Vascular complications after kidney transplantation in children
Stylianos Kykalos1, Georgios C. Sotiropoulos1, Birgitta Kranz2, Udo Vester2, Peter F. Hoyer2
Abstract: Vascular complications after kidney transplantation in children consist a complex problem.
Kinking of the graft due to lack of space, and secondary anastomotic stenosis due to diameter discrepancy of vessel lumen are pure surgical complications. Renal vascular thrombosis (Virchow’s Triad and immunological factors) is the main cause of graft loss. Vascular changes of small vessels after renal transplantation such as thrombotic microangiopathy and graft vasculopathy are further analysed.
Concluding, it comes out that although the risk factors for great vessels are well understood and can be prevented, the changes of small vessels remain an unresolved problem.
Key words: Paediatric kidney transplantation, paediatric surgery, vascular complications, rejection.
Introduction
Vascular complications or vascular problems after kidney transplantation in children are multidimensional. The localisation is oriented to anatomy.
The major vessels are mostly affected by operative and thrombotic complications. In the small vessels the thrombotic microangiopathy, the vascular and the chronic transplant rejections are predominantly responsible. The complications could be also as immunological and non-immunological classified. A classification in the context of kidney transplantation is quite difficult, since it is not always possible to differentiate the immunological from other trigger processes.
Operative complications
Surgical complications rarely happen nowadays, due to the modern state of surgical technique. They are usually caused by vascular characteristics of the transplanted kidney. Thus, if an aberrant vessel can not be anastomosed, it should be ligated with possible complication of a pole-, kidney pelvis- or ureteronecrosis.
The anatomical relationships in childish situs are often narrow. A possible kinking due to compression after abdominal closure, can lead to either renal artery stenosis plus reduction of organ’s perfusion or in venous stasis. Because of the vascular calibre discrepancy between the child's and adult’s graft vessels, secondary anastomotic stenosis, leading to renovascular hypertension, is possible.
Surgical vascular complications should no longer result in graft loss, especially if early postoperative or even in the operating room a routine Doppler monitoring (Figure 1, 2) is
performed. The assessment of diastolic flow velocity and the calculation of resistance index are of crucial importance. A high vascular resistance is found at high parenchyma pressure, by external compression or by swelling of the kidney for example by an acute tubular necrosis. A negative diastolic flow should lead, without
1 Department of General, Visceral and Transplantation Surgery
University Hospital, Essen, Essen Germany
2 Department of Pediatrics II, Pediatric Nephrology, Endocrinology, Gastroenterology and Transplant Medicine, University Hospital, Essen, Essen Germany
Correspondence: Georgios C. Sotiropoulos georgios.sotiropoulos@ uni-due.de Department of General, Visceral and Transplantation Surgery
University Hospital Essen Hufelandstr. 55, 45122 Essen, Germany
Figure 1. Αcute outflow obstruction.
Figure 2. Αcute outflow obstruction after decompression.
delay, to an operational revision, in order to exclude a venous compression or renal vein thrombosis.
Thrombotic complications
30 years ago Lindström et al. had already defined [1] the thrombotic complications as the most common surgical cause of graft loss. Arbus et al. published in 1983 the experience of the paediatric transplantation program in Toronto [2] and concluded that thrombosis occurred more frequently in children less than 6 years who had received a large adult kidney. This phenomenon was particularly pronounced, when the natural kidneys were left with a high rest diuresis in situ. Broyer [3] in 1990 published the experience of the paediatric transplantation program in Paris. A renal vein thrombosis was responsible in 12 from 53 cases of graft loss. Young age of donor or recipient was identified as special risk factors. In contrast, protective effects were found regarding the occurrence of vascular rejection under the use of OKT3. A prospective study conducted in Paris proved that the prophylactic enoxaparin, did significantly reduce the thrombosis rate in the treated patients [4].
The cause of graft failure in about 2000 children was investigated in an analysis of the North American Paediatric Renal Transplantation Cooperative Study (NAPRTCS) [5,6]. Over a study period of 15 years, the chronic rejection with a rate of 33%, followed by acute rejection and renal vascular thrombosis with 15% and 12% respectively, proved to be the main causes of graft loss. The analysis of the last five years resulted in a change of the leading causes: renal vascular thrombosis was in the first place with 21%, followed by chronic and acute rejection with 19% and 9% respectively. The overall incidence of renal vascular thrombosis was 2.1%. The risk factors for the occurrence of renal vascular thrombosis were analyzed in a multivariate analysis (use of IL-2 receptor antibodies, deceased donors’ kidneys, previous transplantation, peritoneal dialysis before transplantation and more than 5 transfusions). Only the use of IL2 receptor antibodies seemed to have a significant effect on decreasing the incidence of renal vascular thrombosis. If this conclusion represents a statistical artifact of registry data, or whether immunological factors do really trigger the occurrence of renal vascular thrombosis can not be answered from this study.
