Correlation of sonographic severity with biochemical markers of synovium and cartilage in knee osteoarthritis patients.

OBJECTIVE: Ultrasonography can be used to detect soft tissue abnormalities within the joints that cannot be assessed using conventional X-rays. This study investigated the relationship between soft tissue and/or bony abnormalities on ultrasonography and the biochemical markers of the synovium and cartilage in the knee of osteoarthritis (OA) patients. METHODS: The knees from 51 OA patients who fulfilled the ACR criteria were enrolled in this study. Knee ultrasonography was performed in the affected knee joints using a 12 MHz linear probe to assess the presence of effusion, synovial proliferation, capsular distention, the length of osteophytes and the cartilage thickness. At the same time, the serum hyaluronic acid (HA) and the cartilage oligomeric protein (COMP) levels were measured by ELISA, and RIA was used to determine the serum osteocalcin levels. RESULTS: The patients with a longer medial osteophyte showed higher serum HA and COMP levels than those with a shorter one. The serum HA levels were significantly higher in those patients with a larger amount of effusion and/or synovial proliferation, which indicated inflammatory changes, than in those without. In addition, the severity of the capsular distention also correlated well with the serum HA and COMP levels. However, the length of the lateral osteophytes and the thickness of the femoral cartilage showed no correlation with the serum HA or COMP levels. In addition, the serum osteocalcin levels did not show any association with the above ultrasonographic parameters. CONCLUSION: This study demonstrated that the serum HA and COMP levels were elevated in the more severe OA patients by knee ultrasonography than in the less severe patients. This suggests that the detailed pathological changes in the soft tissue and/or bone of the OA joints on ultrasonography are directly reflected by the biochemical markers measured in the peripheral blood.

PAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction.

BACKGROUND: Progressive renal disease is characterized by the induction of plasminogen activator inhibitor-1 (PAI-1), suggesting that impaired activity of the renal plasmin cascade may play a role in renal fibrosis. METHODS: To test this hypothesis, the severity of renal fibrosis caused by unilateral ureteral obstruction (UUO) was compared in PAI-1 wild-type (+/+) and PAI-1 deficient (-/-) mice. The extent of interstitial inflammation and fibrosis, renal plasminogen activator and plasmin activity, and renal expression of profibrotic genes was evaluated after 3, 7, and 14 days of UUO. RESULTS: Renal PAI-1 mRNA levels increased 8- to 16-fold in the +/+ mice after UUO surgery, and PAI-1 protein was detected in kidney homogenates. Interstitial fibrosis was significantly attenuated in -/- mice compared with +/+ mice at day 7 and day 14, based on the interstitial area stained with picrosirius red and total kidney collagen content. However, neither the mean renal plasminogen activator nor plasmin activities were increased in -/- mice compared with +/+ mice. The number of interstitial macrophages were significantly lower in the -/- mice three and seven days after UUO; interstitial myofibroblasts were significantly fewer at three days. At the same time points, this altered interstitial cellularity was associated with a significant reduction in renal mRNA levels for transforming growth factor-beta and procollagens alpha 1(I) and alpha 1(III). CONCLUSIONS: These studies establish an important fibrogenic role for PAI-1 in the renal fibrogenic response. The results demonstrate that one important fibrosis-promoting function of PAI-1 is its role in the recruitment of fibrosis-inducing cells, including myofibroblasts and macrophages.

Treatment of chronic hepatitis B with lamivudine in renal transplant recipients.

BACKGROUND: Lamivudine is a potent inhibitor of hepatitis B virus replication. Little has been reported about the efficacy and safety of lamivudine in the treatment of chronic hepatitis B in the setting of renal transplantation. METHODS: Two patients were treated for chronic hepatitis B with lamivudine and subsequently underwent renal transplantation. Four other patients were treated with lamivudine for reactivation of hepatitis B after renal transplantation. Chronic hepatitis B was proven histologically in all the patients. The doses of lamivudine ranged from 100 to 150 mg/day. Hepatic enzyme and viral markers were monitored. RESULTS: Lamivudine was well tolerated for a median duration of 8 months (range, 4-14 months) without significant side effects. Viral replication was suppressed, as evidenced by negative conversion of serum hepatitis B virus DNA in all the patients. Hepatic enzyme was also normalized. Modification of doses of immunosuppressant regimen was not required in using lamivudine in all patients. One patient experienced acute rejection and responded to solumedrol pulse therapy with normalization of graft function. Normal graft function was maintained in other patients while they were treated with lamivudine. CONCLUSION: Lamivudine was a safe and effective therapy for activated hepatitis B in renal transplant recipients in the short term.