, Anna-Lena
    Kämpe, Olle
    Bensing, Sophie
    Clinical and immunological characteristics of Autoimmune Addison's disease: a nationwide Swedish multicenter study2017Ingår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 102, nr 2, s. 379-389Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    CONTEXT: Studies on clinical and immunological features of Autoimmune Addison's disease (AAD) are needed to understand the disease burden and increased mortality.

    OBJECTIVE: To provide upgraded data on autoimmune comorbidities, replacement therapy, autoantibody profiles and cardiovascular risk factors.

    DESIGN, SETTING AND PARTICIPANTS: Cross sectional, population-based study. 660 AAD patients were included utilizing the Swedish Addison Registry (SAR) 2008-2014. When analyzing cardiovascular risk factors, 3,594 individuals from the population-based survey in Northern Sweden, MONICA (MONItoring of Trends and Determinants of CArdiovascular Disease), served as controls.

    MAIN OUTCOME MEASURE: Prevalence of autoimmune comorbidities and cardiovascular risk factors. Autoantibodies against 13 autoantigens were determined.

    RESULTS: Sixty percent of the SAR cohort consisted of females. Mean age at diagnosis was significantly higher for females than for males (36.8 vs. 31.1 years). The proportion of 21-hydroxylase autoantibody positive patients was 83% and 62% of patients had one or more associated autoimmune diseases, more frequently coexisting in females (p<0.0001). AAD patients had lower BMI (p<0.0001) and prevalence of hypertension (p=0.027) compared with controls. Conventional hydrocortisone tablets were used by 89% of patients; with the mean dose 28.1±8.5 mg/day. The mean hydrocortisone equivalent dose normalized to body surface was 14.8±4.4 mg/m(2)/day. Higher hydrocortisone equivalent dose was associated with higher incidence of hypertension (p=0.046).

    CONCLUSIONS: Careful monitoring of AAD patients is warranted to detect associated autoimmune diseases. Contemporary Swedish AAD patients do not have increased prevalence of overweight, hypertension, T2DM or hyperlipidemia. However, high glucocorticoid replacement doses may be a risk factor for hypertension.

  • 236. Danielsson, L
    et al.
    Stenhammar, L
    Ascher, H
    Cavell, B
    Dannaeus, A
    Hernell, Olle
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Ivarsson, Anneli
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och folkhälsovetenskap.
    Lindberg, T
    Lindquist, B
    [Gluten intolerance in children--diagnostic routines in Sweden 1996. Great variations in celiac disease studies]1997Ingår i: Lakartidningen, ISSN 0023-7205, Vol. 94, nr 37, s. 3165-8Artikel i tidskrift (Övrigt vetenskapligt)
  • 237. Danielsson, L
    et al.
    Stenhammar, L
    Ascher, H
    Cavell, B
    Dannaeus, A
    Hernell, Olle
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Ivarsson, Anneli
    Umeå universitet, Medicinska fakulteten, Institutionen för folkhälsa och klinisk medicin, Epidemiologi och folkhälsovetenskap.
    Lindberg, T
    Lindquist, B
    [Proposed criteria for diagnosis of celiac disease in children]1998Ingår i: Lakartidningen, ISSN 0023-7205, Vol. 95, nr 20, s. 2342-3Artikel i tidskrift (Övrigt vetenskapligt)
  • 238.
    Danielsson Niemi, Liza
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för odontologi, Kariologi.
    Hernell, Olle
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Johansson, Ingegerd
    Umeå universitet, Medicinska fakulteten, Institutionen för odontologi, Kariologi.
    Human milk compounds inhibiting adhesion of mutans streptococci to host ligand-coated hydroxyapatite in vitro2009Ingår i: Caries Research, ISSN 0008-6568, E-ISSN 1421-976X, Vol. 43, nr 3, s. 171-178Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Acquisition of mutans streptococci at an early age is a risk factor for later caries development. Following our recent finding that human milk may inhibit adhesion of Streptococcus mutans the aim of the present study was to identify compounds in human milk preventing adhesion of mutans streptococci to saliva- or gp340-coated hydroxyapatite (s-HA and gp340-HA) using an in vitro model system. Superdex 200 fractions of human milk and purified proteins were screened for binding inhibition of the S. mutans strain Ingbritt. Avid inhibition was seen to both s-HA and gp340-HA for caseins, lactoferrin, IgA and IgG, and moderate inhibition for alpha-lactalbumin and bile salt-stimulated lipase, whereas albumin and lysozyme had no effect. The inhibitory epitope in beta-casein was delineated to its C-terminal LLNQELLNPTHQIYPVTQPLAPVHNPISV stretch by use of synthetic peptides. Similarly, a peptide (SCKFDEYFSQSCA) corresponding to the human lactoferrin stretch that is highly homologous to the previously shown inhibitory stretch of bovine lactoferrin was found to inhibit S. mutans Ingbritt binding. Inhibition by human milk, IgA, and the inhibitory beta-casein peptide was universal among 4 strains of S. mutans (Ingbritt, NG8, LT11, JBP) and 2 strains of S. sobrinus (6715 and OMZ176). IgG inhibited 4, alpha-lactalbumin 3 and lactoferrin 2 of these 6 strains. It was also confirmed that none of the milk components coated on HA mediated S. mutans Ingbritt adhesion, which was consistent with the finding that no milk protein was recognized on Western blots by gp340/DMBT1 monoclonal antibodies.