Virchow's triad and thrombotic complications after renal transplantation
In a differentiated approach to the possible causes of vascular thrombosis after kidney transplantation, the classical Virchow's triad is particularly helpful,
since not a single factor, but a combination of them, is responsible for the occurrence of renal vascular thrombosis.
Stasis: risk factors for stasis consist all low flow situations in the transplanted kidney, especially in the transplantation of adult kidneys in an infant recipient, and predominantly in cases where the anastomosis is not between renal arteries and aorta [7], but between renal artery and iliac vessels of the young receiver. The large for size situation leads to a reduction of blood flow velocity. Simultaneous organ swelling with increase in the resistance may also reduce the blood flow velocity. Congestion and compression of the kidney transplant in a young child are additional risk factors that occur more frequently in the transplantation.
Endothelial lesions: reperfusion injury may provoke an endothelial swelling and an increased expression of adhesion molecules on endothelial cells, favoring the adhesion of platelets and leukocytes. Frequently, endothelial lesions do occur during a vascular rejection procedure (Figure3, 4). Calcineurin inhibitors, such as cyclosporine and tacrolimus, may lead to a vascular toxic vasoconstriction. For an older kidney, possible atherosclerosis represents an additional risk factor. Furthermore, the use of additional patches and a long warm ischemia time should be mentioned as surgical causes of endothelial lesions.
Increase of viscosity: this can occur in the framework of dehydration [8], particularly in cases of polyuria. Infants who receive an adult’s organ are, due to high fluid turnover, at particular risk for the development of dehydration. Changes in the coagulation factors, particularly in the direction of hypercoagulability [9] play a significant role. More frequent risk factors for the development of thrombosis are the APC-resistance (hetero-or homozygosity for mutations of factor V), hetero-or homozygosity for mutations in
Figure 3. Αcute vascular rejection.
the prothrombin gene, increased levels of homocysteine, elevated levels of factor VIII and the Lupus anticoagulant. Rarer causes of an increased risk of thrombosis are the degradation of proteins C, S activity, the decreased concentration of ATIII, and the presence of cardiolipin antibodies and lipoprotein a. Very rare causes are dysfibrinogenemia and increased activity of factor IX and XI.
A possible accumulation of the above mentioned risk factors, in the context of Virchow's triad, during kidney transplantation in childhood, sets this age group at high risk of thrombosis.
Strategies to reduce renal vascular thrombosis
In Essen a preoperative screening for coagulation disorders [9] is being routinely performed since 1998, as part of the paediatric kidney transplantations program. The determined factors include prothrombin time, partial thrombin time, fibrinogen, antithrombin III, protein C and S, activated protein C resistance (APC), factor V Leiden mutation (FVR506Q), prothrombin mutation (G20210A), antiphospholipid antibodies and MTHFR mutations.
In 90 studied children, there were found11 cases (12.2%) of increased risk of thrombosis. A factor V Leiden mutation was found in 7 cases, a fibrinogen mutation in two cases, antiphospholipid antibodies were detected in two cases (one child had a history of two graft losses as a result of renal vein thrombosis) and in 5 cases, thrombosis had already occurred in the background without any identifiable cause. The Essen-based therapeutic strategy for patients without risk of thrombophilia consists of a postoperative low dose heparin for 2 weeks. By patients with thrombophilia, the heparinisation begins already intraoperatively and continues for the two first postoperative weeks. All patients receive low-dose aspirin for 1 year.
In the study by Kranz et al. no case of thrombosis occurred, while bleeding complications occurred twice (in one patient without and in one with thrombophilia), but in both cases without any further adverse consequences. The first year Graft Survival rates in patients without and with thrombophilia were 93% and 100% respectively
Vascular changes of small vessels after renal transplantation
Vascular changes in the small vessels occur as a result of thrombotic microangiopathy, of vascular rejections or of the so-called chronic graft vasculopathy.
The thrombotic microangiopathy (Figure 5) is a histopathological description and not a unique entity. Fibrin deposits in the glomerular and pre-glomerular capillaries are found both in the hyperacute rejection as well as the hemolytic-uremic syndrome. In contrast, the vascular toxicity of calcineurin inhibitor is mainly in the arteriole, the so-called typical cyclosporine or tacrolimusassociated arteriolopathy with hyaline necrosis.
