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F Cofan

Publications and source records attributed to F Cofan.

At least 19 recordsLinked to original sources
PubMed2005

Effect of apolipoprotein B polymorphism in kidney transplantation.

INTRODUCTION: In kidney transplant recipients, dyslipidemia is a cardiovascular risk factor that also contributes to the development and progression of chronic allograft nephropathy. Apolipoprotein B (ApoB), present in low-density lipoproteins (LDL), is an important protein component of chylomicrons and very-low-density lipoproteins (VLDL). The del allele of the ApoB signal peptide polymorphism has been associated with elevated levels of total and LDL cholesterol and greater risk of coronary disease. OBJECTIVE: The objective of this study was to assess the influence of ApoB polymorphism on allograft and patient survival among kidney transplant recipients. METHODS: In this study, we analyzed 516 renal transplant recipients (38% were women, 62% were men), aged 46 +/- 15 years, with a minimum follow-up of 12 months (mean, 1854 +/- 806 days). The ApoB signal peptide was analyzed (insertion/deletion) using polymerase chain reaction (PCR) using genomic DNA. Clinical donor-recipient variables were assessed using a Cox multivariate model. RESULTS: Polymorphism distribution was as follows: insertion/insertion (ins/ins) 51%, insertion/deletion (ins/del) 39%, and deletion/deletion (del/del) 9%, with no differences between the genders. Cholesterol levels at 12 months showed no differences between the ins/ins (217 +/- 46), ins/del (228 +/- 50), and del/del (227 +/- 54) groups. Presence of the ApoB signal peptide del/del or ins/del genotype was independently associated with lower patient survival in the group of men younger than 60 years (P < .05). Among the total deaths, cardiovascular causes predominated in the ins/del and del/del groups (50%) as compared with the ins/ins group (33%) (P < .01). CONCLUSIONS: ApoB genetic polymorphism (del allele) seems to have an adverse effect on the long-term survival of kidney transplant recipients.

Adult↗
PubMed2005

Invasive pulmonary aspergillosis in solid organ and bone marrow transplant recipients.

BACKGROUND: Invasive pulmonary aspergillosis (IPA) remains a major cause of mortality in transplant recipients. New strategies in therapy are needed. METHODS: We prospectively followed all solid organ and bone marrow transplant recipients from January 1998 to January 2003 who showed pulmonary infiltrates. We retrospectively analyzed all of the patients diagnosed as having IPA. Clinical and epidemiological data were collected. Influence of new treatment strategies on survival was also analyzed. RESULTS: Thirty-one cases of API were found: 8 definite, 18 probable, 5 possible among recipients of liver (11), bone marrow (9), kidney (7), kidney-pancreas (3), and heart (1) transplants. Five patients (16%) were previously receiving antifungal prophylaxis. The most common symptoms were fever (74%) and dyspnea and dry cough (48%). Six cases (19%) showed dissemination to extrapulmonary sites: central nervous system (CNS) in five and bone in one. The most common radiographic patterns were alveolar infiltrates (58%); the lesions were usually diffuse and bilateral (58%). The most common Aspergillus species identified was A. fumigatus (74%). The test to detect Aspergillus antigen (galactomannan) in serum performed in 13 cases, was positive in eight (61%). The crude mortality rate was 61% (19 of 31), but in patients on mechanical ventilation, it was 94% (OR 88, IC 95%: 7.1-1094), and in patients with CNS involvement, it was 100%. The influence of the different treatment regimens on survival was analyzed in definite and probable cases: Group 1 (12) included patients who received conventional monotherapy and group 2 (12) patients received combination antifungal therapy or liposomal amphotericin B (1-AMB) at high doses. The mortality in group 1 was 83% (10 of 12), and in group 2 it was 42% (5 of 12) (P < 0.05). CONCLUSIONS: The mortality rate of IPA remains high, especially among patients with CNS involvement or those under mechanical ventilation. Combined antifungal therapy or monotherapy with 1-AMB at high doses significantly reduced mortality compared with conventional monotherapy.

