Y. Sakaguchi et al., ABSENCE OF ANTI-TRIFLUOROACETATE ANTIBODY AFTER HALOTHANE ANESTHESIA PATIENTS EXHIBITING NO OR MILD LIVER-DAMAGE, Canadian journal of anaesthesia, 41(5), 1994, pp. 398-403
It has been shown that the circulating antibodies, which bind to rat h
epatic microsomal proteins obtained after in vivo exposure to halothan
e, are detectable by immunoblotting in patients with ''halothane hepat
itis (HH),'' and that rabbit immunized anti-sera against trifluoroacet
ylated rabbit serum albumin (TFA-RSA) recognizes rat microsomal distor
ted polypeptides in almost the same way as do sera from patients with
HH. In this paper, we report first the development of a novel method o
f synthesizing TFA-RSA using p-nitrophenyl TFA, and second the results
of tests for circulating anti-TFA antibodies in the serum of 86 patie
nts who had received halothane anaesthesia and developed no (67 patien
ts) or mild (19 patients, the maximum activity of serum alanine aminot
ransaminase 519 IU.L(-1)) liver damage. Serum was selected from stored
sera of post-transfusion patients. The new method of synthesizing TFA
-RSA war convenient and was able to be done at neutral pH. Rabbit sera
obtained after immunization with the newly synthesized TFA-RSA recogn
ized the same polypeptides (109 kDa, 92 kDa, 80 kDa, 76 kDa, 64 kDa an
d 59 kDa) as the established anti-sera against TFA-RSA, and there reac
tions were inhibited in the presence of TFA-lysine. Circulating antibo
dies were not detected in our patients who had developed no or mild li
ver damage. The present finding supports the hypothesis that the appea
rance of circulating antibodies against microsomal distorted proteins
are specific to patients with HH. Furthermore, we have shown here that
the halothane-induced mild increase in ALT activity is not associated
with the appearance of those circulating antibodies, supporting the p
athophysiological difference between HN and halothane-induced mild hep
atic damage.