The hemolytic-uremic syndrome after kidney transplantation is a complication that has been described since the beginning of transplantation in the 70 years. Originally, it was equated with severe vascular rejection with insufficient immunosuppression (steroids, azathioprine). Furthermore, the hemolyticuremic syndrome after transplantation was thought to be induced by the calcineurin inhibitors- [10], as this phenomenon occurred in isolated cases of cyclosporine treatment, particularly at high but even at low doses. A switch to tacrolimus showed that this phenomenon may occur with tacrolimus as well. In all proposed theories, this phenomenon is still not properly understood. On the other hand, it is certain that the HUS is not only by calcineurin inhibitors triggered, as there are also many described cases after application of mTOR inhibitors [10].
Figure 5. Τhrombotic microangiopathy (1st posttransplantation day)
Figure 4. Αcute chronic vascular rejection.
In cases where a hemolytic uremic syndrome was the cause of renal insufficiency, exists always the danger of disease recurrence in the graft [11,12]. A more detailed recent analysis shows that the risk of recurrence exists exclusively for the atypical HUS. In the so-called typical HUS, which is Verotoxin-induced, the recurrence probability is very low. In a retrospective analysis of patients with loss of the transplanted kidney due to recurrent HUS, the molecular genetic studies revealed frequent defects in the complement system, in particular factor H mutations [13]. Virtually all patients who showed a factor H mutation, have lost their graft in context of a recurrent HUS. In a special investigation in cooperation with Professor Zipfel, Jena, we did demonstrate an antibody against factor H, in a patient with an atypical hemolytic uremic syndrome.
The identification of these risk factors is of great importance, because without new concepts, transplantations in this special group of patients can not promise any success.
Chronic graft vasculopathy
Chronic graft vasculopathy is currently the most common cause of chronic graft dysfunction. The causes are multifactorial. Human immunological factors are likely involved. On the other hand, non-immunological causes, such as arterial hypertension, are considered as pacemaker of chronic graft vasculopathy. Especially in childhood and adolescence, the antihypertensive treatment is often inadequate.[14] Another contributing factor is calcineurin inhibitors. Whether calcineurin inhibitor-free immunosuppressive protocols would resolve this problem, is still open.
The question of endothelial repair processes in the childhood, particularly after an ischemia-reperfusion injury, is unclear. The role of circulating epithelial precursor cells in paediatric graft recipients has not been studied yet, but is eventually indicated by the presence of chimeric endothelial cells in the vascular endothelium of renal transplant (own observations).
Summary
In transplanted children, all vessel segments in the graft kidney could be affected by vascular problems. As risk factors of great vessels complications are easily identifiable, a cautious approach can reduce the problem. Regarding small vessels, many different pathogenetic mechanisms are implicated in thrombotic
microangiopathies, influencing the appropriate therapeutic decision. The problem of chronic graft vasculopathy, which is especially important for the longterm prognosis in children, remains unresolved. Prospective studies with sufficient long-term observation could eventually prove helpful in this direction.
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Hypertension and obesity in children and adolescents
S. Stabouli1, V. Kotsis2
Abstract: Obesity is a chronic disease prevalent in both developed and developing countries, which affects children and adolescents as well as adults. Epidemiological studies have demonstrated a higher prevalence of hypertension in obese than in non-obese children and adolescents in a variety of ethnic and racial groups, using clinic blood pressure measurements. Τhe pathogenesis of obesity induced hypertension implicates adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Evidence is accumulating of early target organ damage in obese young people, emphasizing the fact that the adverse effects of weight gain may be apparent even in childhood. There is compelling evidence that overweight status and elevated blood pressure are closely related and increase cardiovascular risk synergistically. The pathogenetic process of cardiovascular disease appears to begin in childhood, and obesity may accelerate the progression of the disease. Weight loss and exercise remain the cornerstone for the management of obese children and adolescents with hypertension. The presence of left ventricular hypertrophy may be an indication for more aggressive therapy aimed at inducing the regression of silent target organ damage before a clinical event develops. In addition to lifestyle modifications, antihypertensive medication should be considered for obese children with stage 2 hypertension and for those with left ventricular hypertrophy.