Amphotericin B↗
PubMed2005

Effect of calcineurin inhibitors on low-density lipoprotein oxidation.

INTRODUCTION: Low-density lipoprotein (LDL) oxidation is considered a key factor in the biological processes that trigger and accelerate atherosclerosis. Reported data suggest that tacrolimus improves the lipid profile in renal transplant recipients. OBJECTIVE: The objective of this study was to analyze the effect of converting from cyclosporine to tacrolimus on lipoprotein oxidation in renal transplant recipients. METHODS: We studied a group of 12 recipients (6 men and 6 women of mean age 55 +/- 11 years) treated with a cyclosporine-mycophenolate mofetil (MMF)-prednisone combination that was converted to tacrolimus-MMF-prednisone because of gingival hyperplasia. The LDL fraction was isolated by density-gradient ultracentrifugation. Oxidative stress was studied before converting (baseline) and at 6 and 12 weeks, thereafter by in vivo oxidation analysis of LDL, a direct assay of oxidized LDL (oxLDL) and oxLDL autoantibodies (Ab-oxLDL) using enzyme-immunoassay techniques. We measured total cholesterol (TC), triglyceride, LDL-cholesterol, high-density lipoprotein (HDL)-cholesterol, ApoA1, ApoB, and Lp(a) levels. RESULTS: The change to tacrolimus resulted in significant decreases in TC levels, 213 +/- 30 (B) versus 185 +/- 27 (12s) (P < .01); LDL, 129 +/- 24 (B) versus 104 +/- 14 (12s) (P = .002); and ApoB 98 +/- 15 (B) versus 85 +/- 10 (12s) (P < .01). HDL levels significantly increased (45 +/- 10 vs 48 +/- 10 [12s]; P = .018), whereas oxLDL concentrations decreased significantly after conversion (B) (55.42 +/- 10.61 vs 12s 45.76 +/- 10.21; P < .01). Converting to tacrolimus produced a nonsignificant decrease in Ab-oxLDL (baseline 204.88 +/- 134.49 vs 12s 179.51 +/- 143.54). A correlation was observed between LDL and oxLDL (r = 65, P = .02 [B] and r = 0.7, P = .01 [12s]) but not between oxLDL levels and Ab-oxLDL concentration (r = -0.05, P = .87 [3] and r = -0.1, P = .77 [12s]). CONCLUSIONS: In renal transplantation, tacrolimus therapy was associated with a better lipid profile and lower in vivo LDL oxidation when compared with cyclosporine treatment.

Adult↗
PubMed2003

Effect of apolipoprotein polymorphisms in renal transplant recipients.

Cardiovascular disease (CVD) is the main cause of mortality among long-term renal transplant recipients (RTR). On the other hand, allograft chronic nephropathy is the primary cause of graft loss among long-term RTR. Hyperlipidemia is a predisposing factor for both conditions. Polymorphisms of the apolipoproteins modulate lipid metabolism. The aim of the study was to evaluate the effect of apo A-I, apo A-IV and apo C-III genotypes on the long-term results of renal transplantation. Clinical assessment (renal allograft and patient survival) and genotyping for apo A-I (+83C/T), apo C-III (Sst I), and apo A-IV (Thr347Ser and Gln360His) polymorphisms were evaluated in 516 kidney transplant patients and correlated with the clinical evolution over 12 months. The distribution of the apo A-I (+83C/T) polymorphisms was: CC 91.9%, CT 7.9%, and TT 0.2%. The apo C-III genotype showed: S1S1 84.4%, S1S2 15.2%, and S2S2 0.4%. The apo A-IV (Pvu II) polymorphism was: GG 82%, GT 18%, and 0% TT. Finally, the frequency of apo A-IV (Hinf I) polymorphism was: AA 69%, AT 27%, and TT 4%. The frequency of polymorphisms was similar between men and women. In conclusion, there was no significant influence of apolipoprotein polymorphisms on renal and patient survival.

