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S Lamperi

Publications and source records attributed to S Lamperi.

At least 55 records · Page 3Linked to original sources

Cytokine-induced peritoneal fibrosis in CAPD. Effects of Ca++ and 1,25(OH)2D3.

We have demonstrated in some continuous ambulatory peritoneal dialysis (CAPD) patients with ultrafiltration (UF) loss, the role of increased peritoneal lymphocyte (PLy) and macrophage (PMO) Ca++ concentrations in the release of large amounts of gamma-interferon (gamma-IFN) and Interleukin-1 (IL-1), which stimulate peritoneal fibroblast proliferation. We have also shown in vitro and in vivo that the calcium channel blocker verapamil (VPM) is able to normalize the previously high PLy and PM0 Ca++ concentrations, and cytokine release; to decrease fibroblast proliferation; and to increase UF in 60% of the CAPD patients with UF loss due to a cytokine-mediated hyperproliferation of peritoneal fibroblasts, while in the remaining 40% there is little improvement (VPM responders and low-responders, respectively). To evaluate which mechanisms, in addition to passive Ca++ influx, can play a role in the Ca++-dependent activation of peritoneal immune cells, we evaluated the effects in vitro of different doses of Ca++ alone; with VPM; and with 1,25(OH)2D3 on: 1) PLy and PM0 cytoplasmic Ca++ levels; 2) gamma-IFN and IL-1 release by PLy and PM0; and 3) peritoneal fibroblast proliferation in six CAPD VPM low-responder patients. Results showed a direct correlation between Ca++ levels in the medium and PLy and PM0 Ca++ concentrations; IL-1 and gamma-IFN release; and peritoneal fibroblast proliferation. These effects were enhanced by the addition of low doses of 1,25(OH)2D3 to the medium, while both high 1,25(OH)2D3 doses and verapamil abrogated the Ca++-induced PLy and PM0 activation.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol↗

Intraperitoneal therapy with interferon-alpha in CAPD patients with relapsing bacterial peritonitis.

In CAPD patients with relapsing bacterial peritonitis who do not benefit from intraperitoneal therapy with IgG (IgG nonresponders), the authors demonstrated that peritoneal macrophages are deficient in IgG Fc receptors (FcR) and, therefore, unable to kill bacteria, independent of the levels of the opsonic molecule IgG in the peritoneal dialysis effluent (PDE). Because previous studies showed that interferon-alpha (IFN-alpha) is able to increase in vitro the number of PM0 IgG FcR in CAPD patients with relapsing bacterial peritonitis, the authors studied the in vivo effects of IP administration of IFN-alpha (1,000 IU daily in the overnight exchange for 12 months) on: PM0 superoxide generation; PM0 bacterial killing; PM0 IgG FcR; the number of bacteria in the PM0 cytoplasm; and peritonitis relapses in these patients. By the 10th day, IFN-alpha induced a progressive rise in all of the previously depressed PM0 functions tested, the disappearance of bacteria from the PM0 cytoplasm, and no further episodes of bacterial peritonitis were detected during 12 months. These data indicate that IFN-alpha may represent a useful tool for preventing infections in CAPD patients with relapsing bacterial peritonitis.

Adult↗

Intraperitoneal verapamil therapy in CAPD patients with peritoneal hypopermeability. Effects on ultrafiltration.

We found higher peritoneal lymphocyte (PLy) and macrophage (PM0) Ca++ concentrations in CAPD patients with low peritoneal ultrafiltration (UF), than in normal UF patients, as well as the release of greater amounts of lymphomonokines such as interferon-gamma and interleukin-1, which stimulate peritoneal fibroblast proliferation. Since Ca++ is essential in immune-cell activation and lymphomonokine production, the authors analyzed the effects of intraperitoneal (IP) verapamil therapy in 16 CAPD patients with UF loss. The areas studied included: 1) PLy and PM0 Ca++ concentration, 2) peritoneal dialysis effluent (PDE) lymphomonokine levels, 3) peritoneal glucose absorption, 4) UF volume, and 5) peritoneal morphology. In the 10 low UF patients who showed normal glucose absorption and increased peritoneal fibroblast proliferation, of verapamil therapy increased UF volume, decreased the amount of peritoneal fibroblast proliferation, and normalized the previously high PLy and PM0 Ca++ concentrations and PDE lymphomonokine levels. Conversely, UF was not improved by IP verapamil in the six low UF patients showing high glucose absorption and prevalent mesothelial alterations. In conclusion, IP verapamil can be considered a suitable therapy for increasing UF volume in CAPD patients with peritoneal hypopermeability due to a lymphomonokine-mediated hyperproliferation of peritoneal fibroblasts.

Calcium↗

Response of CAPD patients with a high incidence of peritonitis to intraperitoneal immunoglobulin therapy.

This study has demonstrated that in the majority of high-peritonitis-incidence (PI) CAPD patients the defective opsonic activity levels in the peritoneal dialysis effluent (PDE) are restored for 3 weeks by a 12 g IP injection of immunoglobulins (Ig). Further studies showed that in a minority of high-PI CAPD patients who also had low PDE IgG and opsonic activity levels, IP Ig therapy did not significantly reduce the PI. To evaluate this phenomenon we utilized this therapy in 20 high-PI CAPD patients undergoing IP Ig therapy for an average of 24 months daily for 3 weeks (12 g every 3 weeks) and analyzed: 1) PDE IgG levels; 2) PDE opsonic activity; 3) peritoneal macrophage (PM0) membrane-bound IgG; 4) PDE Interleukin-1 (IL-1) levels; 5) PM0 membrane Fc receptor number. The results showed that in the 15 patients in whom Ig therapy reduced PI, there were long-lasting increases in the PDE IgG, opsonic activity and IL-1 levels, as well as a normal PM0 Fc receptor number and PM0 reversibly bound infused Ig. Conversely, the five patients in whom the IP Ig did not reduce the PI showed only transient increases in PDE IgG and opsonic activity levels, no PDE IL-1 increase, and the PM0 were deficient in Fc receptors and, therefore, unable to take up the infused Ig. We conclude that in high-PI CAPD patients there are different peritoneal immune defense abnormalities and that their identification is, therefore, important for the correct choice of therapy to improve these defects.

Adult↗