Key words: Obesity, hypertension, target organ, sympathetic nervous system
1 Paediatric Intensive Care Unit, Hippokration Hospital, Thessaloniki
2 Hypertension-ABPM centre, 3rd Department of Medicine, Papageorgiou Hospital, Thessaloniki, Greece
Correspondence: S. Stabouli sstaboul@med.uoa.gr Paediatric Intensive Care Unit, Hippokration Hospital, Thessaloniki 55132, Kalamaria
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Neonatal Intensive Care Unit (NICU), Child Health Department, University of Ioannina, Greece
Correspondence:
Vasileios Giapros vgiapros@cc.uoi.gr
Neonatal Intensive Care Unit, Child Health Department, University of Ioannina, Greece
Early growth disturbances and development of the metabolic syndrome
V. Giapros, S. Andronikou
Abstract: Individuals who are born either small (SGA) or large (LGA) for gestational age and those who experience early catch-up growth are characterized as having early growth disturbances. These conditions have been related with several parameters of the metabolic syndrome as insulin resistance (IR), diabetes mellitus (DM) type-2, obesity, elevated blood pressure and dislipidemia. Derangements in the production, secretion and action of insulin in SGA children have been observed as early as in the age of 3 years with deterioration with age. These individuals are prone to develop obesity and central fat distribution, which is linked with IR. Individuals with in-utero growth restriction may have a lower nephron endowment and their blood pressure may be elevated at preschool age. Postnatal catch-up growth in SGA children is related with abnormal serum lipids profile while childhood obesity in the same group of children is related with elevated triglycerides. Birth weight and any information about the type, cause, and severity of inutero growth restriction as well as postnatal catch-up growth patterns should be recorded in these children. There is inadequate evidence to recommend special interventions or screening test in individuals with early growth disturbances outside of normal clinical practice.
Key words: Low birth weight, metabolic syndrome, insulin resistance, blood pressure, in-utero growth restriction
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4th Dept of Pediatrics Papageorgiou Hospital
Correspondence: Maria Kavga maroula_k4@yahoo.gr
4th Dept of Pediatrics Papageorgiou Hospital N. Efkarpia, 56403, Thessaloniki, Greece
The role of B type natriuretic peptide in congenital heart disease
Μ. Kavga, G. Varlamis
Abstract: B-type natriuretic peptide (BNP) is a cardiac hormone, secreted mainly by the ventricles in response to volume expansion and pressure load. In the last decades, BNP has been widely recognized as a reliable marker in adult cardiological evaluation, but BNP applications in children have remained limited, and for paediatric patients, age- and sex-related normal values have not yet been compiled.
The data from the few studies published to date suggest that the measurement of BNP may be a useful marker in managing i) children with heart failure of various origins, ii) children treated with antracyclines, and iii) children who have had a cardiac transplantation.
There is growing interest in research on BNP and pro-BNP in children with congenital heart disease. Serum BNP and pro-BNP levels appear to be of future value as effective biomarkers of systolic ventricular dysfunction in paediatric patients with congenital heart disease.
This literature review firstly describes the natriuretic peptide family and secondly summarizes the current state of knowledge regarding the use of BNP in both paediatrics and paediatric cardiology.
Key words: B-type natriuretic peptide, congenital heart disease, children.
είναι ένας ισχυρός, νατριουρητικός, διουρητικός παράγοντας
RAAS (Renin Angiotensin Aldosterone System-ρενίνης-αγγειοτενσίνης-
(5) (Εικόνα 2).
BNP (134
(108 αμινοξέα).
BNP (76
BNP (32
Giannakoulas et
-
επικοινωνία (υπερφόρτωση όγκου), στένωση ισθμού της αορτής (υπερφόρτωση πίεσης) και διατατική μυοκαρδιοπάθεια (συστολική δυσλειτουργία) και διαπίστωσαν
(ventricular septal defect - VSD),
(patent ductus arteriosus - PDA)
(atrial septal defect
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44. Ozhan H, Albayrac S, Uzun H, Ordu S, Kaya A, Yazici M. Correlation of plasma -type natriuretic peptide with shunt severity in Patients with Atrial or Ventricular Septal Defect. Pediatr Cardiol .2007;28:272-275.
45. Nir A, Bar-Oz B, Perles Z, Korach A, Rein AJJT. N-terminal pro-B-type natriuretic peptide: reference plasma levels from birth to adolescence. Elevated levels at birth and in infants and children with heart diseases. Acta Paediatr 2004;93:603–607.
46. Sanjeev S, Pettersen M, Lua J, Thomas R, Shankaran S, L’Ecuyer T. Role of plasma B-type natriuretic peptide in screening for hemodynamically significant patent ductus arteriosus in preterm neonates. J.Perinatol 2005;25:709-713.
