Bone mineral content in primary biliary cirrhosis

Bone mineral content in primary biliary cirrhosis

152 BONE MINERAL O 0 ~ IN PRIMARY BILIARY CIRRHOSIS T Almdal, O Schaadt, J V J~r~ensen, P Lind~reen & L Ranek D i v i s i o n of H e p a t o l o g ...

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152

BONE MINERAL O 0 ~

IN PRIMARY BILIARY CIRRHOSIS

T Almdal, O Schaadt, J V J~r~ensen, P Lind~reen & L Ranek D i v i s i o n of H e p a t o l o g y A - 2 1 5 1 , R i g s h o s p i t a l e t , 9 Blegdamsvej DK-2100 Copenhagen, Denmark. In a c r o s s - s e c t i o n a l s t u d y of 47 n o n - s e l e c t e d f e m a l e w i t h b i o p s y - p r o v e n Primary Biliary Cirrhosis (PBC) the B o n e M i n e r a l C o n t e n t (BMC) of the l u m b a r spine, f e m o r a l n e c k and f e m o r a l s h a f t w e r e d e t e r m i n e d u s i n g d u a l p h o t o n absoptiometry. The B M C - m e a s u r e m e n t s e x p r e s s e d as p e r c e n t of BMC m e a s u r e d in i d e n t i c a l l o c a t i o n in h e a l t h y f e m a l e b e l o n g i n g to the same d e c e n i u m w e r e as f o l l o w s ( m e a n SEM): L u m b a r s p i n e BMC: 8 7 . 5 + 2 . 2 % , F e m o r a l n e c k BMC: 9 1 . 7 + 1 . 9 % a n d F e m o r a l s h a f t BMC: 9 6 . 0 + 1 . 8 % , r e f l e c t i n g a p r e d o m i n a n t loss of t r a b e c u l a r bone. 7% (4/47) of the p a t i e n t s had c r u s h f r a c t u r e s of the spine. T h e s e p a t i e n t s w e r e s i g n i f i c a n t l y o l d e r , 7 1 + l years, t h a n t h o s e w i t h o u t c h r u s h f r a c t u r e s , 57+1 years, a n d h a d s i g n i f i c a n t l y l o w e r a b s o l u t e v a l u e s of l u m b a r s p i n e BMC T h a n t h o s e w i t h o u t f r a c t u r e s , 1 9 . 4 + 0 . 6 U/cm v e r s u s 2 6 . 5 + 0 . 8 U/cm. Patients treated with glucoco~ticoids h a d m e a n v a l u e s of BMC not d i f f e r e n t from o t h e r p a t i e n t s . T h e BMC v a l u e s did not c o r r e l a t e w i t h age, d u r a t i o n of PBC or w i t h any t e s t r e f e l c t i n g i m p a i r m e n t of l i v e r f u n c t i o n or c h o l e s t a s i s , i.e. A l b u m i n , A l k a l i n e P h o s p h a t a s e , B i l i r u b i n or P r o t h r o m b i n index. The S t u d y of p a r a t h y r o i d f u n c t i o n , D - v i t a m i n s a n d D - v i t a m i n b i n d i n g p r o t e i n did not c o n t r i b u t e to an u n d e r s t a n d i n g of the b o n e d i s e a s e of PBC, w h i c h m a i n l y seems to be due to o s t e o p o r o s i s .

153

HEPATITIS B VIRUS SERUM MARKERS AND ALCOHOL ABUSE: EFFECT OF THEIR SINGLE OR COMBINED PRESENCE ON THE PROGNOSIS OF LIVER CIRRHOSIS.

D.Anderlini, G.Cioni, A.Cristani t L.Di Pancrazio t S.Grandi t G. Minetto t M.L. Zeneroli and E.Ventura Clinica Medica III, Universit& di Modena, Italy. It seems well established that markers of hepatitis B are frequent in alcoholic liver disea se patients probably due to a high risk of infection. The aim of the present study was to ev E luate the prognosis of liver cirrhosis patients (LCp) due to alcohol or to hepatitis B with respect to those where both factors seem to be concomitant. In a population of 484 LCp we found 111 posthepatitic (HBsAg positive), 311 alcoholic (mean~SD alcohol intake 136~72 g/day) and 62 LCp with a history of alcohol abuse (115~55 g/day) and with hepatitis B serum marker (HBsAg). In these 3 groups the compensated LCp were respectively 55.9%, 50.2% and 46.8%. The graphs of survival function evaluated by the method of Peto et al. indicated a significant difference between the curve of alcoholic LCp and those of the other 2 groups. In fact the survival graphs of LCp with HBsAg positivity and those of LCp with HBsAg positivity and alcohol abuse were similar each other. The comparison of survival function using the Lee-Desu sta tistic showed significant difference (p < 0.01). The median survival time of alcoholics was 64.3,of HBsAg positives 27.4 and of alcoholics with HBsAg positivity 32.8 months. These data confirm the worse prognosis of posthepatitic LCp in comparison with the alcoholic type and seem to indicate that when both risk factors (alcohol and HBsAg) are present the prognosis is mainly influenced by the virus infection. This observation leads to the consideration that in therapeutic trials or in epidemiological studies, in order to reach a good selection of the patients, it might be more likely to classify these patients in the posthepatitic than in the alcoholic group or alternatively in a group of LCp of "mixed ethiology".

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