Figure 1
Figure 1. Time course of GVHD and CK18F levels in representative patients. (A) Patient UPN 211: slight increase of basal CK18F levels (132 U/L) during acute GVHD I of the skin (day 40, 162 U/L) responding to steroid treatment. CK18F started to rise immediately after steroid reduction and at least 1 week prior to the onset of clinical symptoms of GVHD grade III of the gut. Steroid resistance of the latter episode was reflected by constantly high levels of CK18F after 7 days of high-dose prednisolone treatment. (B) Patient UPN 297: an episode of veno-occlusive disease (VOD) with high serum bilirubin levels following SCT did not coincide with increases in CK18F levels. Liver GVHD developed during reduction of CsA after day 100, which was accompanied by a brisk CK18F increase. This episode of GVHD immediately responded to the restoration of high CsA levels. (C) Patient UPN 275 developed chronic GVHD (liver and wasting syndrome) after CsA reduction. CK18F levels started to rise early after beginning of CsA tapering, whereas liver enzymes became elevated only 50 days thereafter. This episode of GVHD rapidly responded to renewed CsA treatment as shown by normalization of both CK18F and ALAT levels. (D) Patient UPN 301 developed acute GVHD grade IV of skin, liver, and gut as early as 10 days following SCT. Despite high-dose steroid treatment, GVHD progressed and bilirubin levels rose to 10 mg/dL, requiring second-line immunosuppressive treatment (pentostatin). CK18F fell below 300 U/L following steroid and penostatin therapy, which indicated reduced epithelial apoptotic activity and thereby response to treatment. However, this response was not noticed clinically, as the skin rash, diarrhea, and hyperbilirubinemia went unresolved. Therefore, therapy was switched to anti-CD25 (basiliximab), which could not prevent subsequent deterioration (fatal progress of GVHD in all 3 organs). (E) Patient UPN 363 developed GVHD of the skin around day 60. Intestinal symptoms started after day 90 and bilirubin levels rose after day 100. GVHD grade IV of the gut was histologically confirmed. Prednisolone was started on day 90; however, the GVHD progressed and salvage therapies were given. The patient did not respond to any of these treatments and subsequently died. This lack of clinical response was reflected by persistently high levels of CK18F. Note the reduction in sCD25 levels following steroid treatment.

Time course of GVHD and CK18F levels in representative patients. (A) Patient UPN 211: slight increase of basal CK18F levels (132 U/L) during acute GVHD I of the skin (day 40, 162 U/L) responding to steroid treatment. CK18F started to rise immediately after steroid reduction and at least 1 week prior to the onset of clinical symptoms of GVHD grade III of the gut. Steroid resistance of the latter episode was reflected by constantly high levels of CK18F after 7 days of high-dose prednisolone treatment. (B) Patient UPN 297: an episode of veno-occlusive disease (VOD) with high serum bilirubin levels following SCT did not coincide with increases in CK18F levels. Liver GVHD developed during reduction of CsA after day 100, which was accompanied by a brisk CK18F increase. This episode of GVHD immediately responded to the restoration of high CsA levels. (C) Patient UPN 275 developed chronic GVHD (liver and wasting syndrome) after CsA reduction. CK18F levels started to rise early after beginning of CsA tapering, whereas liver enzymes became elevated only 50 days thereafter. This episode of GVHD rapidly responded to renewed CsA treatment as shown by normalization of both CK18F and ALAT levels. (D) Patient UPN 301 developed acute GVHD grade IV of skin, liver, and gut as early as 10 days following SCT. Despite high-dose steroid treatment, GVHD progressed and bilirubin levels rose to 10 mg/dL, requiring second-line immunosuppressive treatment (pentostatin). CK18F fell below 300 U/L following steroid and penostatin therapy, which indicated reduced epithelial apoptotic activity and thereby response to treatment. However, this response was not noticed clinically, as the skin rash, diarrhea, and hyperbilirubinemia went unresolved. Therefore, therapy was switched to anti-CD25 (basiliximab), which could not prevent subsequent deterioration (fatal progress of GVHD in all 3 organs). (E) Patient UPN 363 developed GVHD of the skin around day 60. Intestinal symptoms started after day 90 and bilirubin levels rose after day 100. GVHD grade IV of the gut was histologically confirmed. Prednisolone was started on day 90; however, the GVHD progressed and salvage therapies were given. The patient did not respond to any of these treatments and subsequently died. This lack of clinical response was reflected by persistently high levels of CK18F. Note the reduction in sCD25 levels following steroid treatment.

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