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Biomedical subjects

R Castro

Publications and source records attributed to R Castro.

At least 19 recordsLinked to original sources

Four-year follow-up of a prospective trial of HLA and MICA antibodies on kidney graft survival.

In 2002, 1329 patients with functioning transplants were prospectively tested for HLA antibodies in the 13th International Histocompatibility Workshop. Four years after testing, deceased donor graft survival among 806 patients not having antibodies in 2002 was 81% compared to 58% for 158 patients with HLA antibodies (p < 0.0001) and 72% for 69 patients with MICA antibodies (p = 0.02). Hazard ratio (HR) using death-censored graft survival from multivariate analysis of HLA antibodies was 3.3 (p < 0.00001) and 2.04 for MICA (p = 0.01). In the 14th Workshop, at 1 year follow-up, survival for 1319 patients receiving deceased donor grafts and no HLA antibodies was 96% compared to 94% for 344 patients with HLA antibodies (p = 0.0004) and 83% survival for 33 patients with MICA (p = 0.0005). HR from multivariate analysis: HLA antibodies was 3.6 (p < 0.00001) and 6.1 for MICA (p = 0.006). Twelve patients with donor specific antibodies tested by single antigen beads had a 1 year survival of 64% (p = 0.008), and 27 patients with non-donor specific 'strong' antibodies had a 66% survival (p = 0.0003) compared to 92% survival in those with no antibodies. In conclusion, these two prospective trials, after 1 and 4 years, provided strong evidence that HLA and MICA antibodies are associated with graft failure.

Antibodies↗

Scuticociliate proteinases may modulate turbot immune response by inducing apoptosis in pronephric leucocytes.

The role of proteinases of the histiophagous ciliate Philasterides dicentrarchi, purified by affinity chromatography in bacitracin-Sepharose, on apoptosis (programmed cell death) of turbot pronephric leucocytes (PL) was investigated. The results showed that more than 90% of proteinases purified by bacitracin-Sepharose were cysteine proteinases, which lacked significant caspase-3-like activity and generated three main gelatinolytic bands of molecular weights 36, 45 and 77 kDa as determined by gelatine-SDS-PAGE and immunoblot. Viability of PL cells after 24 h stimulation with P. dicentrarchi cysteine proteinases did not differ from that of non-stimulated cells. Apoptosis was confirmed by: (i) caspase activity, (ii) DNA fragmentation, and (iii) nucleus fragmentation. The caspase-3-like activity in PL incubated for 4h in the presence of 125, 250 and 500 microg/ml of proteinases increased in a dose-dependent fashion. The PL DNA was fragmented following 24-h exposure to P. dicentrarchi cysteine proteinases and characteristic DNA ladders consisting of multimers of approximately 180-200 pb were produced. Morphological changes, such as chromatin condensation and nucleus fragmentation, were observed under fluorescence microscopy after DAPI staining of the PL cells incubated with cysteine proteinase-incubated for 24 h. The results suggest that the pathogenic scuticociliate P. dicentrarchi may induce host leucocyte programmed cell death via the production of cysteine proteinases, as a mechanism of pathogenesis and evasion of the turbot innate immune response.

Animals↗

Homocysteine metabolism, hyperhomocysteinaemia and vascular disease: an overview.

Hyperhomocysteinaemia has been regarded as a new modifiable risk factor for atherosclerosis and vascular disease. Homocysteine is a branch-point intermediate of methionine metabolism, which can be further metabolised via two alternative pathways: degraded irreversibly through the transsulphuration pathway or remethylated to methionine by the remethylation pathway. Both pathways are B-vitamin-dependent. Plasma homocysteine concentrations are determined by nongenetic and genetic factors. The metabolism of homocysteine, the role of B vitamins and the contribution of nongenetic and genetic determinants of homocysteine concentrations are reviewed. The mechanisms whereby homocysteine causes endothelial damage and vascular disease are not fully understood. Recently, a link has been postulated between homocysteine, or its intermediates, and an alterated DNA methylation pattern. The involvement of epigenetic mechanisms in the context of homocysteine and atherosclerosis, due to inhibition of transmethylation reactions, is briefly overviewed.

Animals↗

HOMA, QUICKI and MFfm to measure insulin resistance in morbid obesity.