47. Choi BM, Lee KH, Eun BL, Yoo KH, Hong YS, Son CS, et al. Utility of rapid B-type natriuretic peptide assay for diagnosis of symptomatic patent ductus arteriosus in preterm infants. Pediatrics 2005;115:255-261.
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Γενικό Νοσοκομείο
«Ασκληπιείο Βούλας»,
Φιλίππου Όλγα filiolga@hotmail.com
Β. Παύλου 1, Βούλα, Τ.Κ. 16673
Paediatric Clinic, General Hospital “Asklipeio Voulas”, Voula, Attiki
Correspondence: Olga Filippou filiolga@hotmail.com
1 V. Pavlou St., Voula, TK 16673
The effect on atherogenic factors of a programme modifying dietary and physical exercise habits in overweight and obese children
O. Filippou, C. Vliora, M. Dolianiti, K. Κaranasiou, S. Papadakou-Lagogianni
Abstract
Introduction: This prospective study aimed to evaluate the short-term effects of a 6-month combined dietary and physical activity intervention programme on overweight and obese children and adolescents.
Methods: A total of 170 overweight and obese children (109 boys, 96 obese children) aged 3.5-14 years (mean: 8.9 ± 2.8 years) were included in the study. During their first visit to the outpatient obesity clinic, anthropometric indices, arterial blood pressure and eating and physical activity habits were recorded and their lipid profile was determined. Dietary and physical exercise instructions were given and the participants were invited to attend for follow-up after 3 and 6 months.
results: At the 6 month follow up examination 58 subjects (34.1%) returned for examination. In 19 (32.7%), a reduction in the body mass index (BMI) percentile was observed (mean reduction: -5.241 percentiles, p<0.001). In the measurements carried out before and after intervention, various changes were detected: a mean reduction in total cholesterol (T-C) by -10mg/dl (p=0.009), a mean reduction in LDL-C by –9.9 mg/dl (p=0.007), a mean increase in HDL-C by +2.3mg/dl (p=0.067) and a marginal decrease in blood pressure (p=0.085). A reduction in weekly high-calorie food consumption led to a decrease in levels of T-C and triglycerides (TGL) and in the appearance of normal LDL-C values (p=0.048, p=0.066 και p=0.042 respectively). Taking up systematic physical exercise was significantly associated with a decrease in levels of T-C and LDL-C (p=0.009 and p=0.057, respectively), and in the return of LDL-C to
normal levels (p=0.059). Increase in the frequency of systematic exercise resulted in a borderline drop of BMI (p=0.052).
Conclusions: A combined short-term intervention improved the BMI and atherogenic factors substantially in overweight and obese children.
Key words: Intervention, atherogenic risk factors, BMI, childhood obesity, follow-up.
SDS
αρτηριακή υπέρταση, δυσλιπι-
ΔΜΣ. Η
απώλεια ΒΣ ήταν 2,6 Ε.Θ. (p=0,009),
ΔΜΣ κατά 5,241 Ε.Θ. (p<0,001). Οι μεταβολές του ΒΣ και του ΔΜΣ ήταν ανεξάρτητες
παχυσαρκίας (Πίνακας 2).
Σε 47 παιδιά (27,64%) ελήφθη νέος βιοχημικός έλεγχος (Πίνακας 1). Διαπιστώθηκε σημαντική πτώ-
στις τιμές της Τ-C (μέση μείωση: -10,1mg/dl, p=0,009) και της LDL-C (μέση μείωση: -9,9mg/dl, p=0,007), μη στατιστικά σημαντική ελάτωση στις τιμές των TGL (μέση μείωση: -4,9mg/dl, p=0,470) καθώς και οριακή
της HDL-C (μέση αύξηση: +2,3mg/dl, p=0,067), πριν και μετά την παρέμβαση.
Σε 58 άτομα (34,1%) επανεξετάστηκε
μα μείωσαν οριακά τις τιμές της ΑΠ (p=0,085). Ειδικότερα, το 31,6% των συμμετεχόντων παρουσίασε ελάττωση της ΑΠ, ενώ
Αναψυκτικά 1,6 ± 2 0,6 ± 1 0,001 (φορές/εβδομάδα)
Έτοιμα
(φορές/εβδομάδα)
Μπισκότα
(φορές/εβδομάδα)
Χυμοί
(φορές/εβδομάδα)
Τσιπς
(φορές/εβδομάδα)
Tηλεθέαση
(ώρες/ημέρα)
Οργανωμένο
(ώρες/εβδομάδα)
με οργανωμένο άθλημα, είχε ως αποτέλεσμα την ελάττωση της τιμής της T-C και της LDL-C (p=0,009 και p=0,057, αντίστοιχα), ενώ σχετίστηκε με την επάνοδο παθολογικών τιμών LDL-C, σε φυσιολογικές τιμές (p=0,059). Τέλος, η αύξηση της εβδομαδιαίας συχνότητας
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διά της Ν.Α. Αττικής. Επίδραση του σύγχρονου τρόπου
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30.
