蛋白喪失性腸症の病因に関する臨床的, 実験的研究

抄録

Six cases with protein-losing enteropathy, four with intestinal lymphangiectasia and two with constrictive pericarditis, were studied clinically with aid of RISA test, ¹³¹I-PVP test, peritoneoscopic examination, lymphangiography and thoracic duct cannulation.
In the former, it was concluded that the duration of intestinal lymph congestion caused abnormal intestinal protein loss, and that the lymph congestion was attributed to the stenotic lesions of the lymphatic system located between mesenteric lymphatics and thoracic duct.
In the latter, it was the primary cause of intestinal protein loss that the elevated venous pressure increased unusually lymph production and disturbed moreover lymph reflex to venous veins.
Experimental study was designed to make clear the mechanism of abnormal intestinal protein loss in intestinal lymphangiectasia.
The male rats fed on basal diet were injected intravenously with 2μc of ¹³¹I-PVP.
The fecal excretion of ¹³¹I-PVP within 24 hours after injection were determined.
When the mesenterial lymphnodes were resected as many as possible, no difference between normal and five days group was found. Abnormal fecal excretion of ¹³¹I-PVP were demonstrated in about half numbers of each group from one to seven weeks. That is, about one week duration of lymph congestion seemed to be necessary for giving rise to abnormal intestinal protein loss. After the thoracic duct ligation, abnormal fecal ¹³¹I-PVP excretion was seen in each group from one to four weeks. But it was not demonstrated after five weeks, suggesting that the collateral formation of lymph vessles saved the intestine from lymph congestion and abnormal protein loss.
In the immunized group with isologous lymphnode homogenate incorporated in Freund's complete adjuvant, abnormal ¹³¹I-PVP excretion were shown in four of six animals at five weeks after thoracic duct ligation. The collateral lymph vessles formation was believed to be disturbed by this immunological procedure. Even in the immunized group with Freund's complete adjuvant only, abnormal ¹³¹I-PVP excretion were demonstrated at five weeks after thoracic duct ligation.
Accordingly, the disturbance of collateral lymph vessles formation was attributed to the lymphatic tissue damage, which was developed presumably on the basic of either specific or non-specific hyper-immune reaction of lymphatic tissue.
Besides, some case of the above-mentioned two kinds of immunized groups, who received no ligation of thoracic duct, revealed also abnormal ¹³¹I-PVP excretion.
It was supporsed that the stenotic lesion of lymphatic tissue and the disturbance of collateral lymph vessles formation were could be originated by these immunological procedures.