K. J. Van Acker
University of Antwerp
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Featured researches published by K. J. Van Acker.
Diabetes Research and Clinical Practice | 2000
K. J. Van Acker; M Oleen-Burkey; L De Decker; R. Vanmaele; P van Schil; Giovanni Matricali; H Dys; I. De Leeuw
This prospective observational study was carried out to assess the annual preventive and curative treatment costs for diabetic foot problems. Measures of resource use over the 1-year study period were taken for 151 patients whose lesions covered the entire Wagner classification. Treatment was provided under the current protocols of a multidisciplinary team. The 1993 market prices for health services were used to convert units of health service utilization to expenditures by the social insurance system and the patients. The severity of the foot problems determined the medical cost. Preventive care (47 cases), represented an average cost per case of US
European Journal of Pediatrics | 1992
K. Melis; J. Vandevivere; C. Hoskens; A. Vervaet; A. Sand; K. J. Van Acker
880 (1US
European Journal of Pediatrics | 1990
A. M. Roodhooft; E. R. Baumgartner; Jean-Jacques Martin; W. Blom; K. J. Van Acker
1993=BEF 30.65). Curative care (120 cases), including diagnostic tests, wound dressings, antibiotic therapy, revascularization and off loading techniques resulted in a mean cost of US
European Journal of Pediatrics | 1990
A. M. Roodhooft; K. Van Dam; D. Haentjens; G. A. Verpooten; K. J. Van Acker
5227 per ulcer. Care for the 16 most severe wounds and amputations involved hospitalization and surgery at a mean cost per ulcer of US
Pediatric Nephrology | 1990
A. M. Roodhooft; Robert H. McLean; E. Elst; K. J. Van Acker
31716. The most important cost contributers were hospitalizations (72%), drugs (11%) and diagnostic examinations (4%). Preventive treatment for diabetic foot problems can represent a significant saving for the social insurance system as well as for the patients.
Clinical Nephrology | 1981
H. A. Simmonds; K. J. Van Acker; M. J. Dillon; T. M. Barratt; C. F. Potter; A. Sahota; J.S. Cameron
SummaryWe performed99mTc dimercaptosuccinic acid (DMSA) scan and ultrasonography in 146 children during the acute phase of a proven urinary tract infection (UTI). In 99 a micturating cysto-urethrography and in 83 an intravenous urography was also done. The occurrence of fever and increased WBC count, CRP and ESR were also studied. It appeared from this retrospective study that 47% of the kidneys had a cortical or patchy pattern of decreased uptake of99mTc DMSA, as compared to 23% with abnormal findings on US. Vesico-ureteral reflux was present in 38% of the kidneys with parenchymal involvement on99mTc DMSA scan. Although fever, leucocytosis and elevated CRP and ESR were significantly correlated with abnormal99mTc DMSA scan, they were also observed in children without renal parenchymal involvement. Our results suggest that99mTc DMSA scan is a sensitive method for the detection of parenchymal involvement during acute UTI. The exact nature of these lesions and their relation with scars need, however, to be defined.
European Journal of Pediatrics | 1987
A Deprettere; K. J. Van Acker; M. V. L. Du Caju
In a patient with methylmalonic acidaemia (MMAA), persistent neurological symptoms were observed in addition to the acute episodes of metabolic dysequilibrium. CT scan and magnetic resonance imaging revealed bilateral symmetrical necrosis of the globus pallidus. Different episodes of metabolic decompensation, one with severe acidosis, had occurred. Persistent neurological symptoms in patients with MMAA who are appropriately treated suggest irreversible brain damage which appears to occur preferentially at the level of the basal ganglia.
Advances in Experimental Medicine and Biology | 1977
H. A. Simmonds; K. J. Van Acker; J.S. Cameron; A. McBurney
In a child who probably received an overdose of sodium valproate, progressive coma, intermittent tonic-clonic seizures and anuria developed. Laboratory investigations revealed coagulopathy, anaemia and mildly disturbed liver function. Progressive renal insufficiency, probably due to rhabdomyolysis and myoglobulinuria, occurred later. Treatment consisted of supportive measures, combined haemoperfusion and haemodialysis and IV thiopentone. Clinical and biochemical normalisation was observed after 11 days.
Diabetes Research and Clinical Practice | 1991
L. Van Gaal; G. Vansant; K. J. Van Acker; I. De Leeuw
In a girl with recurrent haemolytic uraemic syndrome (HUS), persistently low serum levels of C3 were found. Analysis of complement phenotype revealed a hypomorphic variant of C3 Fast in the patient (C3fS) and a normal heterozygous pattern in both parents and the brother (C3FS). Other complement aberrations in the patient were: the presence of a null gene for C4A and C4B and low serum levels of factor H. The father also had partial factor H deficiency. It is hypothesized that the hypomorphic C3 variant may predispose to recurrent HUS. In the acquired forms the role of uraemia in alteration of C3F should be considered.
European Respiratory Journal | 1996
J. H. Pauwels; H. P. Van Bever; Kristine Desager; M. Willemen; Wouter L. Creten; K. J. Van Acker; P. Vermeire
Purine nucleotides important for normal cellular metabolism are derived endogenously from de novo synthesis and also from recycling of pre-formed purines via the so-called salvage pathway (Figure 1). The latter pathway contains a number of enzymes, the absence of which can lead to disturbances of purine metabolism and also severe clinical symptoms1. An example is the deficiency of the salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRT) which can lead either to the Lesch-Nyhan syndrome or X-linked gout1.