BACKGROUND: The relationship between morbid obesity (MO) and insulin resistance (IR) has been widely demonstrated. The euglycemic-hyperglycemic clamp method for diagnosis of IR is neither practical nor cost-effective for population-based studies. However, the application of mathematical models (HOMA, QUICKI and Mf(fm) indices) can be useful. METHODS: The data from 171 patients were retrospectively evaluated. We recorded general anthropometric parameters and the basal levels of glucose, triglycerides and insulin and calculated the metabolic indexes both before surgery (Capella gastric bypass) and 6, 12, 24, 36 and 48 months after the operation. RESULTS: Before surgery, patients could be classified according to their waist-hip ratio (WHR) into 2 groups. Group A (n = 131, 108 females and 23 males) with WHR values 1.10 +/- 0.1 SD for males and 0.94 +/- 0.1 for females (central obesity); and Group B (n = 40, 34 females and 6 males) with WHR values 0.90 +/- 0.1 for males and 0.84 +/- 0.1 for females (peripheral obesity). Group A patients showed elevated serum levels of glucose, triglycerides and insulin and high values of the HOMA index with low values of QUICKI and Mf(fm). Group B patients showed lower levels of glucose, triglycerides, insulin and HOMA index and higher values of QUICKI and Mf(fm). These abnormal levels began to decrease 6 months after bypass and the QUICKI and Mf(fm) began to increase. CONCLUSIONS: The high baseline levels of insulin and the high prevalence of hypertension, diabetes or both conditions in patients with central obesity confirm that they suffer a metabolic syndrome, Meanwhile, patients with peripheral obesity with lower levels of chemical parameters and of the metabolic indices suffer peripheral resistance against insulin. Clinical application of these mathematical indices can be useful in patients with MO; they are easily performed and lack the high costs and risks associated with the clamp technique.

Adolescent↗

Humoral and cellular responses to cow milk proteins in patients with milk-induced IgE-mediated and non-IgE-mediated disorders.

BACKGROUND: Cow milk allergy (CMA) is one of the most common food allergies in childhood. Patients with CMA present with a wide range of immunoglobulin (Ig)E- and non-IgE-mediated clinical syndromes. Limited information is known about the specific humoral and cellular responses to cow milk proteins in these various forms of CMA. OBJECTIVE: The aim of the study was to determine IgE, IgA, IgG1 and IgG4 antibody levels and lymphocyte proliferative responses to the major cow milk allergens in patients with IgE- and non-IgE-mediated CMA. METHODS: One hundred and forty cow milk allergic patients, 6 months to 22 years of age, were included in the study. One hundred and thirteen patients had IgE-mediated CMA, 11 had milk protein-induced enterocolitis syndrome and 16 had allergic eosinophilic gastroenteritis. Twenty-one patients without food allergy, 8 months to 18 years of age, served as controls. Serum IgE, IgA, IgG1 and IgG4 antibodies to alpha-, beta-, and kappa-casein, alpha-lactalbumin and beta-lactoglobulin were measured using enzyme-linked immunosorbent assays. For a subset of these patients, we performed lymphocyte proliferation assays to the various milk allergens. RESULTS: Patients with IgE-mediated CMA had higher specific IgE concentrations to casein compared with whey proteins (P < 0.001). In this group of patients, there was a positive correlation between IgE levels and levels of the other isotypes for all four milk proteins (P < 0.001). In general, the caseins were the more allergenic and antigenic proteins in all groups of patients. Patients with enterocolitis syndrome produced less milk protein-specific IgG4 (P < 0.05) and had a trend for higher IgA antibody levels when compared to the control group. Lymphocyte proliferative responses in all groups with CMA were significantly higher than controls (P < 0.05), although this response was similar in patients with IgE- and non-IgE-mediated CMA. CONCLUSION: There is a distinct pattern of humoral antibody response in the different forms of CMA. Patients with IgE-mediated CMA have an elevated polyisotypic response to cow milk protein. The relative lack of specific IgG4 production in patients with enterocolitis syndrome may be involved in the pathogenesis of the disease. In general, caseins appear to be the predominant allergen in patients with CMA.

Adolescent↗

Morbid obesity, hypertensive disease and the renin-angiotensin-aldosterone axis.

