Search PubMed⌕ Search

Biomedical subjects

G Kaplanski

Publications and source records attributed to G Kaplanski.

At least 37 records · Page 2Linked to original sources
PubMed2001

[Acquired factor V inhibitor: etiology, bleeding risk and therapeutic management with regard to three cases].

INTRODUCTION: Acquired factor V inhibitor is rare and clinical symptoms are quite variable. Bleeding is the leading symptom but some patients are asymptomatic. Several diseases or conditions are associated with factor V inhibitors. Various treatments have been attempted but randomized or prospective trials are not available. EXEGESIS: Here we report three cases of acquired factor V inhibitor. These reports highlight the clinical variability of this disorder. Pathogenesis and therapy with reference to the literature are discussed. CONCLUSION: Factor V inhibitors are rare and associated to several diseases or conditions. Pathogenesis is still unclear except in patients exposed to bovine thrombin. The majority of the cases developed after surgery. In a few cases there is an association to a malignant or autoimmune disease. Plasmapheresis and platelet transfusions might be the best treatment in case of severe bleeding. High-dose intravenous immunoglobulin infusions have been used successfully in some cases and we report here their efficacy in two cases.

Aged↗
PubMed2000

Increased soluble vascular cell adhesion molecule 1 concentrations in patients with primary or systemic lupus erythematosus-related antiphospholipid syndrome: correlations with the severity of thrombosis.

OBJECTIVE: Recent studies have shown that in vitro endothelial cells are activated by antiphospholipid antibodies and may support leukocyte adhesion. We studied levels of soluble intercellular adhesion molecule 1 (sICAM-1, sCD54), soluble vascular cell adhesion molecule 1 (sVCAM-1, sCD106), and soluble E-selectin (soluble endothelial leukocyte adhesion molecule 1 [sELAM-1, sCD62E]) in sera from patients with primary antiphospholipid syndrome (primary APS), and compared them with those from patients with systemic lupus erythematosus-associated APS (SLE-APS) or pure SLE, as well as with those from 2 control groups composed of healthy volunteers and patients with thrombosis unrelated to autoimmune diseases. METHODS: Serum samples from 24 patients with primary APS, 15 patients with SLE-APS, 22 patients with pure SLE, 48 control patients with thrombosis, and 18 healthy volunteers were examined using enzyme-linked immunosorbent assays specific for sICAM-1, sVCAM-1, and sELAM-1. RESULTS: Serum levels of sVCAM-1, but not sICAM-1 or sELAM-1, were significantly increased in all patient study groups compared with thrombosis control patients and healthy volunteers, but did not differ between the groups of patients with primary APS, SLE-APS, or pure SLE. Concentrations of sVCAM-1 were significantly higher in primary APS or SLE-APS patients with severe, recurrent thrombosis and were negatively correlated with platelet counts in primary APS patients. In patients with primary APS, sVCAM-1 levels were higher if there was thrombotic kidney involvement and correlated with creatinemia. CONCLUSION: Serum sVCAM-1 concentrations are increased in patients with primary APS, especially those with repeated thrombotic events or kidney involvement. These findings suggest that endothelial/ monocyte interaction may be important in the pathogenesis of primary APS.

Adult↗
PubMed2000

[Acute neuromyocarditis secondary to diet-induced beriberi. Case report].

INTRODUCTION: Thiamine deficiency can be determined by various clinical signs; some of these symptoms may be acute, and require an urgent diagnosis. In countries such as ours with a high standard of living, this disorder is more commonly observed in cases of severe alcoholism, and cases of diet-associated thiamine deficiency are rare, and therefore not easily recognized. The metabolic disorders resulting from vitamin B1 deficiency are responsible for the well-known central or peripheral neurological symptoms, and also for the less common and often more acute cardiovascular reactions. Immediate thiamine/vitamin B1 supplementation is of major importance. The rapid reversal of symptoms following this treatment is often considered as a diagnostic index. EXEGESIS: In this study, an original case of diet-associated thiamine deficiency has been reported, with clinical symptoms including myocarditis and subacute peripheral nerve involvement in a young adult. The disorder was the result of a thiamine deficiency in the diet, which was exclusively based on milled rice. CONCLUSION: The present report is interesting both as regards its clinical aspects and its etiology, and it emphasizes the importance in the differential diagnosis of a given case of taking the possibility of diet-related thiamine deficiency into account, although this is an uncommon etiology in developed countries.