The protective role of breastfeeding against pyelonephritis in infants with urinary tract infection
D. Doganis, D.
Delis, M. Mavrikou, G. Issaris, A. Martirosova, L. Stamoyiannou, K. Siafas
Abstract
Background: Much evidence shows that breastfeeding protects infants from infection and especially urinary tract infections, but the possible protective effect of breastfeeding against the development of lesions of acute pyelonephritis (APN) among infants with first time urinary tract infection (UTI) has not yet been sufficiently evaluated.
Methods: We studied 137 infants (males: 78, females: 59) aged 0.5-12 months (median 3.1) admitted to the hospital with their first time UTI and we evaluated the effect of breastfeeding on the findings of Technetium-99m-dimercaptosuccinic acid (DMSA) scintigraphy performed within 28 days of the diagnosis of UTI (median time: 5 days).
results: Findings of APN on DMSA scan were documented in 31/69 (45%) of currently breastfed infants, in 25/45 (56%) of infants who had been breastfed in the past for different periods of time and in 16/23 (70%) infants, who had never been breastfed. Among boys, APN was detected in 52%, 48% and 56% of infants with ongoing breastfeeding, prior breastfeeding and no breastfeeding respectively (p=ns) whereas among girls the corresponding percentages were 29%, 62.5% and 79% (p=0.008).
Conclusions: A protective role of breastfeeding against the development of acute pyelonephritis lesions on DMSA scan was noted only in girls with UTI.
Key words: Breastfeeding, infants, acute pyelonephritis.
1st and 3rd Paediatric Clinics, “P. & A. Kyriakou” Children’s Hospital, Athens Correspondence: Dimitrios Doganis doganisd@gmail.com 1st Paediatric Clinic, “P. & A. Kyriakou” Children’s Hospital, Athens, Greece
Ladomenou
Βιβλιογραφία
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Neonatal Intensive Care Unit, “P. and A. Kyriakou” Children’s Hospital, Athens, Greece
Correspondence: S. Mouskou stelli_m@yahoo.com 15 Efessou St., Papagou 15669, Athens
Hereditary spherocytosis in newborn infants. Case report
S. Mouskou,
A. Nika, N. Mastrantonaki, , G. Kourakis
Abstract: Hereditary spherocytosis is the most common haemolytic anaemia due to a red cell membrane defect. It is the result of abnormalities in the membrane proteins which leads to loss of the erythrocyte shape and their early destruction in the spleen. The disease is transmitted by autosomal dominant inheritance. A significant number of patients, however, represent de novo mutations. The clinical course is extremely variable; some children have severe haemolytic anaemia and jaundice, and need blood transfusions early in their life, while others are asymptomatic, with mild haemolysis which is detected incidentally. Splenectomy is the indicated treatment after the age of 5 years. The cases are presented of 2 neonates with jaundice and haemolytic anemia. Only one had positive family history for spherocytosis. The 2 infants had a different clinical course during their hospitalization.
Key words: Hereditary spherocytosis, haemolytic anaemia, jaundice, neonate.
Εξήλθε
3
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binding to band 3 and Rh-related proteins forms the basis of a screening test for hereditary spherocytosis. Br J Haematol 2004;124:106
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1st Paediatric Department, “P. & A. Kyriakou” Children’s Hospital
Correspondence: A. Papadopoulou papadop5@otenet.gr
1st Paediatric Department, “P. & A. Kyriakou” Children’s Hospital Athens, Greece
Topics of Pediatric Allergy in “Pediatriki”
P. Maggina
1rst Pediatric Clinic
Children’s Hospital
“P. & A. Kyriakou”
Correspondence:
Paraskevi Maggina vivian.maggina@hotmail.com
1rst Pediatric Clinic
Children’s Hospital
“P. & A. Kyriakou” 11527, Athens, Greece
2006; 69(3):167-168
http://www.e-child.gr/oldmagazines/Paediatriki_2006_69_167_168.pdf
69(3):193-198
http://www.e-child.gr/oldmagazines/Paediatriki_2006_69_193_198.pdf
Παιδιατρική 2005; 68(6):399-408
http://www.e-child.gr/oldmagazines/Pediatriki_2005_68_No6_P399_408.pdf
2006; 69(3):169-177
http://www.e-child.gr/oldmagazines/Paediatriki_2006_69_169_177.pdf
2006; 69(6): 417-424
http://www.e-child.gr/oldmagazines/Paediatriki_2006_69_p_417_424.pdf
Παιδιατρική 2007; 70(5):416-419
http://www.e-child.gr/oldmagazines/Paediatriki_2007_70_p_416_419.pdf
Αντιφλεγμονώδης
Παιδιατρική 2006; 69(6): 425-431
http://www.e-child.gr/oldmagazines/Paediatriki_2006_69_p_425_431.pdf
Νεφελοποιημένη
M.Β.