BACKGROUND: Resistance to insulin and secondary hyperinsulinemia seem to be the putative link between morbid obesity (MO) and hypertensive disease (HD). Adipose tissue can secrete leptin and angiotensinogen, among other substances. Leptin activates the sympathetic nervous system, leading to HD. Angiotensinogen is a substrate for renin, therefore taking part in the renin-angiotensin-aldosterone axis and the regulation of blood pressure. In MO, both hypertrophy and hyperplasia of the adipocytes lead to an increase in the secretion of both substances, leading to loss of the equilibrium between the levels of both hormones. The aim of the present study was to evaluate these abnormalities and their potential reversibility following bariatric surgery. METHODS: Data from 100 patients with MO was retrospectively evaluated. Anthropometric data, the plasma renin activity (PRA), plasma levels of aldosterone, ACE, potassium and sodium were collected both prior to surgery and 6, 12, 24 and 36 months after surgery. RESULTS: The waist-hip ratio (WHR) before surgery allowed classification of our patients in two groups: central obesity (WHR > or =0.90 in men and > or =0.85 in women); peripheral obesity (WHR <0.90 in men and <0.85 in women). In patients with central obesity, high levels of PRA, aldosterone and ACE with sodium retention and potassium loss and high insulin levels, were found. These changes were not found in patients with peripheral obesity. After gastric bypass, these abnormalities tended to disappear, mainly in the first 6 months. CONCLUSIONS: The reduction of BMI and WHR after gastric bypass confirmed this operation to be effective against MO. The high basal levels of insulin and the high rate of HD and diabetes in patients with central obesity seem to indicate that they suffer a metabolic syndrome with significant hormonal imbalances and sodium retention. Patients with peripheral obesity only showed a peripheral resistance against insulin, probably with a shorter duration of the hormonal action, but they did not show hormonal abnormalities or sodium retention. After gastric bypass these abnormal hormone levels tended to normalize.

Adolescent↗

Morbid obesity and gastric bypass surgery: biochemical profile.

BACKGROUND: Morbid obesity (MO) and the pathologies associated with it constitute an important public health problem, accounting for 7% of the health expenditure in industrialized countries. An important percentage of this expense is attributed to the different biochemical tests performed in these patients, who suffer from several metabolic derangements. We evaluated the basic biochemical abnormalities in MO patients and their reversibility by weight loss after gastric bypass, to standardize the surveillance of the different metabolic abnormalities in obese patients. METHODS: By a retrospective analysis on 125 patients operated in our hospital, we evaluated anthropometric and biochemical data before and 1, 3, 6, 12 and 24 months after gastric bypass. RESULTS: Preoperatively hyperinsulinemia, hyperglycemia, dyslipidemia and hypertensive disease were present, and began to improve 1 and 3 months after surgery (although not significantly) and significantly at 6, 12 and 24 months after it. We also observed deficient protein nutrition and a deficiency of micronutrients both before bypass and during the follow-up. CONCLUSION: After gastric bypass, a marked decrease in insulin occurred, with normalization of blood pressure and the biochemical parameters associated with the metabolic syndrome. We propose a biochemical follow-up protocol for MO patients.

Adolescent↗

5,10-Methylenetetrahydrofolate reductase 677C-->T and 1298A-->C mutations are genetic determinants of elevated homocysteine.

BACKGROUND: Methylenetetrahydrofolate reductase (MTHFR) is one of the main regulatory enzymes of homocysteine metabolism. Elevated plasma total homocysteine (tHcy) is a major risk for cardiovascular disease. A common 677C-->T mutation in the MTHFR gene results in decreased enzymic activity, and contributes to increased plasma tHcy, in association with low plasma folate. A recently described 1298A-->C mutation in the MTHFR gene clearly reduces MTHFR activity (although to a lesser extent than the 677C-->T) but its effect on plasma tHcy levels is not yet clear. AIM: To investigate the frequency of these two MTHFR polymorphisms in a Portuguese population, and to correlate the MTHFR genotype with the biochemical phenotype at the level of homocysteine and folate concentrations. DESIGN: Prospective population survey. METHODS: We studied 117 healthy volunteers (71 females, 46 males). The 677C-->T and 1298A-->C mutations were screened by PCR-RFLP. Levels of plasma tHcy and folate, and red blood cell folate, were determined. RESULTS: The allele frequencies of the 677C-->T and 1298A-->C mutations were 0.33 and 0.28, respectively. Homozygotes for the 677C-->T mutation had significantly elevated plasma tHcy and RBC folate levels and significantly lowered plasma folate concentrations than subjects without the mutation. The 1298A-->C mutation showed a significant effect on plasma tHcy, but not on plasma folate or RBC folate levels. DISCUSSION: The observed 677T allele frequency is not consistent with the idea of a north-south gradient as previously suggested. The 1298A-->C mutation is common in Portugal. Both MTHFR mutations showed effects on plasma tHcy levels.