Adult↗
PubMed2000

Dietary soybean phosphatidylcholines lower lipidemia: mechanisms at the levels of intestine, endothelial cell, and hepato-biliary axis.

The beneficial metabolic effects of dietary soybean lecithin on lipid metabolism are now more clearly established. The intestinal absorption of cholesterol is decreased by soybean phosphatidylcholine-enriched diet and results in a cholesterol-lowering effect. There is an enhancement of the cholesterol efflux by endothelial cells incubated with soybean phosphatidylcholines, and a stimulation of the reverse cholesterol transport by high density lipoprotein-phosphatidylcholines. As a result of all these processes, phosphatidylcholines provided by the soybean lecithin metabolism appear to be key molecules controlling the biodynamic exchanges of lipids. They regulate homeostasis of cholesterol and fatty acids by decreasing their synthesis and promoting cholesterol oxidation into bile salts. Finally, the outcome is the increase in bile secretion of these lipids and/or their metabolite forms. Such findings constitute promising goals in the field of nutritional effects of soybean lecithin in the treatment or prevention of hyperlipidemia and related atherosclerosis.

Journal Article↗
PubMed1998

Thrombin-activated human endothelial cells support monocyte adhesion in vitro following expression of intercellular adhesion molecule-1 (ICAM-1; CD54) and vascular cell adhesion molecule-1 (VCAM-1; CD106).

Thrombin, a central molecule in coagulation, is also involved in inflammation. Notably, thrombin induces endothelial neutrophil adhesion, P- and E-selectin expression, and chemokine production. We show here that thrombin induces expression of intercellular adhesion molecule-1 (ICAM-1; CD54) and vascular cell adhesion molecule-1 (VCAM-1; CD106) on human umbilical vein endothelial cells (HUVECs) associated with increased adhesion of monocytes. Thrombin increased mRNA steady-state levels and expression of ICAM-1 over 24 hours. Thrombin-induced VCAM-1 expression exhibited unusual kinetics, reaching maximum levels after 6 to 12 hours, but decreasing to near baseline after 24 hours. Thrombin activity on HUVECs was mediated through interaction with its specific receptor, because ICAM-1 and VCAM-1 expression were similarly induced by the 14-amino acid thrombin receptor-activating peptide. Thrombin-induced ICAM-1 and VCAM-1 expression was significantly inhibited by hirudin, but not by interleukin-1 receptor antagonist or anti-tumor necrosis factor alpha monoclonal antibody (MoAb). Thrombin-activated HUVECs significantly increased greater numbers of adhering THP-1 macrophagic cells, peripheral blood mononuclear cells, or purified monocytes than unstimulated HUVECs. This adhesion was inhibited by anti-CD18 and anti-CD49d MoAb, demonstrating that thrombin-induced ICAM-1 and VCAM-1 were functional. These results show that, in addition to selectins, thrombin directly induces a cytokine-independent expression of adhesion molecules of the Ig superfamily on HUVECs that may support firm leukocyte attachment during inflammation.

Antibodies, Monoclonal↗
PubMed1998

Ribavirin in hepatitis C related cryoglobulinemia.

OBJECTIVE: An open, uncontrolled trial of ribavirin, an oral guanosine nucleoside analog for treatment of hepatitis C, in patients with hepatitis C virus (HCV) associated cryoglobulinemia intolerant to interferon. METHODS: Five patients with cryoglobulinemia related to HCV infection unresponsive to interferon therapy received oral ribavirin (100 to 1200 mg daily) for 10 to 36 months. RESULTS: Patients treated with ribavirin had prompt decrease in serum aminotransferase levels and marked improvement of manifestations of cryoglobulinemia within a few weeks. Ribavirin did not eradicate HCV RNA from the sera, but a decrease in viral load was observed in 3 patients, from 232 to 86 x 10(5) copies HCV/ml. Relapse occurred within 3 months once therapy was discontinued. The drug was well tolerated, but mild dose related hemolysis was common. CONCLUSION: Ribavirin monotherapy may be effective in patients with symptomatic cryoglobulinemia related to HCV infection, but this effect is not sustained when ribavirin therapy is discontinued.

Aged↗
PubMed1997

Thrombin induces endothelial type II activation in vitro: IL-1 and TNF-alpha-independent IL-8 secretion and E-selectin expression.

