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  • 1. Albertsson Wikland, K
    et al.
    Alm, F
    Aronsson, S
    Gustafsson, J
    Hagenäs, L
    Häger, A
    Ivarsson, S
    Kriström, Berit
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Marcus, C
    Moëll, C
    Nilsson, K O
    Ritzén, M
    Tuvemo, T
    Westgren, U
    Westphal, O
    Aman, J
    Effect of growth hormone (GH) during puberty in GH-deficient children: preliminary results from an ongoing randomized trial with different dose regimens.1999In: Acta Paediatrica. Supplement, ISSN 0803-5326, Vol. 88, no 428, p. 80-4Article in journal (Refereed)
    Abstract [en]

    This paper reports results from an ongoing, randomized, multicentre national trial. The aim is to elucidate whether a dose of growth hormone (GH) of 0.2 IU/kg (0.07 mg/kg), given either as once-daily or twice-daily injections during puberty, is more effective than a once-daily dose of 0.1 IU/kg/day (0.03 mg/kg/day) in improving final height in children with GH deficiency (GHD). The twice-daily regimen comes closer to the spontaneous GH secretion pattern in puberty. Ninety-two children with GHD who had been receiving GH therapy for at least 1 year, and with spontaneous puberty or who were prepubertal and due to be started on replacement therapy to induce puberty, were randomly assigned to receive GH as follows: group A, 0.1 IU/kg/day (0.03 mg/kg/day), administered once daily; group B, 0.2 IU/kg/day (0.07 mg/kg/day), administered once daily; and group C, 0.2 IU/kg/day (0.07 mg/kg/day), divided into two equal injections given at 12-hour intervals. Pubertal height gain was 0.7, 0.7 and 1.3 SDS for groups A, B and C, respectively. The gain in height during puberty was thus most marked in group C. Mean final height, when corrected for parental height, was between 0 and 1 SDS in all treatment groups. All but seven children reached a final height within +/- 2 SD of the general population. There was a wide range of final heights in all three treatment groups. This variation in response suggests the need to individualize treatment in order to achieve an appropriate final height for most individuals.

  • 2.
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Potentials and pitfalls in neonatal screening for type 1 diabetes.1999In: Acta Paediatrica. Supplement, ISSN 0803-5326, Vol. 88, no 432, p. 80-2Article in journal (Refereed)
    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.

  • 3.
    Dahlquist, Gisela
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    The aetiology of type 1 diabetes: an epidemiological perspective.1998In: Acta Paediatrica. Supplement, ISSN 0803-5326, Vol. 425, p. 5-10Article in journal (Refereed)
    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.

  • 4. Örtqvist, Å
    et al.
    Blennow, M
    Carlsson, R-M
    Hansson, LÅ
    Lindberg, A
    Lindqvist, I
    Magnusson, M
    Nilsson, L
    Norlund, A
    Nyrén, O
    Olcén, P
    Olin, P
    Silfverdal, Sven Arne
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Paediatrics.
    Säwe, J
    Söderström, A
    Trollfors, B
    Vaccination of children: a children systematic review2010In: Acta Paediatrica. Supplement, ISSN 0803-5326, Vol. 99, no s461, p. 1-192Article in journal (Refereed)
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