  • 239. Davidsson, J
    et al.
    Paulsson, K
    Lindgren, D
    Lilljebjörn, H
    Chaplin, T
    Forestier, Erik
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Andersen, M K
    Nordgren, A
    Rosenquist, R
    Fioretos, T
    Young, B D
    Johansson, B
    Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations.2010Ingår i: Leukemia, ISSN 0887-6924, E-ISSN 1476-5551, Vol. 24, nr 5, s. 924-31Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Although childhood high hyperdiploid acute lymphoblastic leukemia is associated with a favorable outcome, 20% of patients still relapse. It is important to identify these patients already at diagnosis to ensure proper risk stratification. We have investigated 11 paired diagnostic and relapse samples with single nucleotide polymorphism array and mutation analyses of FLT3, KRAS, NRAS and PTPN11 in order to identify changes associated with relapse and to ascertain the genetic evolution patterns. Structural changes, mainly cryptic hemizygous deletions, were significantly more common at relapse (P<0.05). No single aberration was linked to relapse, but four deletions, involving IKZF1, PAX5, CDKN2A/B or AK3, were recurrent. On the basis of the genetic relationship between the paired samples, three groups were delineated: (1) identical genetic changes at diagnosis and relapse (2 of 11 cases), (2) clonal evolution with all changes at diagnosis being present at relapse (2 of 11) and (3) clonal evolution with some changes conserved, lost or gained (7 of 11), suggesting the presence of a preleukemic clone. This ancestral clone was characterized by numerical changes only, with structural changes and RTK-RAS mutations being secondary to the high hyperdiploid pattern.

  • 240. Davies, E H
    et al.
    Erikson, A
    Umeå universitet, Medicinsk fakultet, Klinisk vetenskap, Pediatrik.
    Collin-Histed, T
    Mengel, E
    Tylki-Szymanska, A
    Vellodi, A
    Outcome of type III Gaucher disease on enzyme replacement therapy: review of 55 cases.2007Ingår i: J Inherit Metab Dis, ISSN 1573-2665, Vol. 30, nr 6, s. 935-42Artikel i tidskrift (Övrigt vetenskapligt)
  • 241.
    de Chateau, Peter
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Neonatal care routines: influences on maternal and infant behaviour and on breast feeding1976Doktorsavhandling, sammanläggning (Övrigt vetenskapligt)
  • 242. de Chateau, Peter
    et al.
    Andersson, Yvonne
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Left-side preference for holding and carrying newborn infants. II:Doll holding and carrying from 2 to 16 years.1976Ingår i: Developmental Medicine & Child Neurology, ISSN 0012-1622, E-ISSN 1469-8749, Vol. 18, s. 738-44Artikel i tidskrift (Refereegranskat)
  • 243.
    De Chateau, Peter
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Wiberg, Britt
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Long-term effect on mother-infant behaviour of extra contact during the first hour post partum: I. First observations at 36 hours1977Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 66, nr 2, s. 137-143Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Abstract The immediate post partum period may be particularly important for the developing relationship between mother and infant; little is as yet known, however, of the long-term effects of hospital practice during this period. This study examines the effect of extra contact during the first hour following delivery. An extra skin to skin contact and suckling contact was given to 22 primiparous mothers and their infants. One control group of 20 primiparous mothers and infants and a second one of 20 multiparous mothers and infants was given routine care immediately after birth. All mothers and infants were healthy with normal pregnancies and deliveries. At 36 hours a first observation was made of maternal and infant behaviour during breast feeding in all three groups. At this stage primiparae with extra contact showed behaviour much more like the behaviour of multiparae with routine care. Infants of primiparae with routine care cried most frequently. The behaviour of mothers of boys differed more from group to group than did that of mothers of girls.