5,10-Methylenetetrahydrofolate Reductase (FADH2)↗

Current role of simplified upper tract approach in the surgical treatment of ectopic ureteroceles: a single centre's experience.

OBJECTIVE: Despite renewed interest in either endoscopic decompression or complete reconstruction as primary approaches in ectopic ureterocele's (EU's) treatment, we advocate that a simplified upper tract approach is an optimal choice in a large subset of these patients. We review our surgical results to evaluate the effectiveness of different surgical procedures used in the treatment of EU, based on an individualized approach. PATIENTS AND METHODS: We retrospectively analysed all patients with EU and without previous treatment (n = 59) operated in this centre between the years 1991 and 2000. This disorder was bilateral in three patients (62 EU) and associated with duplex ureters in 60 cases. Vesicoureteral reflux (VUR) was diagnosed pre-operatively in 49.1% of patients. Treatment and choice of procedure was based on patients' age, clinical manifestations, associated abnormalities and function of the ureterocele-bearing moiety. Patients were divided in three separate groups according to the initial surgical approach. Group 1-11 patients submitted to endoscopic puncture (six urgent ureterocele decompression, four infants with obstruction of a functional ureterocele-bearing moiety and another with both lower pole ureter and mild bladder outflow obstruction). Group 2-30 patients (31 EU) submitted to a simplified upper tract approach--pyeloureterostomy (1), heminephrectomy (29) and nephrectomy (1) (all patients but one with non-viable renal segments; VUR, grade < or = III, present in six cases). Group 3-18 patients (20 EU) submitted to complete primary reconstruction (all patients with high-grade and/or contralateral reflux, with or without function of the ureterocele-bearing moiety). Success (clinically asymptomatic patients, without obstruction or VUR) and complication rates from the different approaches were analysed. For statistical evaluation, we used Fisher's exact test with p < or = 0.05 considered significant. RESULTS: The success rate of endoscopic treatment, simplified upper tract approach and complete reconstruction were 18.2%, 80% and 83.3%, respectively. Major complications occurred in two patients from group 3. CONCLUSION: Endoscopic puncture is our first option when immediate ureterocele decompression is required, although it seldom affords definitive treatment. Complete primary reconstruction is necessary in complex cases. Cure rates are high but there is a potential risk for serious complications. A simplified upper tract approach is curative in most patients without associated reflux. Heminephrectomy remains our first choice in a large subset of patients with non-viable or hypofunctional renal segments and without high-grade reflux.

Case-Control Studies↗

[Effectivity versus toxicity of minoxidil as antiproliferative agent for lens epithelial cells. In vitro study].

PURPOSE: To evaluate the inhibitory effect of minoxidil on cultured proliferating lens epithelial cells (LECs) versus cytotoxic effect over corneal endothelial cells in culture, because minimum side effects over anterior chamber structures and particularly on corneal endothelium are required for successful therapy and prevention of posterior capsular opacification (PCO). METHODS: New Zealand Rabbit LECs and corneal endothelium were cultured in DMEM at 35 degrees C in 5% CO2 in multiwells during 7 days. Both types of cells were exposed to minoxidil (1, 2 and 4 mM) for 1 and 24 hours. Control group and balanced salt solution group were included. After seven days multiwells were processed for light microscopy study. Morphometric study of cellular population of LECs and corneal endothelium cells were done using a computed planimetry system. RESULTS: Dose-dependent effect on LECs proliferation was noted and non-confluent colonies of cells were observed on all treated groups. Morphologic changes in normal appearance of corneal endothelial cells after 1 hour of minoxidil treatment was observed and intracellular alterations were confirmed even with the lowest dose exposure. CONCLUSIONS: Although effectiveness of minoxidil suppressing in vitro LECs proliferation could be suggest as a useful therapeutic agent to prevent PCO, however the inhibitory effect of different concentrations on corneal endothelial cells conditioned its possible use on ocular surgery.

Animals↗

[The prevalence of antibodies against hepatitis B abs c virus in odontology students].

