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L I V ~ Fl~Cl'IO~ I)~I~ DIABETIC K E T O A ~
LIVER STEATOSlS AND HCV INFECTION
R.Koeid,M.Milenovid,M.Veloji6,S.Radenkovi6~Z.Burazor G.KoradevidtG.Kocid.Clinic for Endocrinology and Institut of Biochemistry,University Ni§,Yugoslavia
G.Montalto,M. Soresi,F.Arasona,C.M.Barbasallo,A.Carroccio,S.Tripi,A.Notarbartolo. Cattedra dl Medicina Interna, Universit~ di Palermo, Italy.
Long-term poorly controled Insulin-dependent diabetes mellitus is characterised by the pathophysiological alteration of many organs and systems,including liver.The study was performed with theaa~mto evaluate how diabetic ketoacidosis can affect liver function.Moreover,the other question was if the level of serum enzymes correlate with the glucose and insulin level.The study included 14 diabetic patients(6 women and 8 men)with the diabetic ketoacidosis, evaluated by the clinical and laboratory tests. Results:In spite of clinicaly registrated nausea, abdominal pain and vomiting,hepatomegaly was present in 35,71%.In men sAST was 40,13+4,16, sALT36,52+3,84 sAP 50,44+5,35,insulin 3,22+O,3~,glucose 25,34+~,86. In women,~AST was 46,31+6,~2,sALT 42,48+2,65 ~AP 57,32+6,18(IU/l).Serum i~sulin was 2,98+T, 18 and glucose 29,34+8,32(mmol/l).Evaluating t~e level of the correlation it has been concluded that it was negative with the serum Insulin,bu positive with the p~mum ~ucose level: r Ins./sAST r Ins./aALT r Ins./AP men -0,33 -0,18 -0,24 women -0,47 -0,23 -O,48 r Gluc./sAST r Gluc./sAiT r Gluc./AP men 0,36 0,38 O,19 women 0,47 0,39 0,34 In conclusion,given results indicate that liver function is affected during diabetic ketoacidosis.
RANDOMIZED DOUBLE-BLIND TRIAL OF URSODEOXYCHOLIC ACID (UDCA) VS PLACEBO FOR TOTAL PARENTERAL NUTRITION-ASSOCIATED LIVER DYSFUNCTION T,E, Kowalski. M. Bosse. J,L, Mullen, P,R. Holt*. G.$, Tint**. P.F. M a l ~ Depts. of Medicine & Surgery, U of Pennsylvania & VAMC, Philadelphia & *St. Luke'sRoosevelt Hosp., New York & **VAMC, E. Orange, USA. Liver dysfunction may affect 10-20% of patients on longterm total parenteral nulrition (TPN). Aim; to evaluate in a controlled fashion the effect of UDCA on serum liver enzymes in TPN-associated liver dysfunction. Methods: patients on long-term home TPN with 1.5 times elevation of_> 2 liver enzymes in whom other etiologies were excluded were randomized to receive in a double-blind fashion either UDCA (300 mg bid) or placebo for 6 months with serial liver enzymes & serum UDCA levels. Study m'O~lp: Of 61 patients on long-term TPN, 18 (29%) had 1.5 times elevation of liver enzymes. 6 were excluded: 3 had other etiologies, 1 was gravely ill & 2 were already receiving UDCA. Of the remaining 12, 4 declined and 8 were randomized. Results: baseline liver enzymes were similar in both groups; at 6 months, the UDCA group showed a significant (p<0.05) decrease in: (+ or- change from baseline+_SE for placebo (n--4) & UDCA (n--4) groups, respectively): AST: +3.3+_3.3 vs -36+7, ALT: +3.5+_3.5 vs -88+17, GGT: +54+25 vs 75+13 and alkaline phosphatase: +23+13 vs -72~12. Serum UDCA levels increased to 2.3_+0.5 p.g/ml in the UDCA group vs 0.4_+0.4 in the placebo group. Conclu~i0n: UDCA significantly reduced liver enzymes in patients on long-term TPN with liver dysfunction; whether it also alters histology or natural history remains unanswered.
We determined the frequency of liver steatosis and its relationship with a number of lipid parameters in a group of anti-HCV positive (RIBA II confirmed) patients with chronic active hepatitis (CAH), hlsto logically proved. No patients had other pathologies associated with liver steatosis. At biopsy, the fol lowing were assayed: total cholesterol, triglycerldes, HDL-cholesterol, Apoprotein A1 and B, and lipoprotein (a). Steatosis were divided into macro and microvacuolar types and a semiquantitative score, ranging from 0 to 4 (from absent to severe) was calculated. Steatosis prevalence was 83%, macro vacuolar 61% and microvacuolar 22%. No statistically significant differences were found in any of the lipid parameters between patients with and those wi thout steatosis and between macro and microvacuolar steatosls. The graduated steatosis score was only statistically significant for stafe 4 vs the others for triglyceride values (p<.05). In conclusion, our data suggest a high frequency of steatosis in antiHCV positive patients, with no relationship with circulating lipid levels. There is probably an intrahepatic interference by virus C on lipid metabolism, and further studies are necessary to determine the mechanism involved.
E F F E O ~ B OF C A F F E I N E O N P O L Y A M I ~ OXIDASE AND DIAMINE OXIDASE ACTIVITY IN ~ LIVER OF ~w~ R A T J . N i k o l i 6 and G. B S e l a k o v i 6 , I n s t i t u t e of B i o c h e m i s t r y , F a c u l t y of M e d i c i n e , Ni§ University, Yugoslavia C a f f e i n e , w h i c h is p r e s e n t in coffe, tea or o t h e r f o o d p r o d u c t s , is one of the mo st w i d e l y c o n s u m e d drug. It has b e e n sho w n that its c o n s u p t i o n leads to a l t e r a t i o n of m a n y m e t a b o l i c p r o c e s e s . The aim 9~this s t u d y is to i n v e s t i g a t e th~ i n f l u e n c e of c a f f e i n e on m e t a b o l i s m of p o l y a m i n e s . We h a v e i n v e s t i g a t e d the a c t i v i t y of p o l y a m i n e o x i d a s e a n d d i a m i n e o x i d a s e a c t i v i t y a f t e r acute and c h r o n i c ad m i n i s t r a t i o n of c a f f e i n e to rats. E n z y mes a c t i v i t y was d e t e r m i n e d in the l i v e r h o m o g e n a t e on the b a s i s of the p r o d u c e d aminoaldehydes ( B u c h r a c h and R e c h e s , 1 9 6 6 ) One h o u r a f t e r a d m i n i s t r a t i o n of c a f f e ine in a d o s e of @ O m g per rat, d i a m i n e o x i d a s e a c t i v i t y was d e c r e a s e d , w h i l e , p c l y a m i n e o x i d a s e was not c h a n g e d . 5 d a y s t r e a t m e n t of r a t s w i t h c a f f e i n e leads to e l e v a t i o n of b o t h e n z y m e s . ~nese r e s u l t s i n d i c a t e t h a t c a f f e i n e int ake a l t e r s the a c t i v i t y of e n z y m e s w h i c h p a r t i c i p a t e in m e t a b o l i s m of p o l y a m i n e s .