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8 A C T A M E D I C A M A R T I N I A N A 2 0 0 5 5/3 15. Liekens S, De Clerq E, Neyts J. Angiogenesis: regulators and clinical applications. Biochemical Pharmacology 2001; 61: 253-270 16. Tonini T, Rossi F, Claudio PP.Molecular basis of angiogenesis and Cancer. Oncogene 2003; 22: 6549-6556 17. Nor JE, Polverini PJ. Role of endothelial cell survival and death signals in angiogenesis. Angiogenesis 1999; 3: 101- 106 18. Ferrara N. The role of vascular endothelial growth factor in pathological angiogenesis. Breast Cancer Res Treat 1995; 36:127-137 19. Mecklenburg L, Tobin DJ, Muller-Rover S et al. Active hair growth (anagen) is associated with angiogenesis. J Invest Dermatol 2000; 114: 909-916 20. Hubler WR, Wolf JE. Melanoma, tumor angiogenesis and human Neoplasia. Cancer 1976; 38: 187-192 21. Pepper MS, Ferrara N, Orci L et al. Potent synergism between vascular endothelial growth factor and basic fibroblast growth factor in the induction of angiogenesis in vitro. Biochem Biophys Res 1992; 189: 824-831 22. Hannah D, Folkman J. Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis. Cell 1996; 86: 353-364 23. Marcoval J, Moreno A, Graelis J et al. Angiogenesis and malignant melanoma – angiogenesis is related to the development of vertical tumorigenic phase. J Cutan Pathol 1997; 24: 212-218 24. Kashani-Sabet M, Sagebiel RW, Ferreira CMM et al. Tumor vascularity in the prognostic assessment of primary cutaneous melanoma. J Clin Oncol 2Q002, 20 (7): 1826-1831 25. Jonjic N, Zamolo G, Stifter S et al. Cytomorphological variations, proliferation and angiogenesis in the prognosis of cutaneous melanoma. Clin and Exp Dermatol 2003; 28: 310-314 26. Straume O, Salvesen HB, Akslen LA. Angiogenesis is important in vertical growth phase melanomas. Intern J Oncol 1999; 15: 595-599 27. Neitzel LT, Neitzel CD, Magee KL et al. Angiogenesis correlates with metastasis in melanoma. Ann Surg Oncol 1999; 6 (1): 70-74 28. Urgurel S, Rappl G, Tilgen W, Reinhold U. Increased serum concentration of angiogenic factors in malignant melanoma patients correlates with tumor progression and survival. J Clin Oncol 2001;19 (2): 577-583 29. Staibano S, Boscaino A, Salvatore G et al. The prognostic significance of tumor angiogenesis in nonaggressive and aggressive basal cell carcinoma of the human skin. Hum Pathol 1996; 27 (7): 695-700 30. Razon MJ, Kraling BM, MullikenJB at al. Increased apoptosis coincides with onset of involution in infantile hemangioma. Microcirculation 1998; 5: 189-195 31. Boye E, Yu Y, Paranya G et al. Clonality and altered behavior of endothelial cells from hemangiomas. J Clin Invest 2001; 107: 745-752 32. Beck L, D’Amore PA. Vascular development: cellular and molecular regulation. FASEB J 1997; 11 (5): 365-373 33. Dosquet C, Coudert MC, Wassef M et al. Importance of bFGF for diagnosis and treatment of hemangiomas. Ann Dermatol Venereol 1998; 125(5): 313-316 34. Barker JNWN. Pathophysiology of psoriasis. Lancet 1991; 338:227-230 35. Braverman IM, Yen A. Ultrastructure of the capillary loops in the dermal papillae of psoriasis. J Invest Dermatol 1977; 68: 53-60 36. Braverman IM, Simbley BA. Role of microcirculation in the treatment and pathogenesis of psoriasis. J Invest Dermatol 1982; 78: 12 -17 37. Creamer D, Sullivan D, Bicknell R et al. Angiogenesis in psoriasis. Angiogenesis 2002; 5: 231-236 38. Bushan M, McLaughlin B, Weiss JB et al. Levels of endothelial cell - stimulating angiogenesis factor and VEGF are elevated in psoriatic epidermis. Br J Dermatol 1999; 141: 1054-1060 39. Creamer D, Allen M, Sousa A at al. Altered vascular endothelium integrin expression in psoriasis. Am J Pathol 1995; 147: 1661-1667 40. Kuroda K, Sapadi A, Shoji T et al. Altered expression of angiopoetins and Tie 2 receptor in psoriasis. J Invest Dermatol 2001; 116:713-720 41. Rosen L. Antiangiogenic Strategies and agents in clinical trials. The Oncologist 2005; 5: 20-27 Received: August, 8, 2005 Accepted: November, 2, 2005
