Forty two examinations utilizing F-18 FDG-PET were performed in 23 patients with Hodgkin's disease to study for involved lymphoma regions and compared to conventional staging procedures. Twenty stagings were performed at diagnosis of untreated Hodgkin's disease or at first relapse, and 22 restagings during and after chemoradiotherapy. At diagnosis in 5 of 20 patients PET and other procedures revealed different extranodal manifestations and in 3 patients established different clinical staging. PET seemed to be accurate in the assessment of lymphoma involvement in nodal sites. During follow up, in 10 out of 22 investigations different results and discrepancy were recorded, mostly due to the different extent of F-18-FDG metabolism in residual masses in lymphatic tissues compared to CT, X-ray or ultrasonography. The results indicate that PET may have advantages in the assessment of remissions in nodal sites. Less conclusive results were observed with regard to extranodal involvement or inflammatory disease. In conclusion PET may be sufficient for the staging of the majority of patients with Hodgkin's disease and particularly for assessing remission status in nodal sites, but PET may have disadvantages in the evaluation of extranodal lymphoma and inflammatory disease.

It is known that more than 95% of the serum ALP activity is derived from hepatocytes and osteoblasts. Therefore, in patients with normal liver function, serum ALP seems available as the index of bone formation. Indeed, serum ALP as well as BAP levels were elevated in our case after bortezomib-combined therapy. Bisphosphonate has been reported as the potent inhibitor of osteoclastic activity and to reduce the skeletal complications in MM. 4 But our patient did not show the definite elevation of serum ALP levels after prior incadronate-containing salvage therapy, and the inability of bisphosphonate to repair lytic bone lesions indicates that the functional defect of osteoblasts is also important in the lytic process. 5 In this case, he showed the remarkable elevation of serum ALP as well as BAP levels after receiving bortezomib in combination with incadronate and dexamethasone. Our case suggested that bortezomib might have an effect on the osteoblastic activity in addition to antimyeloma activity. The possible mechanism is the rapid disappearance of myeloma cells induced by bortezomib. Myeloma cells secrete at least two molecules that modulate the bone microenvironment in a manner favorable to tumor growth. Receptor activator of NF-kB ligand (RANKL) acts to stimulate osteoclast formation and activity, leading to bone erosion, whereas dickkopf1 (DKK1) appears to inhibit osteoblasts by the Wnt signal pathway, thus preventing repair of the lesions. 5 Thus, removal of myeloma cells decreased the inhibition of DKK1 on canonical Wnt signal pathway, resulting in osteoblast differentiation. 6 Activation of canonical Wnt pathway induces ALP activity. 7 Another mechanism is that bortezomib directly inhibited the secretion of DKK1 from osteoblasts, which results in the activation of Wnt signal pathway and osteoblast differentiation. Recently, Oyajobi et al demonstrated that bortezomib inhibited DKK1 expression in cell lines of mesenchymal origin, and stimulated the new bone formation in neonatal mouse calvariae. 8 This case suggests the presence of new action of bortezomib on bone formation, and this effect might benefit the bone disease in patients with MM. Further studies are required to clarify this hypothesis.