  • 244.
    de Chateau, Peter
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Wiberg, Britt
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Long-term effect on mother-infant behaviour of extra contact during the first hour post partum: II. A follw-up at three months1977Ingår i: Acta Paediatrica, ISSN 0803-5253, E-ISSN 1651-2227, Vol. 66, nr 2, s. 145-151Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Abstract Primiparous mothers and their infants who had an extra 15–20 minutes' suckling and skin to skin contact during the first hour after delivery, behaved differently at 36 hours post partum compared with a control group without this extra contact. The present study is a 3-month follow-up of these mothers and infants by means of direct observation of mother-infant free play and a personal interview with the mothers. Mothers in the extra contact group spent more time kissing and looking en face at their infants; these infants smiled more often and cried less frequently. A greater proportion of the mothers with extra contact were still breast feeding at 3 months. The influence of extra contact on behaviour was more pronounced in boy–mother than in girl–mother pairs.

  • 245.
    de Chateau, Peter
    et al.
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Wiberg, Britt
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Long-term effect on mother-infant behaviour of extra contact during the first hour post partum: III. Follw-up at one year1984Ingår i: Scandinavian journal of social medicine, ISSN 1403-4948 Print; 1651-1905 Online, Vol. 12, nr 2, s. 91-103Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    The present prospective study examined, one year after delivery, the possible effects of early extra contact during the first hour following delivery. An extra skin-to-skin contact and suckling contact was allowed 22 primiparous mothers and their infants (P+ group). One control group of 20 primiparous mothers and their infants were given routine care immediately after birth (P group). During observation of a physical examination of the infant, ‘extra contact mothers’ held and touched their infants more frequently and more often talked positively to their infants than did mothers given routine care. ‘Extra contact mothers’ had returned to their professional employment outside the home to a lesser extent than had routine care mothers. A greater proportion of ‘extra contact’ infants slept in a room of their own. In the P+ group, mothers who had returned to gainful employment were also able to have their babies sleep in a room of their own—no such correspondence was found in the P group. The Gesell Developmental Schedules revealed that, in four parts out of five, infants with extra contact immediately after birth, were ahead of those in the control group. On the other hand, the Vineland Social Maturity Scale and the Cesarec Marke Personality Scheme did not reveal any major differences between the two groups. Mothers with early extra skin-to-skin contact and suckling contact breast-fed their infants on an average for 2 1/2 months longer than did routine care mothers. No other differences in feeding habits were found. The influence of extra contact was more pronounced in boy–mother than in girl–mother pairs.

  • 246. Decker, Ralph
    et al.
    Albertsson-Wikland, Kerstin
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Halldin, Maria
    Dahlgren, Jovanna
    Decreased GH dose after the catch-up growth period maintains metabolic outcome in short prepubertal children with and without classic GH deficiency2012Ingår i: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 77, nr 3, s. 407-415Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    OBJECTIVE: Few studies have evaluated metabolic outcomes following growth hormone (GH) treatment in short prepubertal children during different periods of growth. Previously, we found that individualized GH dosing in the catch-up period reduced the variation in fasting insulin levels by 34% compared with those receiving a standard GH dose. We hypothesized that the GH dose required to maintain beneficial metabolic effects is lower during the prepubertal growth phase after an earlier catch-up growth period.

