Biomedical subjects
Publications and source records attributed to A Segarra.
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Hemoperitoneum is a well-known form of hepatocellular carcinoma presentation and represents a frequent complication in countries with a high incidence of hepatocellular carcinoma, but it is rarely seen in Western countries. Our aim was to report the results and describe the arteriographic and CT-scan characteristics in a series of seven consecutive patients. They were admitted to our hospital because of hemoperitoneum due to ruptured tumor as a first manifestation of hepatocellular carcinoma, and the rupture was effectively controlled by transcatheter arterial embolization. From April 1989 to April 1998, 440 consecutive patients were admitted to our liver unit with the diagnosis of hepatocellular carcinoma and liver cirrhosis. Fourteen patients (3%) presented with acute hemoperitoneum due to tumor rupture as a first manifestation of hepatocellular carcinoma. We here report our experience in the group of patients treated by transcatheter arterial embolization. Mean age was 67.1+/-5 years (range, 61-73). All patients presented with sudden abdominal pain, abdominal distension, and four patients had symptoms of acute anemia. In all cases the ruptured tumor was subcapsular. The procedure was effective in the control of bleeding in all cases, without significant impairment in liver function or treatment-related deaths. In six of the seven patients, a self-limited postembolization syndrome was observed. Mean survival time was 273+/-488.7 days (range: 15-1290). Three patients survived more than six months but at the time of evaluation, only one patient was alive. In conclusion, the present results confirm that transcatheter arterial embolization is an effective and well-tolerated treatment in the management of hemoperitoneum due to ruptured hepatocellular carcinoma in patients with liver cirrhosis.
The chemokine receptors CCR5 and CXCR4 play a key role in HIV-1 infection as co-receptors for viral entry. In the placenta, an important natural barrier to HIV, the expression and regulation of these receptors has yet to be elucidated. In this study, we determined the expression of CCR5 and CXCR4 co-receptors on placental macrophages (PM) and the effect of interleukin-10 (IL-10) on co-receptor expression. PM were isolated from term placentae of HIV-uninfected mothers and cultured for up to 11 days. The cells were stimulated with IL-10 for 24 h and stained with specific antibodies to CCR5, CXCR4, CD4, CD3, CD11c and CD14 for flow cytometry. Unstimulated PM expressed significantly more CCR5 than CXCR4. Expression of both co-receptors was upregulated by stimulation with IL-10 at 24 h post-stimulation. In vivo expression of these co-receptors from frozen sections revealed a higher percentage of CCR5 positive cells. This is the first study in which expression of both co-receptors is detected on the PM membrane. These results are consistent with previous studies performed in our laboratory where PM were readily infected by CCR5-using HIV strains but could not be productively infected by HIV strains that exclusively use CXCR4 as a co-receptor.
We have investigated the effects of high arginine (Arg) levels (7.5 mg/100 g body weight per hour) on the early integration of biocompatible mesh grafts into the rat abdominal wall. Studies were performed over implantation intervals of 6, 12, 24 or 48 hours (n=12, each). Arginine and related compounds were quantified in plasma, wound fluids and multiple tissues. Plasma nitric oxide (NO) production was studied. Strips were taken from the polypropylene fiber-host tissue interfaces (PTIs) for optical microscopic analysis and for immunohistochemical analysis using rat-specific antibodies against type I and type III collagens. Exogenous Arg was metabolized at the peripheral tissues but reliably reached the wound space. High amounts of Arg and ornithine (Orn) were detected in the specimens considered. No changes on citrulline (Ctr) or NO concentrations were observed, overall suggesting that, during the period studied, the arginase pathway predominated. The acute scarring response differed significantly in the two placements considered. The P-SS interface evidenced more extensive new tissue growth than the P-DS interface. Forty-eight hours after mesh implantation cellular infiltration, fibroblast proliferation, and mesh-surrounding angiogenesis were higher in the arginine-treated rats. Type III collagen staining was related to arginine treatment, being higher (++) in the study group. In conclusion, and independently of the site of mesh placement, supplemental Arg seemed to favorably affect early local collagen deposition. This could be potentially helpful to ameliorate the integration of biomaterials into the tissues and, consequently, to allow for the design of more selective therapeutic strategies to prevent hernia recurrence rates.
