Reduced pain with use of proprietary hyaluronic acid with lidocaine for correction of nasolabial folds: a patient-blinded, prospective, randomized controlled trial.

BACKGROUND: Pain during and after implantation of dermal gel fillers is a consistent complaint of patients undergoing soft tissue augmentation. Reduction of pain during injection would increase patient comfort and improve the overall patient experience. OBJECTIVE: To evaluate pain at the injection site during and after the injection of Prevelle SILK or Captique and to evaluate outcomes after 2 weeks. METHODS & MATERIALS: In a patient-blinded, prospective, randomized, split-face design trial, a non-animal-derived hyaluronic acid based filler formulated with lidocaine (Prevelle SILK) was injected in one nasolabial fold (NLF), and the same filler without lidocaine (Captique) was injected in the contralateral NLF of 45 enrolled patients. Injection site pain was measured using a visual analogue scale at injection (time 0) and 15, 30, 45, and 60 minutes after injection. Patients were asked to return for an evaluation after 2 weeks and to complete a self-assessment questionnaire during the follow-up visit. RESULTS: There was more than 50% less pain associated with the dermal gel with lidocaine than with the same filler without lidocaine at all time points (p<.05). The greatest difference in pain was recorded at the time of injection, and then the effect gradually declined over the 60-minute period. Both fillers were well tolerated, and there was no difference in outcome after 2 weeks. CONCLUSION: Addition of lidocaine to a filler resulted in significantly less pain associated with the procedure without compromising outcomes.

Hemodialysis leukopenia and complement function with different dialyzers.

The relationship between leukopenia and the complement system during hemodialysis was re-examined by studying not only the in vivo effects of four different dialyzer membranes (cellulose hydrate, cuprophan, cellulose acetate, and polyacrilonitrile) on leukocyte counts and complement levels, but especially by investigating the effects of these membranes on complement function in vitro. Whereas from in vivo studies no definite conclusions could be drawn, in vitro investigations provided clear-cut information. When more sophisticated technical approaches were undertaken, it became evident that hemodialysis leukopenia has to be thought of in terms of chemotactic factor generation. In fact, a strict correlation was demonstrated between the degree of leukopenia induced by the dialyzers tested and the ability of the relative membrane to generate chemotactic activity in vitro. Moreover, the previously observed ability of polyacrilonitrile membrane to induce a decrement in complement function was due to the ability of polyacrilonitrile to adsorb complement activity and did not correspond to effective complement consumption. This finding explained why polyacrilonitrile dialysis is not accompanied by a decrease in circulating granulocytes. Taken together, our data strongly point to a pivotal role of complement system in the pathogenesis of hemodialysis leukopenia.

Cell mediated immunity in idiopathic glomerulonephritis.

Various recent reports have suggested the presence of a functional defect of lymphocyte subpopulations in minimal-change nephropathy during the active phase. A probable role of inhibitory humoral factor(s) has been hypothesized. However, other authors have been unable to detect a significant difference between plasma from patients with nephrotic syndrome due to minimal-change nephropathy and plasma from other glomerulonephritis in the degree of inhibition of mitogen-induced lymphocyte transformation. In our study, T cell function, as measured by the response to PHA in autologous plasma, was depressed only in patients with minimal-change nephrotic syndrome and in patients with membranoproliferative glomerulonephritis. The lymphocyte function returned to normal when lymphocytes were cultured in homologous plasma. The lymphocyte responsiveness of patients with other glomerulonephritis with or without nephrotic syndrome was normal in both autologous and homologous plasma. Moreover, only plasma from patients with minimal-change nephropathy in the active phase and with membranoproliferative glomerulonephritis were able to induce inhibition of mitogenesis of lymphocytes from healthy donors. These data seem to confirm the presence of specific humoral inhibitory factor(s) in the plasma of these patients. Finally, preliminary findings seem to demonstrate an increase of the number of TG cells in patients with minimal-change nephropathy in remission who relapse early in the subsequent follow-up.