A C T A M E D I C A M A R T I N I A N A 2 0 0 5 5/3 9 POSTNATAL PROPHYLAXIS OF EARLY-ONSET GROUP B STREPTOCOCCAL INFECTIONS IN NEWBORNS – A PILOT STUDY LUCIA ŠTILLOVÁ, MIRKO ZIBOLEN, INGRID KRAUSOVÁ, ZUZANA STRECHOVÁ Department of Neonatology, Jessenius Faculty of Medicine, Comenius University, Faculty Hospital of Martin, Martin, Slovakia A b s t r a c t Recently, Streptococcus agalactiae or group B Streptococcus (GBS), is the leading cause of early-onset infections in newborns. Neonatal Early-Onset Group B Streptococcal Disease (EOGBSD) is manifested mostly as sepsis, and it remains the most frequent cause of morbidity and mortality in neonatal period. Maternal intrapartum GBS colonization is a major risk factor for EOGBSD. Maternal intrapartum antibiotic prophylaxis (IAP) does not prevent all cases of the disease. Management of asymptomatic neonates of GBS colonized mothers is problematic. Evidence supports the use of postnatal intramuscular penicillin in newborns to prevent EOGBSD. The authors of the article prefer IAP combined with postnatal antibiotic prophylaxis (PAP) in a defined group of newborns at risk of the disease, using strict indication criteria. The aim of the pilot study is to design an optimal strategy for administering PAP. The authors have created a protocol for management of a full-term infant born to a GBS colonized mother. The study is prospective, the study sample consists of 100 full-term newborns with adequate postnatal adaptation. Out of 100 infants, PAP was administered to 9 infants. In 8 of them the indication criteria included leucocytosis, in 1 case additional obstetrical risk factors. In the study group there was no case of clinically manifest infection, and no case of sepsis, either suspected or proven. The authors suggest that the strategy of selective PAP using penicillin, may be an effective and safe method in order to reduce morbidity and mortality from streptococcal infections. They recommend a combination of IAP and selective PAP. K e y w o r d s : neonatal sepsis, early-onset infection, Streptococcus agalactiae, Group B Streptococcus (GBS), penicillin prophylaxis INTRODUCTION Today, Streptococcus agalactiae or Lancefield group B Streptococcus (GBS), is identified as the leading cause of invasive bacterial infections in neonates (1). At our clinic there were 11.6 % of preterm newborns affected with early-onset infection and the culture showed that the most frequent pathogen found in mothers was GBS (16.2 %) (2). Sepsis remains the most frequent cause of morbidity and mortality in neonatal period. Incidence of sepsis is the highest in neonatal period in comparison to other periods of life (3, 4). Early-onset neonatal sepsis is defined if clinical signs are developed within the first 72 hours of life (5). It is associated with severe, mostly fulminant course and high case fatality rate. Still, there is no appropriate laboratory marker for early diagnosing of neonatal sepsis (3).Although neonatal Early-Onset Group-B Streptococcal Disease (EOGBSD) is rare, it is the most common cause of serious infection in newborn babies. The EOGBSD or perinatal form of GBS disease, typically occurs within the first 24 hours of life in most of the patients (6), with fulminant sepsis or pneumonia and less often with meningitis. The attack rates for the EOGBSD range from 0.5 or 1 to 4 cases per 1,000 live births (7, 8). Earlyonset disease accounts for approximately 80 % of GBS cases (9). The reported case fatality rate is 5 - 20 %, even 20 – 60 % (10, 8). Maternal intrapartum GBS colonization is a major risk factor for EOGBSD in infants. Women with prenatal GBS colonization were 25 times more likely than women with negative prenatal cultures to deliver infants with the disease (1). The prevalence of recto-vaginal colonization among pregnant women ranges from 15 to 40 % (11). The colonization is dynamic, and it is usually asymptomatic. Carriers are identified by bacteriological testings. Colonization of newborns Address for correspondence: Lucia Štillová, Gen. Svobodu 84, 03601 Martin, Slovakia Phone: +421 904 445 271 e-mail: lucanovalucia@zoznam.sk
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