Published online Feb 15, 1999. doi: 10.3748/wjg.v5.i1.61
Revised: November 22, 1998
Accepted: December 13, 1998
Published online: February 15, 1999
AIM To investigate the pathophysiologic basis of syndrome of Liver-Qi stagnation and parame-ters for clinical differentiation.
METHODS Plasma L-ENK, AVP, ANP and serum gastrin were determined by RIA in 84 patients with neurasthenia, mastodynia, chronic gastri-tis, and chronic cholecystitis presenting the same syndrome of Liver-Qi stagnation in tr adi-tional Chinese medicine (TCM). Healthy subjects served as controls in comparison with patients having the same syndrome but with different diseases.
RESULTS Among the patients with Liver-Qi stagnation, the plasma L-ENK, ANP and gastrin levels were 38.83 ng/L ± 6.32 ng/L, 104.11 ng/L ± 29.01 ng/L and 32.20 ng/L ± 6.68 ng/L, being significantly lower than those in the healthy controls (P < 0.01, t = 3.34, 6.17, 4.48). The plasma AVP of the patient group (52.82 ng/L ± 19.09 ng/L) was significantly higher than that of the healthy contr ols (P < 0.01, t = 5.79). The above changes in patients having the same symptom complex but different diseases entities showed no significant differences, P > 0.05.
CONCLUSION The syndrome of Liver-Qi stagnation is closely related to the emotional modulatory abnormality of the brain, with decrease of plasma L-ENK, ANP and gastrin, and increase of plasma AVP as the important pathophysiologic basis.