    DESIGN: Short prepubertal children with isolated GH deficiency or idiopathic short stature were randomized to individualized GH treatment (range, 17-100 μg/kg/day) or a standard dose in a preceding 2-year study. After achieving near mid-parental height(SDS) (,) children receiving an individualized dose were randomized to either a 50% reduced individualized dose (RID, n=28) or an unchanged individualized dose (UID, n=37) for 2 years. The dose remained unchanged in 33 children initially randomized to receive a standard dose (FIX, 43 μg/kg/day).We evaluated whether the variations in metabolic parameters measured during maintenance growth diminished in RID compared with UID or FIX.

    RESULTS: We observed less variation in fasting insulin levels (-50%), insulin sensitivity as assessed by homeostasis model assessment (-55.1%), lean soft tissue (-27.8%) and bone mineral content (-31.3%) in RID compared with UID (all p<0.05), but no differences compared with FIX.

    CONCLUSIONS: Continued individualized GH treatment after the catch-up growth period is safe and reduces hyperinsulinism. Individualized GH dose can be reduced once the desired height(SDS) is achieved to avoid overtreatment in terms of metabolic outcome.

  • 247. Decker, Ralph
    et al.
    Albertsson-Wikland, Kerstin
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Halldin, Maria
    Gustafsson, Jan
    Nilsson, Nils-Östen
    Dahlgren, Jovanna
    GH Dose Reduction Maintains Normal Prepubertal Height Velocity After Initial Catch-Up Growth in Short Children2019Ingår i: Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, E-ISSN 1945-7197, Vol. 104, nr 3, s. 835-844Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Context: GH responsiveness guides GH dosing during the catch-up growth (CUG) period; however, little is known regarding GH dosing during the prepubertal maintenance treatment period.

    Objective: To evaluate whether SD score (SDS) channel parallel growth with normal height velocity can be maintained after CUG by reducing the GH dose by 50% in children receiving doses individualized according to estimated GH responsiveness during the catch-up period.

    Design and Settings: Prepubertal children (n = 98; 72 boys) receiving GH during CUG (GH deficient, n = 33; non–GH deficient, n = 65), were randomized after 2 to 3 years to either a 50% reduced individualized dose (GHRID; n = 27; 20 boys) or unchanged individualized dose (GHUID; n = 38; 27 boys). Another 33 children (25 boys) continued a standard weight-based dose [43 µg/kg/d (GHFIX)].

    Main Outcome Measures: The primary endpoint was the proportion of children with ΔheightSDS within ±0.3 at 1 year after GH dose reduction compared with two control groups: GHUIDand GHFIX. The hypothesis was that heightSDS could be maintained within ±0.3 with a reduced individualized GH dose.

    Results: For the intention-to-treat population at 1 year, 85% of the GHRIDgroup maintained ΔheightSDS within ±0.3 vs 41% in the GHUIDgroup (P = 0.0055) and 48% in the GHFIXgroup (P = 0.0047). The ΔIGF-ISDS in the GHRID group was −0.75 ± 1.0 at 3 months (P = 0.003) and −0.72 ± 1.2 at 1 year compared with the GHUID group (0.15 ± 1.2; P = 0.005) and GHFIX group (0.05 ± 1.0; P = 0.02).

    Conclusions: Channel parallel growth (i.e., normal height velocity) and IGF-ISDS levels within ±2 were maintained after completed CUG using a 50% lower individualized dose than that used during the CUG period.

