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20 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 ters when comparing to other three drugs, least of all. We enrolled in our transversal study all registered patients with JIA who met the basic research requirements. Six of them were treated with triamcinolone before. Cumulative doses and duration of each drug administration were studied retrospectively. This is the reason why also patients treated with this drug were enrolled. Duration of corticosteroid therapy influenced somatic parameters in a very interesting way. Children treated with prednisone were expected to be influenced negatively most of all, but only two significant correlations of duration of prednisone therapy were found in oligoarticular patients. The most significant dependences of somatic parameters on duration of administration were found in children with systemic JIA form treated with methylprednisone. For comparing somatic parameters of individual JIA forms within the whole group of 81 children the analysis of variance was used. Systemic JIA was statistically different from oligoarticular and polyarticular in thirteen somatic parameters (81%). Only in wrist circumference and BMI no statistically significant differences were found. Statistically significant differences between JIA types in children treated with corticoids were found in ten somatic parameters (62.5%), always in relation to the systemic disease. Our results show that in children treated with corticoids there were no statistically significant differences among JIA types in six somatic parameters only. We found out, that systemic JIA differed from oligoarticular and polyarticular in all other parameters. The results of our study confirm the negative influence of corticoids on the body growth of children with JIA. No statistically significant differences in somatic parameters were found between boys and girls. Neither the child’s age of illness manifestation, nor the illness duration influenced somatic parameters of our patients with JIA. The most negative influence was proved in methylprednisone and systemic JIA form. REFERENCES 1. Jacobs JC. Pediatric rheumatology for the practitioner. New York: Springer-Verlag; 1993. 2. Still GF. On a form of chronic joint disease in children. Med Chir Trans 1897; 80: 47. 3. Ansell BM, Bywaters EGL. Growth in Still_s disease. Ann Rheum Dis 1956; 15: 295-319. 4. Bacon MC, White PH, Raiten DJ, Craft N, Margolis S, Levander OA. Nutritional status and growth in juvenile rheumatoid arthritis. Seminars in Arthritis and Rheumatism 1990; 20: 97-106. 5. Bennett AE, Silverman ED, Miller JJ, Hinty R. Insulin - like growth factor I and II in children with systematic onset juvenile arthritis. J Rheumatol 1998; 15: 655-668. 6. Cassidy JT, Hillman LS. Abnormalities in skeletal growth in children with juvenile rheumatoid arthritis. Pediatr Rheumatol 1997; 23: 499-522. 7. Polito C, Strano CG, Olivieri AN, Alessio M, Iammarrone CS, Todisco N, Papale MR. Growth retardation in nonsteroid treated juvenile rheumatoid arthritis. Scan J Rheumatol 1997; 26: 99-103. 8. Saha MT, Verronen P, Laippala P. Growth of prepubertal children with juvenile chronic arthritis. Acta Paediatr 1999; 88: 724-28. 9. Truckenbrodt H, Häfner R. Allgemeine und lokale Wachstumsstörungen bei chronischer Arthritis im Kindesalter. Schweiz Med Wschr 1991; 121: 608-20. 10. Zerin JM, Rockwell DT, Garn SM, Schlesinger AE, Sullivan DB. Carpo-metacarpal growth disturbance and the assessment of carpal narrowing in children with juvenile rheumatoid arthritis. Invest Radiol 1991; 26: 727-33. 11. Bláha P. et al. Antropometrie československé populace od 6 do 55 let. Československá spartakiáda 1985. Praha: ÚNZ VS; 1986. 12. Laaksonen AL. A prognostic study of juvenile rheumatoid arthritis. Acta Pediatr Scan 1966; 55: Supl. 13. Kotaniemi A. Growth retardation and bone loss as determinants of axial osteopenia in juvenile chronic arthritis. Scan J Rheumatol 1993; 26: 14-18. 14. Kotaniemi A, Savolainen A, Kautiainen H, Kröger H. Estimation of central osteopenia in children with chronic polyarthritis treated with glucocorticoids. Pediatrics 1993; 91: 1127-29. 15. Reeve J, Loftus J, Hesp R, Ansell BM, Wright DJ, Woo PMM. Biochemical prediction of changes in spinal bone mass in juvenile chronic (or rheumatoid) arthritis treated with glucocorticoids. J Rheumatol 1993; 20: 1189-95. 16. Kuhns JG, Swaim LT. Disturbances of growth in chronic arthritis in children. Am J Dis Child 1932; 43: 1118. Received:August, 8, 2005 Accepted: October, 27, 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 21 ASSESSMENT OF THE IN SITU COMPONENT IN DUCTAL INVASIVE CARCINOMAS BY VAN NUYS CLASSIFICATION KAROL KAJO 1 , PAVOL ŽÚBOR 2 , KATARÍNA MACHÁLEKOVÁ 1 , SILVESTER GALO 2 1 Department of Pathology, Jessenius Faculty of Medicine, Comenius University and Martin Faculty Hospital, 2 Department of Obstetrics and Gynaecology, Jessenius Faculty of Medicine, Comenius University and Martin Faculty Hospital, A b s t r a c t The purpose of this study was to assess the in situ component in ductal invasive carcinomas by Van Nuys classification – VNC and to provide correlations of ductal carcinoma in situ - DCIS together with other prognostic indices in ductal invasive carcinoma - DIC (histological grade, vascular invasion, hormone receptor status and Nottingham prognostic index - NPI). 106 cases of DIC with DCIS were analyzed in the study. DCIS were evaluated by the Van Nuys classification and divided into three groups (VNC1-3). We have taken the architectonic classification in consideration (comedo type, cribriform, solid, micropapillary type) when we were making enlistments. General agreement between VNC groups of DCIS and ductal invasive carcinoma grades was in 79 cases (75%). DIC cases with high grade (n G3 =54) achieved this agreement in 93%. Differences between VNC groups and grade, vascular invasion, NPI and hormone receptors reached the level of statistical significance (p
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