K.Ν.
Παιδιατρική 2008; 71(3):231-234
http://www.e-child.gr/oldmagazines/Paediatriki_2008_71_p_231_234.pdf
Παιδιατρική 2007; 70(4):330-335
http://www.e-child.gr/oldmagazines/Paediatriki_2007_70_p_330_335.pdf
http://www.e-child.gr/sites/default/files/Pediatriki_73_2_90_102.pdf
A. Σοφιανού-Κατσούλη, G. Du Toit, G. Lack
Παιδιατρική 2005; 68(5):337-341
http://www.e-child.gr/oldmagazines/Paediatriki_2005_68_No5_P337_341.pdf
http://www.e-child.gr/oldmagazines/Paediatriki_2008_71_p_475_481.pdf
http://www.e-child.gr/oldmagazines/Paediatriki_2008_71_p_486_492.pdf
Crohn
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versus enteroclysis in the detection of small-bowel involvement in Crohn's disease: a prospective trial. Clin Gastroenterol Hepatol 2005, 3(8):772-776.
19. Attard TM, Horton KM, DeVito K, Darbari A, OlivaHemker M, Thompson R, Cuffari C: Pediatric jejunoileitis: a severe Crohn's disease phenotype that requires intensive nutritional management. Inflammatory bowel diseases 2004, 10(4):357-360.
20. Wagtmans MJ, Verspaget HW, Lamers CB, van Hogezand RA: Clinical aspects of Crohn's disease of the upper gastrointestinal tract: a comparison with distal Crohn's disease. The American journal of gastroenterology 1997, 92(9):1467-1471.
21. A Papadopoulou, MO Rawashdeh, GA Brown, AS Mc Neish, IW Booth Remission following an elemental diet or prednisolone in Crohn's disease. Acta Paediatrica 1995; 84:79-83.
ΥΠΟΥΡΓΕΙΟ ΥΓΕΙΑΣ ΚΑΙ
ΚΟΙΝΩΝΙΚΗΣ ΑΛΛΗΛΕΓΓΥΗΣ
ΔΙΟΙΚΗΣΗ 6η ΥΓΕΙΟΝΟΜΙΚΗΣ ΠΕΡΙΦΕΡΕΙΑΣ
ΠΕΛΟΠΟΝΝΗΣΟΥ- ΙΟΝΙΩΝ ΝΗΣΩΝ-ΗΠΕΙΡΟΥ
& ΔΥΤ. ΕΛΛΑΔΑΣ
ΑΓΙΟΣ ΔΙΟΝΥΣΙΟΣ
ΓΡΑΦΕΙΟ ΔΙΟΙΚΗΤΗ
ΠΛΗΡ.: Σ. Δρόσσου
Έχοντας υπόψη : 1. Τις
13 του Ν. 1965/91
άρθρου 84 του Ν.2071/92. της παρ.1 του άρθρου 5 του Ν. 2194/94.
39 του Ν.2737/99
του Ν.2716/99
του άρθρου 10 του του Ν.2955/01
του άρθρου 19 του Ν.3106/03
του Ν.3172/03
του άρθρου 3 του Ν.3527/07
το Π.Δ. 131/87 (ΦΕΚ73/Α/87)
της παρ.2 του άρθρου 43 του Ν.1759/88
Ν.2072/92.