UNLABELLED: It is accepted that the practice of odontology implies a risk of BBV and HCV transmission but the study of does not. This work tries to determine the prevalence of HBv Ac and HCV Ac (by ELISA) in odontology students and whether there is any relation to the year of study and/or the presence of other risk factors. 188 students in their last three years of studies were investigated, all the participants filled out a clinical epidemiological form. 89 women (47.3%) and 99 men (52.7%), x age was 24.8. 50 (26.7%) had other risk factors. 160 (85.1%) fulfilled biosecurity norms and 40 (21.2%) had a labour accident. RESULTS: None of the analyzed sera were positive for HCV Ac (0%) and 1 was positive for HbcAc. CONCLUSION: The prevalence of HBv Ac and HCV Ac is extremely low with no relation to the year of study or any other risk factors.

Adult↗

RenaGel efficacy in severe secondary hyperparathyroidism.

BACKGROUND: Haemodialysis patients frequently have simultaneous hypercalcemia and hyperphosphatemia, posing a therapeutic dilemma for the traditional calcium--and aluminum--based binders. RenaGel (sevelamer hydrochloride) is an effective phosphate binder without changes in serum calcium or aluminum levels. However being an expensive medication it is currently used mainly for patients with moderate to severe secondary hyperparathyroidism. However most of the previous studies have not included patients with severe secondary hyperparathyroidism. METHODS: Our purpose is to determine RenaGel binder efficacy in haemodialysis patients with severe secondary hyperparathyroidism. As a secondary purpose we have followed the variations of parathyroid hormone, serum calcium, serum lipids [low- and high-density lipoprotein cholesterol, triglycerides and Lipoprotein(a)], uric acid and bicarbonate. All phosphate binders previously used were suspended one week before RenaGel prescription. Our study included 18 adult haemodialysis patients, with PTHi of 810 +/- 330 pg/ml after the "pre-treatment" washout. The binder was administered during 12 weeks, beginning with a mean dose of 2.4 +/- 0.4 g daily and adjusted to obtain serum phosphorus under 6.5 mg/dl (at the end of the study, the mean RenaGel dose was 2.8 +/- 0.6 g daily. RESULTS: The mean changes after RenaGel in serum phosphorus was -0.7 +/- 1.5. mg/dl (P < 0.05), in serum calcium was 0.5 +/- 1.0 mg/dl (P < 0.05) and in calcium x phosphate product of -4.0 +/- 12.4 mg/dl (P = NS). "Post-treatment" the PTHi levels remained stable (820 +/- 360 pg/ml vs 810 +/- 330) but serum alkaline phosphatase increased (14.3 +/- 14.4 U/l; P < 0.01). LDL cholesterol serum levels decreased by -35 +/- 10 mg/dl (P < 0.01), HDL cholesterol showed a trend to increase (3.0 +/- 8.1 U/l; P = NS), triglycerides decreased by 38 +/- 56 mg/dl (P < 0.05) and Lipoprotein(a) remained stable. Serum albumin increased by 0.1 +/- 0.2 g/L (P < 0.05), uric acid decreased -0.8 +/- 1.2 mg/dl (P < 0.05) and bicarbonate remained unchanged. CONCLUSIONS: RenaGel is an effective phosphate binder, even in haemodialysis patients with severe secondary hyperparathyroidism. The lipid profile improved with the treatment, with the exception of Lipoprotein(a) stabilization. Selection of patients with severe secondary hyperparathyroidism at the beginning of RenaGel disposal, for economic reasons is debatable, but could be correct.

Adult↗

Determination of quaternary ammonium pesticides by liquid chromatography-electrospray tandem mass spectrometry.

A method for the direct determination of paraquat, diquat, chlormequat and difenzoquat in water samples, using an on-line solid-phase extraction-liquid chromatography-tandem mass spectrometry system was developed. No sample preparation was required and the detection limits were below the European Union maximum residue levels. The chromatographic separation was performed using an XTera MS C8 column. The concentration of the ion pair reagent, the pH and the gradient elution were optimized to give high recoveries and good chromatographic resolution between quats. The detection was carried out using an ion trap as mass analyzer. Parameters such as the magnitude and duration of the resonant excitation voltage and the magnitude of the trapping RF voltage for full scan tandem mass spectrometry (MS-MS) experiments were studied to establish the optimal experimental conditions. Moreover, the accurate optimization of these parameters allowed MS-MS experiments of low mass ions, below m/z 200, providing unambiguous peak identification. Finally, the reproducibility of the proposed method was shown by good run-to-run and day-to-day precision values and its applicability to the determination of quats in drinking water was evaluated using spiked samples.

