Antinuclear Antibodies in Primary Biliary Cirrhosis

Abstract

Ethanol connumption had been shown t o r e s u l t i n an increase in hepatocyte s i z e which is due t o ap increase i n i n t r a c e l l u l r r water (Orrego et al mechanism by which this could occur is by an effect on the membrane bound encyme Na+, K+-ATPaae. The purpose of the present study WM t o investigate t h e possible d i r e c t e f f e c t s of ethanol and its m a i n metabolite acetaldehyde on the a c t i v i t y of t h i s enzyme and other pl-a membrane bound enzymes, Mg++ ATPase and FNucleot i h e (5-Nt). libllowing the in vitro addition of e t h m o l or acetaldehyde, enzyme a c t i v i t i e s were meamred spectrophotolaetricdly from the releese of inorganic phosphate from ATF'or AMP i n isolated rat hepatocyte plagra membranes. No significant inhibition of Na+, K+-ATPMe a c t i v i t y by ethanol WM seen over a concentration range of 8 mmol/L t o 100 mol/L (50 mg% t o 500 a&). b a n bMal a c t i v i t y , following 8 m o l / L and 100 m o l / L ethanol were: 23'9+SD 2.7. 2).2+SD 2.5, 22.6+sD 3.2 umol Pi& protdn/h'; reupectively. Lack of inhibition of enzyme a c t i v i t y with acetaldehyde over a range of 10 umolh t o 3 mol/L was also found. A c t i v i t i w of Mg++ ATPaae and 5-Nt were also unaffected by both ethanol and acetaldehyde at these concentration ranges. However, at higher concentrations, a generalised non-competitive inhibition of these enzyme8 W M found: inhibits: Na+, K+-ATpase 19% (pCOo.O1), Ug++ ATPM~ 15% (N.S.), 5-Nucleotidase 3.2% (N.S.). Alcohol (494.6 mol/L): 64%. %% and 13% respectively (p<O.01, i n each case). Acetaldehyde (6 mol/L): 18% (p~O.ol), 6% (N.S.)and 21% (pt0.01) respectively. Acetaldehyde (56 mmol/L) 508% 21% and 85% respectively (p<O.OOl in each carre). We conclude t h a t the acute administration of ethanol and its main metabolite acetaldehyde, i n concentrations up t o those found i n the blood of heavy drinkers, has no d i r e c t e f f e c t on the a c t i v i t y of N+, K+-ATPUe.

Differential recognition of the 52-kd Ro(SS-A) antigen by sera from patients with primary biliary cirrhosis and primary Sjogren's syndrome

“…Two PBC patients who were not included in the PBC/SS group expressed anti-52-kd antibodies without sicca symptoms, as previously reported by others. 7,25 Both patients' sera contained anti-52-kd Ro(SS-A) antibodies comparable to those in PBC/SS serum samples and recognized fragments A1, E, and A1-2, respectively. Moreover, three patients with classical secondary Sjögren's syndrome did not contain antibodies to Ro(SS-A).…”

“…Different rheumatological manifestations of PBC patients, various Protein E, carrying AA 197-245, was found to show a strikingly lower reactivity with the same sera than with frag-PBC patient subsets, or patients with overlap syndromes such as PBC/SS, PBC/scleroderma, or PBC/Calcinosis, Ray-ments A1 and F. This constellation could be explained by the hypothesis that a considerable part of the major immunonaud, Esophagus dysmotility, sclerodactylie, Teleaugiest syndrome have been described. 1,[3][4][5][6][7][8][25][26][27][28][29] Frequently, character-genic region is not linear, 30,31 but that this region may be discontinuous or conformational and may even require furistic disease-associated autoantibodies such as anticentromere, anti-Scl-70, and anti-Ro(SS-A)/La(SS-B) antibodies ther N-terminal sequence modification to acquire full antigenicity. Serological characteristics in primary biliary cirrhosis associated with to be both qualitatively and quantitatively different from that sicca syndrome.…”

Differential recognition of the 52-kd Ro(SS-A) antigen by sera from patients with primary biliary cirrhosis and primary Sjogren's syndrome

“…Different rheumatological manifestations of PBC patients, various Protein E, carrying AA 197-245, was found to show a strikingly lower reactivity with the same sera than with frag-PBC patient subsets, or patients with overlap syndromes such as PBC/SS, PBC/scleroderma, or PBC/Calcinosis, Ray-ments A1 and F. This constellation could be explained by the hypothesis that a considerable part of the major immunonaud, Esophagus dysmotility, sclerodactylie, Teleaugiest syndrome have been described. 1,[3][4][5][6][7][8][25][26][27][28][29] Frequently, character-genic region is not linear, 30,31 but that this region may be discontinuous or conformational and may even require furistic disease-associated autoantibodies such as anticentromere, anti-Scl-70, and anti-Ro(SS-A)/La(SS-B) antibodies ther N-terminal sequence modification to acquire full antigenicity. …”