του Ν.3204/03
του Ν.3754/2009 όπως τροποποιήθηκε
2. Την ΔΥ13α/39832/97 (ΦΕΚ1088/97 τ.Β’) απόφαση
αξιολόγησης υποψήφιων για
ΑΔΑ: 4Α194690ΒΞ-Μ
ΑΝΑΡΤΗΤΕΑ ΣΤΟ
ΖΑΚΥΝΘΟΣ 4-3-2011
Α.Π.: 1219
Σχετ. 1089/24-2-11, 219/14-1-11
3868/10
3. την ΔΥΙγ/οικ.41255/92 (ΦΕΚ 97/25-2-93 τ.Β’) Υπουργική Απόφαση όπως
με την ΔΥΙγ/οικ.25338/10-5-93 (ΦΕΚ 376/93 τ.Β’) όπως
ΔΥ13α/29804/15-9-97 (ΦΕΚ 859/26-9-97 τ. Β’).
4. Τον οργανισμό του Γ.Ν. Ζακύνθου.
5. Την υπ' αριθμ. 7465/3-11-2010 άγονη προκήρυξη
6. Την υπ' αριθμ. 7705/10-11-2010άγονη
8. Την υπ' αριθμ. Υ10α/162918/24-12-10 (Φ.Ε.Κ. 1250/31-12-2010) απόφαση της Υ.Υ.
9.
ΑΔΑ: 4Α194690ΒΞ-Μ
17-21 ιανουαρίου 2011 Pediatric Emergency Medicine: Sarasota, ΗΠΑ
An Evidence-Based Approach
Contact: Christy or Kathryn
Tel.: 1-866-267-4263
Fax: 1-941-365-7073
E-mail: mail@ams4cme.com
22
Makedonia Palace
Πληροφορίες: Global Events
Τηλ.: 2310 247743
Fax: 2310 247746
E-mail: info@globalevents.gr
17-20 Φεβρουαρίου 2011 the first Global congress for consensus in
Pediatrics and Child Health
Contact: CIP Sectretariat
Tel.: 41-0-22-533-0948
Fax: 41-0-22-580-2953
E-mail: cip@cipediatrics.org
13-17 Mαρτίου 2011 6th World Congress on Pediatric Critical Care
World Federation of Pediatric Intensive and Critical Care Societies (WFPICCS)
Phone: +61 2 9265 0700, Fax: +61 2 9267 5443
Email: pcc2011@arinex.com.au
17 Μαρτίου 2011
- «Μητώ» Τηλ: 210 68 69000 www.mitera.gr 7-10
2011 AlAPE Updates in Pediatrics Panama City, Contact: Astrid Sender
Tel.: 41-0-22-533-0948
Fax: 41-0-22-580-2953
E-mail: asender@paragon-conventions.com
22nd Annual Congress of ESPU
European Society for Paediatric Urology
E-mail: meeting@espu.org 4 - 6
2nd European Conference on Pediatric and ΜontreuxNeonatal Cardiac Intensive Care
Tel. (+41-22) 839 84 84. Fax (+41-22) 839 84 85
Email : info@epncic.com www.epncic.com
11-14 Μαΐου 2011 3rd International Congress on
lymphoma-leukemia-Myeloma
Contact: Ipek Durusu
Tel.: 90-312-490-9897
Fax: 90-312-490-9868
E-mail: admin@thd.org.tr
12-15
Μαΐου 2011
3-6 ιουνίου 2011
10th European Symposium on Pediatric Αθήνα Cochlear Implantation
Divani Apollon Palace
Πληροφορίες: GOLDAIR Congress
Τηλ.: 210 3274570
Φαξ: 210 3311021
E-mail: congress@goldair.gr
2nd Summer School of Pediatric dermatology Aegean Sea
European Society of Pediatric Dermatology & Hellenic Cruise, Greece
Society of Pediatric Dermatology
Πληροφορίες: Erasmus Conferences Tours & Travel S.A.
Τηλ: 210 7257693, 210 7257531
Ε-mail: info@espdsummerschool2011.org www.espdsummerschool2011.org
15-18 ιουνίου 2011 International Association of Paediatric dentistry Αθήνα
23rd Congress (IAPd 2011)
Πληροφορίες: Μαρία Ράντου
Τηλ.: 210 6889130
Φαξ: 210 6844777
E-mail: iapd2011@candc-group.com
23-26 ιουνίου 2011 5th Europaediatrics
European Paediatric Association (EPA/UNEPSA)
Tel.: +30 210 6889130, Fax: +30 210 6844777
E-mail: europaediatrics2011@candc-group.com
14-17 Οκτωβρίου 2011
Βιέννη, Αυστρία
52nd Annual Meeting of the European Society Newcastle, for Paediatric research Αγγλία
European Society for Paediatric Research
Tel: +41 22 908 0488, Fax: +41 22 906 9140
E-mail: espr@kenes.com