  • 248.
    Decker, Ralph
    et al.
    Department of Pediatrics, Gothenburg Pediatric Growth Research Center (GP-GRC), University of Gothenburg, Institute of Clinical Sciences, The Queen Silvia Children’s Hospital, Gothenburg.
    Albertsson-Wikland, Kerstin
    Department of Pediatrics, Gothenburg Pediatric Growth Research Center (GP-GRC), University of Gothenburg, Institute of Clinical Sciences, The Queen Silvia Children’s Hospital, Gothenburg.
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Nierop, Andreas F M
    Muvara bv, Multivariate Analysis of Research Data, Leiderdorp, Netherlands.
    Gustafsson, Jan
    Department of Women’s and Children’s Health, Uppsala University, Uppsala.
    Bosaeus, Ingvar
    Department of Clinical Nutrition, Research Centre for Endocrinology and Metabolism, Sahlgrenska, University Hospital, Gothenburg, Sweden.
    Fors, Hans
    Department of Pediatrics, Gothenburg Pediatric Growth Research Center (GP-GRC), University of Gothenburg, Institute of Clinical Sciences, The Queen Silvia Children’s Hospital, Gothenburg.
    Hochberg, Ze'ev
    Division of Pediatric Endocrinology, Rambam Medical Centre, Haifa, Israel.
    Dahlgren, Jovanna
    Department of Pediatrics, Gothenburg Pediatric Growth Research Center (GP-GRC), University of Gothenburg, Institute of Clinical Sciences, The Queen Silvia Children’s Hospital, Gothenburg.
    Metabolic outcome of GH treatment in prepubertal short children with and without classical GH deficiency2010Ingår i: Clinical Endocrinology, ISSN 0300-0664, E-ISSN 1365-2265, Vol. 73, nr 3, s. 346-354Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Context  Few studies have evaluated the metabolic outcomes of growth hormone (GH) treatment in idiopathic short stature (ISS). Moreover, children with ISS appear to need higher GH doses than children with GH deficiency (GHD) to achieve the same amount of growth and may therefore be at increased risk of adverse events during treatment. The individualized approach using prediction models for estimation of GH responsiveness, on the other hand, has the advantage of narrowing the range of growth response, avoiding too low or high GH doses.

    Design  Short prepubertal children with either isolated GHD (39) or ISS (89) participated in a 2-year randomized trial of either individualized GH treatment with six different GH doses (range, 17–100 μg/kg/day) or a standard dose (43 μg/kg/day).

    Objective  To evaluate if individualized GH treatment reduced the variance of the metabolic measures as shown for growth response and to compare changes in metabolic variables in children with ISS and GHD.

    Hypothesis  Individualized GH dose reduces the range of metabolic outcomes, and metabolic outcomes are similar in children with ISS and GHD.

    Results  We observed a narrower variation for fasting insulin (−34·2%) and for homoeostasis model assessment (HOMA) (−38·9%) after 2 years of individualized GH treatment in comparison with standard GH dose treatment. Similar metabolic changes were seen in ISS and GHD. Delta (Δ) height SDS correlated with Δinsulin-like growth factor I (IGF-I), Δleptin and Δbody composition. Principal component analysis identified an anabolic and a lipolytic component. Anabolic variables [Δlean body mass (LBM) SDS and ΔIGF-I SDS] clustered together and correlated strongly with Δheight SDS and GH dose, whereas lipolytic variables [Δfat mass (FM) SDS and Δleptin] were clustered separately from anabolic variables. Regression analysis showed GH dose dependency in ISS, and to a lesser degree in GHD, for ΔLBM SDS and Δheight SDS, but not for changes in FM.

    Conclusions  Individualized GH dosing during catch-up growth reduces the variance in insulin and HOMA and results in equal metabolic responses irrespective of the diagnosis of GHD or ISS.