Apolipoprotein A-I↗
PubMed2001

Platelet procoagulant activity induced in vivo by muromonab-CD3 infusion in uremic patients.

BACKGROUND: Muromonab-CD3 is a murine monoclonal antibody (MoAb) that is used in the prophylaxis and treatment of acute graft rejection. Activation of coagulation and fibrinolysis following anti-CD3 administration have been reported in some patients to lead to irreversible intragraft thrombosis. DESIGN AND METHODS: We have studied the effect of muromonab-CD3 infusion on platelets using flow cytometry in six patients who received three daily doses of muromonab-CD3 as prophylaxis of rejection before receiving a living donor renal transplant. Samples were collected before, 15 and 60 min after muromonab-CD3 infusion. Immunolabeling of platelets was performed in whole blood using dual-color analysis. The following conjugated MoAb were used: anti-CD41a, -CD36, -CD42b, -CD62P, -CD63, -factor V/Va and nonspecific Ig. Samples were analyzed with a FACScan flow cytometer (Becton Dickinson, Mountain View, CA, USA). RESULTS: After muromonab-CD3 infusion, an increase in the binding of MoAb anti-factor V/Va to platelets was seen, which was only statistically significant (2.2% vs. 12.8%, P=.04) after 15 min of the second dose. No significant changes were seen in the other MoAbs studied. No thrombotic complications were observed after transplantation. INTERPRETATION AND CONCLUSION: In uremic patients receiving muromonab-CD3 infusion as prophylaxis of graft rejection, an increase in the binding of anti-factor V/Va, denoting an increased exposure of anionic phospholipids in platelets, was seen. This increase in platelet procoagulant activity might contribute to the appearance of thromboses within renal graft seen in some patients who received muromonab-CD3.

Adult↗
PubMed2000

Cortical laminar necrosis caused by immunosuppressive therapy and chemotherapy.

We report three patients in whom neurologic symptoms and cortical laminar necrosis developed after immunosuppressive treatment (cyclosporin A and FK 506) and polychemotherapy (vincristine and methotrexate). Initial neuroradiologic studies showed cortical and white matter involvement. Follow-up studies showed cortical hyper-intense lesions on T1-weighted MR images, consistent with cortical laminar necrosis. The clinical and radiologic data indicate that a transient hypoxic-ischemic process could have been responsible for the encephalic lesions in these three patients.

Adolescent↗
PubMed1999

Uremic tumoral calcinosis in patients receiving longterm hemodialysis therapy.

OBJECTIVE: To analyze a series of uremic tumoral calcinosis (UTC) in patients receiving longterm dialysis therapy. METHODS: Twelve patients receiving longterm hemodialysis affected by tumoral calcinosis were analyzed. Clinical, radiological, and pathological features were evaluated and pathogenic factors were reviewed. RESULTS: The most common sites for UTC were the elbow, hip, hand, and wrist. The lesions were multiple (67%, n = 8), of large size, and symptomatic with joint mobility impairment (75%, n = 9) as well as nerve compression (33%, n = 4). High serum calcium and phosphate concentrations were detected in 50% (n = 6) and 100% of the patients, respectively. An increased calcium-phosphorus product (Ca x P) was observed in all patients, either due to overt secondary hyperparathyroidism (42%, n = 5), or secondary to iatrogenic hypercalcemia and/or severe hyperphosphoremia of multifactorial etiology (i.e., prolonged and excessive administration of calcitriol and calcium carbonate, insufficient dialysis and inadequate phosphorus chelating therapy, etc.) (58%, n = 7). Several treatment strategies were followed (surgical excision, parathyroidectomy, renal transplant) in combination with aggressive medical therapy to decrease Ca x P product, achieving complete remission in 83% of the patients. CONCLUSION: UTC lesions show clinical and pathogenic features that differ from those of idiopathic tumoral calcinosis. The most important pathogenic factor involved in UTC is an increase in Ca x P, not necessarily related to hyperparathyroidism. Combined treatment strategies allow complete remission in a high proportion of patients. A low Ca x P is necessary to prevent development of UTC.

Adult↗