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  • 1
    ISSN: 1432-1076
    Keywords: HIV ; Children ; Intravenous immunoglobulins ; Zidovudine ; CMV
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract From 1988 to 1991 the long-term efficacy of a combined therapy with a polyvalent immunoglobulin/cytomegalovirus (CMV) hyperimmunoglobulin, oral low dose zidovudine, oral cotrimoxazole or inhaled pentamidine was investigated in three groups of human immunodeficiency virus (HIV)-infected children. Group 1A consisted of three perinatally infected children with a CD4 cell decrease of 〉400, cells/μl per year. Group 1B were 17 perinatally infected children with a CD4 cell decrease of 〈400 cells/μl per year. Group 2 comprised eight haemophilic children infected by clotting factors. Despite combined therapy none of group 1A survived longer than 12 months showing a rapid loss of CD4 cell counts, progressive encephalopathy, wasting syndrome and severe bacterial, fungal and CMV reactivation. Under pure intravenous immunoglobulin (IVIG) therapy severe bacterial infections were seen in 1 of 12 children in group 1B. The majority of these patients showed increases or stabilisation of length and weight percentiles. In this group low dose zidovudine therapy was of benefit in HIV-associated neurological symptoms. Nevertheless combined therapy could not prevent further deterioration of CD4 cell counts. In group 2 severe bacterial infections were not seen under IVIG therapy. In this group a temporary increase (6 months) of CD4 cell counts under IVIG/zidovudine combined therapy occurred.Pneumocystis carinii pneumonia (PCP) prophylaxis with oral cotrimoxazole or inhaled pentamidine successfully prevented PCP in all three groups. Under CMV hyperimmunoglobulins (n=22), ten out of ten patients did not acquire primary CMV infection, whereas CMV reactivations mainly located in the CNS could not be prevented in 5 of 12 patients. Our findings indicate that this combined therapy showed remarkable differences in therapeutic efficacy in children with different modes of HIV progression. These modes must be considered for correct timing, dosage and evaluation of therapeutic measures.
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  • 2
    ISSN: 1432-1076
    Keywords: AbbreviationsA2T zidovudine ; 3TC lamivudine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1076
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 4
    ISSN: 1432-1076
    Keywords: Key words Childhood venous thrombosis ; FV G1691A mutation ; Protein C ; Protein S ; Antithrombin ; Lipoprotein (a)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To evaluate the role of multiple established and potential causes of childhood thrombophilia, 285 children with a history of thrombosis aged neonate to 18 years (first thrombotic onset) were investigated and compared with 185 healthy peers. APC- resistance (FV:Q506), protein C, protein S, antithrombin, heparin cofactor II (HCII), histidine-rich glycoprotein (HRGP), and prothrombin (F.II), factor XII (F.XII), plasminogen, homocysteine and lipoprotein (a) (Lp(a)) were investigated. In 59% of patients investigated one thrombotic defect was diagnosed, 19.6% showed two thrombotic risk factors, while in 21.4% of children investigated no risk factor could be identified. Single defects comprised established causes of inherited thrombophilia: FV:Q506 (homozygous n = 10, heterozygous n = 69), protein C (homozygous n = 1; heterozygous n = 31), heterozygous type I deficiency states of protein S (n = 7), antithrombin (n = 7) and homocystinuria (n = 6); potentially inherited clotting abnormalities which may be associated with thrombophilia: F.XII (n = 3), plasminogen (n = 2), HCII (n = 1), increased HRGP (n = 4); new candidate risk factors for thrombophilia: elevated plasma levels of Lp(a) (n = 26), F.II (n = 1). Heterozygous FV:Q506 was found in combination with heterozygous type I deficiency states of protein C (n = 2), protein S (n = 13), antithrombin (n = 8) and HCII (n = 1), increased Lp(a) (n = 13), and once each with elevated levels of F.II, moderate hyperhomocysteinemia, fibrinogen concentrations 〉700 mg/dl and increased HRGP. In addition to the association with FV:Q506, heterozygous protein C type I deficiency was combined with deficiencies of protein S (n = 2), antithrombin (n = 1), and increased Lp(a) (n = 3). One patient showed protein C deficiency along with familially increased von Willebrand factor 〉250%. Besides coexistence with FV:Q506 and protein C deficiency, protein S deficiency was combined with decreased F.XII and increased Lp(a) in one subject each. Furthermore, we found combinations of antithrombin deficiency/elevated Lp(a), hyperhomocysteinemia/Lp(a), deficiency of HCII/plasminogen, and plasminogen deficiency along with increased Lp(a) each in one. Increased prothrombin levels were associated with fibrinogen concentrations 〉700 mg/dl and with HCII deficiency in one child each. Carrier frequencies of single and combined defects were significantly higher in patients compared with the controls. Conclusion In conclusion, data of this multicentre evaluation indicate that paediatric thromboembolism should be viewed as a multifactorial disorder.