In addition to its role in coagulation, thrombin is involved in the inflammatory process by inducing vessel neutrophilic infiltration. Thrombin induces endothelial P-selectin expression and platelet activating factor release, which participate to induce early neutrophil adhesion and activation. We employed HUVEC and now show that thrombin induces the production of the chemokine IL-8 in a time- and dose-dependent fashion. Similarly, thrombin induced E-selectin expression on HUVEC. Both IL-8 secretion and E-selectin expression were preceded by an increase in steady state levels of the respective mRNAs. Thrombin action on HUVEC was inhibited by the specific thrombin inhibitor, hirudin. In addition, these effects of thrombin on HUVEC were mimicked by the 14-amino acid thrombin receptor agonist peptide, which triggers the native thrombin receptor in a similar fashion to thrombin itself. Although IL-1 and TNF-alpha also induce IL-8 and E-selectin, the thrombin effects in these experiments were not mediated by those cytokines, since neither IL-1 receptor antagonist nor anti-TNF-alpha Ab inhibited the effects of thrombin. Furthermore, IL-1alpha, IL-1beta, and TNF-alpha were not detected in the supernatants of thrombin-activated HUVEC. Although intracellular IL-1alpha was found in thrombin-activated HUVEC, antisense IL-1alpha had no inhibitory effect on IL-8 secretion. These results demonstrate that in addition to short term endothelial activation, thrombin also functions as a long acting proinflammatory agent by inducing endothelial synthesis of the mediators required for neutrophils activation and extravazation during inflammation.

Cells, Cultured↗
PubMed1997

Increased levels of soluble adhesion molecules in the serum of patients with hepatitis C. Correlation with cytokine concentrations and liver inflammation and fibrosis.

Lymphocyte adhesion to endothelium, extravasation, and adhesion to hepatocytes are mediated by adhesion molecules and constitute important steps in the liver inflammation due to chronic hepatitis C (HCV-CH). We measured soluble intercellular adhesion molecule (sICAM-1, sCD54), vascular cell adhesion molecule (sVCAM-1, sCD106), E-selectin (sCD62E), as well as interleukin (IL)-1 beta, IL-8, and tumor necrosis factor-alpha (TNF-alpha) concentrations in the serum of 22 patients with HCV-CH in comparison to 20 seronegative healthy volunteers. sICAM-1, sVCAM-1, sCD62E, TNF-alpha, and IL-8 but not IL-1 beta concentrations were significantly elevated in patients. sICAM-1 and sCD62E correlated with TNF-alpha and aspartate amino transferases levels. sICAM-1 correlated with liver lobular inflammation whereas sVCAM-1, sCD62E, and IL-8 correlated with liver fibrosis. Measurement of soluble adhesion molecules may be an easy way to follow liver inflammation and fibrosis during HCV-CH.

Adult↗
PubMed1997

Dapsone for chronic autoimmune thrombocytopenic purpura: a report of 66 cases.

Sixty-six adults with chronic autoimmune thrombocytopenic purpura AITP and platelet count <50 x 10(9)/l were treated with dapsone (75-100 mg orally). A response was observed in 33 patients. The median duration of treatment required to obtain a response was 21 d (range 8-90). The median maximal platelet count on treatment was 130 x 10(9)/l (range 71-355). Dapsone was continued in 20/33 responders for a median of 12.5 months (range 1-48) and the response persisted in 19. Treatment was intentionally withdrawn in the other 13 responders and thrombocytopenia immediately recurred in 12. Reversible side-effects required cessation of treatment in seven patients. These results demonstrate that dapsone is an effective, inexpensive, and well-tolerated treatment for chronic AITP.

Adult↗
PubMed1997

Interaction with autologous platelets multiplies interleukin-1 and tumor necrosis factor production in mononuclear cells.

The effect of activated platelets on cytokine production by human peripheral blood mononuclear cells (PBMC) was investigated. When PBMC were coincubated with activated autologous platelets amid lipopolysaccharide (LPS, 50-100 pg/mL) for 8 h, the production of interleukin (IL)-1alpha increased 11- to 18-fold and tumor necrosis factor (TNF)-alpha 3- to 5-fold compared with PBMC without platelets. Activated platelets in a dual-chamber well that prevented platelet-PBMC contact but permitted passage of soluble factors enhanced IL-1alpha production (P < .01). Platelet-PBMC contact in the chamber resulted in a further enhancement of IL-1alpha production. These data suggest that platelet-PBMC interaction, both directly and with platelet-derived factors, enhances production of shock-producing IL-1alpha and TNF-alpha, albeit differently. The interaction of platelets with monocytes may play an important role in the pathophysiology of sepsis and disseminated intravascular coagulation.

Blood Platelets↗