Chlormequat↗

Regulation of Ca(2+) signals in a parotid cell line Par-C5.

The Ca(2+) signaling system in an established immortalized rat parotid acinar cell line, Par-C5, was examined using the Ca(2+)-sensitive fluorescent indicator fura-2 and by measuring inositol 1,4,5-trisphosphate (IP(3)) formation. Agonist-induced increase in intracellular Ca(2+) ([Ca(2+)](i)) by mobilization of intracellular stores and influx across the cell membrane was stimulated by acetylcholine (ACh) and ATP, whereas noradrenaline-(NA)-induced a small [Ca(2+)](i) increase mediated primarily by release from intracellular Ca(2+) stores. [Ca(2+)](i) increase by ACh and ATP was mediated through the phosphoinositide signal pathway since both agonists significantly increased 1,4,5-IP(3) formation and Ca(2+) mobilization was abolished by the phospholipase C inhibitor U73122. In Ca(2+)-free medium, ACh or ATP discharged the IP(3)-sensitive Ca(2+) store and essentially abolished subsequent [Ca(2+)](i) response to thapsigargin (TG). Exposure to ionomycin and monensin after TG induced a further mobilization of Ca(2+), suggesting IP(3)-insensitive stores are present. Furthermore, depletion of IP(3)-sensitive Ca(2+) stores by TG, ACh and ATP enhanced plasmalemmal Ca(2+)-entry pathways. Exposure to tumor necrosis factor-alpha (TNF-alpha), a cytokine associated with lymphocyte invasion of salivary epithelial cells in autoimmune disorders, significantly reduced ACh-stimulated Ca(2+) mobilization. TNF-alpha inhibitory effect on Ca(2+) mobilization was not directly due to an interaction on muscarinic receptors since ACh-induced 1,4,5-IP(3) formation was not altered. These results in the Par-C5 cell line indicate 1) [Ca(2+)](i) is regulated by muscarinic and P2Y-nucleotide receptors and partly by alpha(1)-adrenergic receptors; 2) IP(3)-sensitive and -insensitive Ca(2+) stores exist; 3) Ca(2+) influx activated by ACh, ATP or TG is mediated by the store-operated Ca(2+) entry pathway; and 4) muscarinic agonist-stimulated Ca(2+) mobilization is altered by the cytokine TNF-alpha.

Adrenergic alpha-Agonists↗

Location of superoxide production sites in turbot neutrophils and gilthead seabream acidophilic granulocytes during phagocytosis of glucan particles.

Here we show, by spectrophotometry and enzyme cytochemical methods, that turbot neutrophils and gilthead seabream acidophils responded in a similar way when incubated with PMA or with particulate glucans. Cells stimulated with PMA released high amounts of superoxide both intra- and extracellularly. However, O2- was mainly released intracellularly when cells were incubated with particulate glucans. Small glucan particles were quickly phagocytosed and O2- was initially produced in intracellular vesicles and tubular structures that later fused with the phagosome or with the cell membrane. Large glucan filaments that were not phagocytosed also induced cell stimulation and O2- was also produced in intracellular vesicles which then appeared to fuse with the cell membrane. We conclude that, in stimulated turbot neutrophils and gilthead seabream acidophils, superoxide production is carried out initially in intracellular compartments that are very similar to those described in mammalian neutrophils.

Animals↗

Vaginal shedding of hepatitis C virus.

A group of 14 women infected with hepatitis C virus (HCV) was evaluated for vaginal shedding of the virus. The HCV-RNA detection was performed in plasma, peripheral blood mononuclear cells (PBMC) and in supernatant and pellet of vaginal washings. HCV-RNA positive results were obtained in all plasma samples, in 57% of the PBMC samples, in 36% pellets obtained following centrifugation of vaginal washings and in 36% of the supernatants. In 21% of the women a positive result was found, at the same time, in every analysed product. The HCV genotypes identified in the plasma samples (1a: 38%; 1b: 36%; 3a: 13% and 1b+3a: 14%) matched with those in PBMC and vaginal washings in every sample, with the exception of cases where mixed infection (1b+3a) was detected. In these, genotype 1b was only detected in plasma. HCV viral load was not associated with the presence of HCV-RNA in PBMC or in vaginal washings (either cells or supernatant).

Female↗