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  • 5
    ISSN: 1432-1076
    Keywords: Key words Stroke ; Coagulation ; Children
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Many studies have shown a high percentage of venous thromboses in children to be associated with haematological disorders. However, studies assessing the influence of haemostaseological disorders on paediatric stroke are rare. We compared 26 children with cerebral infarction (median age 2 months, range 0–16.2 years) and 17 with venous thrombosis (median age 4.5 years, range 0–17 years) with regard to prothrombotic risk factors. Prothrombotic disorders were found in 8 out of 26 patients with cerebral infarction (FV Leiden mutation: n = 4; protein C deficiency: n = 1; FV Leiden mutation + protein C deficiency: n = 2; prothrombin mutation G20210A: n = 1) and in 13 out of 17 with venous thrombosis (FV Leiden mutation n = 3; protein C deficiency n = 5; elevated HRGP + PAI: n = 1; combined deficiency of AT, protein C and plasminogen: n = 1; F XII deficiency: n = 1; lupus anticoagulans n = 1; FV Leiden + F XII deficiency + lupus anticoagulans + PAI: n = 1). Comparison of these prevalences with those of 150 healthy paediatric controls showed in children with FV Leiden mutation and/or protein C deficiency an increased risk of cerebral infarction (patients vs. controls: 26.9% vs. 6%; OR 5.77; 95%-CI 1.92–17.3; P = 0.0031) as well as of venous thrombosis (53% vs. 5.3% 19.9; 95%-CI 6–65.6; P 〈 0.0001). This result is in contrast with reports on thrombophilia in cerebral infarction in adult patients. Conclusion Our results indicate that FV Leiden mutation and protein C deficiency may contribute to the multifactorial aetiology of stroke in early childhood.
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  • 6
    ISSN: 1432-1076
    Keywords: Key words Haemophilia ; Intracranial haemorrhage ; Prevalence ; Neurological outcome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A survey among centres of the paediatric group of the GTH was performed to evaluate the prevalence and outcome of haemophiliacs with intracerebral haemorrhage. A questionnaire sent to the centres covered the following points: number of patients with severe, moderate and mild haemophilia A and B; for each patient with ICH: birth date, age at bleeding, aetiology and neurological sequelae. Overall, 30 ICH in 744 haemophiliacs (4.0%) were reported by 17/40 centres (42.5%). There was no significant difference between the prevalence of patients with haemophilia A and B (3.5% vs. 6.3%) and among the age groups. Bleeding was diagnosed within 1 week of birth in 11/27 patients (41%). For 3 patients, no age-related information was given. The most important factor was trauma (17/30 = 57%), either during birth (9/30 = 30%) or later in life (8/30  = 27%). Seizures were common, occurring in 19/30 patients (63%). As 1 patient died after posttraumatic ICH, the neurological outcome of 29 patients could be evaluated. Psychomotor and statomotor retardation and cerebral palsy were reported in 17/29 (59%), 15/29 (51%) and 13/29 (45%) patients respectively. Only 7/29 (24%) showed no neurological sequelae. Severity of deficits was not correlated with birth date but to age at bleeding. Older children showed a better neurological outcome than neonates. Conclusion The frequency and outcome of ICH in haemophiliacs have not changed in our cohort over the past 20 years. Trauma at birth is an important risk factor for ICH in patients with haemophilia A or B. lntracranial haemorrhages in older children are rare, and a better outcome may be expected.
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  • 7
    ISSN: 1432-1076
    Keywords: Key words Haemophilia A ; Thrombosis ; Continuous infusion ; F V Leiden ; Thrombolysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We report on a 14-year-old boy with severe haemophilia A who developed a portal vein thrombosis during continuous infusion of F VIII. For treatment of a posttraumatic intramural jejunal haematoma with extension into the mesenterium the patient received continuous infusion (CI) of a high purity F VIII concentrate, starting with an initial bolus injection of 100 IU F VIII/kg bw and followed by 4–5 IU F VIII/kg bw/h i.v. F VIII plasma activity ranged between 47 and 88%. Resorption of the haematoma was proven by abdominal ultrasonic follow-ups. After 3 weeks of CI a thrombus formation in the portal vein was detected by ultrasound and confirmed by duplex ultrasound. Subsequent to diagnosis the patient was heparinised with unfractionated heparin (UFH 300–450 IU/kg/d i.v.). In order to induce further resorption of the haematoma, F VIII concentrate was given concomitantly (50 IU/kg bw twice daily) during the initial phase of treatment. After 14 days of anticoagulant therapy with UFH, the regimen was changed to low molecular weight heparin (LMWH; Fraxiparin 0.3™; 2850 IU anti-X activity/d s.c.; bw 60 kg). F VIII dosage was gradually reduced with advanced resorption of the haematoma and thereafter switched to prophylaxis (40 IU/kg bw 3 times weekly). Complete lysis of the thrombus was observed after 6 months of treatment with UFH and LMWH respectively without any further complications. Thereafter LMWH was discontinued. Thrombophilic screening revealed no abnormalities except heterozygous F V G1691A. Conclusion The coexistence of a common prothrombotic risk factor and haemophilia may cause severe complications, in particular if the bleeding disorder has to be corrected temporarily by administration of the concerning deficient agent.
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  • 8
    ISSN: 1432-1076
    Keywords: Key words Antithrombin concentrate ; Children ; Septicaemia ; Acquired antithrombin deficiency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Consumption coagulopathy is a serious problem in childhood. In addition to treatment of the underlying disease, consumption coagulopathy was previously treated with heparin. Nowadays it is treated by substitution of coagulation factors, especially antithrombin (AT) concentrate, alone or in combination with heparin. In this pilot study we administered AT concentrate (dosage 80 U/kgbw/d), without additional heparin treatment, to 29 children beyond infancy with acquired AT deficiency. Antithrombin, platelet count, fibrinogen, PT, and APTT were assayed before and during the course of AT substitution. These coagulation parameters returned to normal 48 hours after normalisation of the plasma AT level. AT levels normalised within 24 h of initial substitution in all children. Lethal outcome due to the underlying disease was observed in only two children. Conclusion Data of this pilot study suggest that, concomitantly with the treatment of the underlying disease, consumption coagulopathy in childhood can be managed successfully with early substitution of AT concentrate.
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  • 9
    ISSN: 1432-1076
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 10
    ISSN: 1432-1076
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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