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The possible association between lipoprotein(a) [Lp(a)] and albumin excretion rate (AER) is a topic that generates conflicting views. In addition, Lp(a) phenotypes have not previously been considered as factors influencing AER. In order to clarify this issue, we studied 70 non-insulin-dependent diabetes mellitus (NIDDM) patients without clinically detectable macroangiopathy, 27 with microalbuminuria and 43 without it. Both groups were matched for the known variables that could influence AER and serum Lp(a) levels. Lp(a) was determined by enzyme-linked immunosorbent assay (ELISA), and Lp(a) phenotypes were assessed by electrophoresis followed by immunoblotting. Lp(a) phenotypes were grouped as follows: 'small' (F, S1 and S2), 'big' (S3 and S4) and 'null'. The NIDDM patients with microalbuminuria presented higher serum Lp(a) concentrations than the patients without it [15.7 mg dL-1 (95% CI 0.5-36.5) vs. 4.5 mg dL-1 (95% CI 0.1-18.5); P < 0.001] and a direct correlation between Lp(a) and AER was observed (r = 0.34; P < 0.01). AER was significantly different when Lp(a) phenotypes were considered ['small': median 19 micrograms min-1 (range 1-195); 'big': median 9.5 micrograms min-1 (range 1-186); 'null': 4 micrograms min-1 (range 1-9); P = 0.04]. None of the NIDDM patients with a 'null' phenotype showed an AER of > 10 micrograms min-1. In conclusion, this case-control study provides evidence that microalbuminuria is associated with high serum Lp(a) in NIDDM without clinically detectable macroangiopathy. Furthermore, NIDDM patients with a 'null' phenotype could be considered at low risk for the development of microalbuminuria.
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In order to investigate the effects of lovastatin on adrenal and gonadal function, we prospectively determined the basal and gonadorelin-stimulated concentrations of testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and the cortisol response to adrenocorticotropic hormone (ACTH) in a sample of 25 male patients with advanced chronic renal failure, hypercholesterolemia and proteinuria. Hormone studies were done prior to and after lovastatin treatment. The values of these patients were compared with those of a matched healthy control group. Before starting treatment with lovastatin, the patients showed significantly lower testosterone concentration and higher LH concentration than the control group. After stimulation with gonadorelin, they also showed a lower increase in testosterone and LH. After 12 months of lovastatin treatment, a significant decrease in the concentration of cholesterol, LDL C, VLDL C and apo B was observed, but neither the basal testosterone concentration nor the response to gonadorelin stimulation was modified. Before treatment, basal and ACTH-stimulated serum cortisol levels did not differ from those of the control group. After lovastatin treatment, neither the basal serum cortisol levels nor the response to ACTH was modified. We conclude that in the patients studied, although the decrease in testosterone concentration may be partially attributable to a decrease in its synthesis, lovastatin treatment does not increase testosterone deficit. This is either because this drug does not inhibit gonadal hydroxymethylglutaryl CoA reductase at the does given or because the cholesterol which LDL C provides the cell with is enough to maintain testosterone synthesis.
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In order to analyze the relationship between lipoprotein (a) [Lp (a)] and other lipoproteins during chronic renal failure and once renal function is restored after kidney transplantation, we determined the serum levels of total lipoprotein, high-density lipoprotein, low-density lipoprotein, and very-low-density lipoprotein cholesterols, total and very-low-density lipoprotein triglycerides, apolipoproteins A-I, B, C-II, C-III, and E, and E, and Lp (a) in 30 patients with chronic renal failure before and 12 months after renal transplantation. During the 1st year after transplantation, all patients were treated only with ciclosporin and prednisone and had serum creatinine levels < 1.6 mg/dl (140 mumol/l) and proteinuria < 500 mg/day. No patients had chronic hepatic disease. To determine reference values we studied a control group of 60 healthy volunteers. Before renal transplantation, the study group showed higher concentrations of triglycerides, very-low-density triglycerides, very-low density lipoprotein cholesterol, apolipoproteins, C-II and C-III, and Lp(a) than the control group. There was no correlation between Lp(a) and any of the studied variables. After renal transplantation, the serum levels of total lipoprotein, high-density lipoprotein, and low-density lipoprotein and apolipoproteins A-I and B increased significantly. Apolipoproteins C-II and C-III and Lp(a) decreased and normalized. After these changes had taken place, there was no relationship between Lp(a) and other parameters of lipoprotein metabolism. We conclude that the increase in Lp(a) during the chronic renal failure phase is basically related to the loss of renal function and does not depend on the resultant alterations which are produced in other lipoprotein variables.
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BACKGROUND: Isotopic renogram allows renal function to be estimated in both kidneys independently. The glomerular filtrate in ischemic kidneys is largely dependent on the tone of the efferent glomerular arteriolae and therefore on the concentration of circulating angiotensin II. METHODS: In 42 patients with severe high blood pressure in whom renal angiographic study was carried out for suspicion of vasculo-renal hypertension, an isotopic renogram using 99m Tc-DTPA as a tracer was performed in basal conditions and following the administration of 50 mg of oral captopril. RESULTS: In 21 patients both the angiographic examination and the post-captopril renogram were normal. In 16 patients in whom uni or bilateral stenosis higher than 50% of the lumen of renal artery was observed on angiographic examination, the post-captopril renogram showed changes. In 5 patients the angiography was normal while the renogram showed evaluable changes. No false negatives were observed in the post-captopril renogram, however the basal renogram was not demonstrative in 6 patients with stenosis of the renal artery. Sensitivity of the test was thus 100% and specificity 80%. The positive predictive value was 76% and the negative predictive value 100%. CONCLUSIONS: The post-captopril renogram may be a useful test in the functional study of renal behaviour in patients with vasculo-renal hypertension.
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