  • 249.
    Decker, Ralph
    et al.
    Göteborg Pediatric Growth Research Centre (GP-GRC), Department of Pediatrics, Institute of Clinical Sciences, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Nygren, Anders
    Göteborg Pediatric Growth Research Centre (GP-GRC), Department of Pediatrics, Institute of Clinical Sciences, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Kriström, Berit
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Nierop, Andreas F. M.
    Muvara bv, Multivariate Analysis of Research Data, Leiderdorp, Netherlands.
    Gustafsson, Jan
    Department of Women’s and Children’s Health, Uppsala University, Uppsala, Sweden.
    Albertsson-Wikland, Kerstin
    Göteborg Pediatric Growth Research Centre (GP-GRC), Department of Pediatrics, Institute of Clinical Sciences, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Dahlgren, Jovanna
    Göteborg Pediatric Growth Research Centre (GP-GRC), Department of Pediatrics, Institute of Clinical Sciences, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
    Different thresholds of tissue-specific dose-responses to growth hormone in short prepubertal children2012Ingår i: BMC Endocrine Disorders, ISSN 1472-6823, E-ISSN 1472-6823, Vol. 12, s. 26-Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Background: In addition to stimulating linear growth in children, growth hormone (GH) influences metabolism and body composition. These effects should be considered when individualizing GH treatment as dose-dependent changes in metabolic markers have been reported. Hypothesis: There are different dose-dependent thresholds for metabolic effects in response to GH treatment. Method: A randomized, prospective, multicentre trial TRN 98-0198-003 was performed for a 2-year catch-up growth period, with two treatment regimens (a) individualized GH dose including six different dose groups ranging from 17-100 mu g/kg/day (n=87) and (b) fixed GH dose of 43 mu g/kg/day (n=41). The individualized GH dose group was used for finding dose-response effects, where the effective GH dose (ED 50%) required to achieve 50% Delta effect was calculated with piecewise linear regressions. Results: Different thresholds for the GH dose were found for the metabolic effects. The GH dose to achieve half of a given effect (ED 50%, with 90% confidence interval) was calculated as 33(+/- 24.4) mu g/kg/day for Delta left ventricular diastolic diameter (cm), 39(+/- 24.5) mu g/kg/day for Delta alkaline phosphatase (mu kat/L), 47(+/- 43.5) mu g/kg/day for Delta lean soft tissue (SDS), 48(+/- 35.7) mu g/kg/day for Delta insulin (mU/L), 51(+/- 47.6) mu g/kg/day for Delta height (SDS), and 57(+/- 52.7) mu g/kg/day for Delta insulin-like growth factor I (IGF-I) SDS. Even though lipolysis was seen in all subjects, there was no dose-response effect for Delta fat mass (SDS) or Delta leptin ng/ml in the dose range studied. None of the metabolic effects presented here were related to the dose selection procedure in the trial. Conclusions: Dose-dependent thresholds were observed for different GH effects, with cardiac tissue being the most responsive and level of IGF-I the least responsive. The level of insulin was more responsive than that of IGF-I, with the threshold effect for height in the interval between.

  • 250. Demmelmair, Hans
    et al.
    Prell, Christine
    Timby, Niklas
    Umeå universitet, Medicinska fakulteten, Institutionen för klinisk vetenskap, Pediatrik.
    Lönnerdal, Bo
    Benefits of Lactoferrin, Osteopontin and Milk Fat Globule Membranes for Infants2017Ingår i: Nutrients, ISSN 2072-6643, E-ISSN 2072-6643, Vol. 9, nr 8, artikel-id 817Artikel, forskningsöversikt (Refereegranskat)
    Abstract [en]

    The provision of essential and non-essential amino acids for breast-fed infants is the major function of milk proteins. In addition, breast-fed infants might benefit from bioactivities of milk proteins, which are exhibited in the intestine during the digestive phase and by absorption of intact proteins or derived peptides. For lactoferrin, osteopontin and milk fat globule membrane proteins/lipids, which have not until recently been included in substantial amounts in infant formulas, in vitro experiments and animal models provide a convincing base of evidence for bioactivities, which contribute to the protection of the infant from pathogens, improve nutrient absorption, support the development of the immune system and provide components for optimal neurodevelopment. Technologies have become available to obtain these compounds from cow's milk and the bovine compounds also exhibit bioactivities in humans. Randomized clinical trials with experimental infant formulas incorporating lactoferrin, osteopontin, or milk fat globule membranes have already provided some evidence for clinical benefits. This review aims to compare findings from laboratory and animal experiments with outcomes of clinical studies. There is good justification from basic science and there are promising results from clinical studies for beneficial effects of lactoferrin, osteopontin and the milk fat globule membrane complex of proteins and lipids. Further studies should ideally be adequately powered to investigate effects on clinically relevant endpoints in healthy term infants.

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