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Biomedical subjects

S Aguado

Publications and source records attributed to S Aguado.

At least 19 recordsLinked to original sources

Herpes simplex virus encephalitis in a renal transplant patient: diagnosis by polymerase chain reaction detection of HSV DNA.

A case of herpes simplex virus (HSV) encephalitis with disseminated primary HSV infection in a renal transplant patient is described. The diagnosis of the disease was achieved by nested polymerase chain reaction (PCR)-DNA in cerebrospinal fluid (CSF). Other diagnostic measures (immunoglobulin [Ig] M and virological cultures both in blood and CSF) were negative. Blood IgG gave a false-positive signal. Although ganciclovir is not the drug of choice, its concomitant administration in our patient as a prophylactic measure against CMV infection may have decreased the usual severity normally expected in this kind of primary HSV infection. The subsequent increase in ganciclovir dose to full therapeutic range, which was implemented before the diagnosis was achieved, led to the disappearance of symptoms. The detection of PCR-DNA in CSF will probably become the diagnostic method of choice. One of its great advantages, in addition to its diagnostic reliability, is that it may obviate the performance of many cerebral biopsies.

Adult↗

Treatment of cyclosporin-induced gingival hyperplasia with azithromycin.

BACKGROUND: Gingival hyperplasia is a known complication of cyclosporin therapy. Although plaque control has been shown to be of benefit, gingival surgery is occasionally necessary. The aim of this study was to review the effect of a short-course therapy with azithromycin in renal transplant patients with cyclosporin-induced gingival hyperplasia. METHODS: Thirty-eight patients received 500 mg/day of azithromycin for 3 consecutive days. The degree of gingival hyperplasia was classified as: 0, no gingival overgrowth; 1, mild overgrowth; 2, moderate overgrowth, and 3, severe overgrowth. Gingival bleeding and evolution of gingival hyperplasia were determined at 0 (pretreatment), 7, 30, 90 and 180 days. Cyclosporin, serum creatinine and ALT levels were simultaneously determined on the same days. RESULTS: Seven patients were excluded, leaving a total of 31 included in the trial. Eleven had a score of 3, 17 a score of 2, and 3 a score of 1. The degree of gingival hyperplasia was unrelated to the dose and levels of cyclosporin. Gingival hyperplasia improved in all patients (P < 0.001, Friedman test). The degree of improvement was better when the degree of hyperplasia was lower. In 27 patients gingival hyperplasia remained absent 6 months later, 3 patients required a second course of treatment, and another required gingival surgery. Gingival bleeding, present in 28 patients when diagnosed, disappeared in all cases in 2.2 +/- 1.2 (1-7) days. No adverse effects were observed. Cyclosporin, serum creatinine, and ALT levels were not affected by treatment. CONCLUSIONS: Azithromycin improves cyclosporin-associated gingival hyperplasia, especially when administered early in the process.

Adult↗

A family with a milder form of adult dominant polycystic kidney disease not linked to the PKD1 (16p) or PKD2 (4q) genes.

Autosomal dominant polycystic kidney disease (ADPKD) is a genetically heterogeneous disease. Most families show positive linkage to polymorphic markers around the PKD1 (16p13.3) or PKD2 (4q21-23) loci. The PKD1 and PKD2 genes have been cloned and mutations defined in a number of patients. Several clinical studies have described a milder phenotype for PKD2 patients. More recently, evidence for a third genetic locus has been found in one Portuguese, one French-Canadian, and one Italian family. We identified a Spanish family with negative linkage to the PKD1 and the PKD2 loci. This family showed a very mild clinical phenotype compared to the other forms of ADPKD, including the non-PKD1/non-PKD2 families previously described.

Adult↗

[Bacteremia in patients undergoing chronic hemodialysis in a 16-year period].

OBJECTIVE: To determine the incidence of bacteremia among patients on hemodialysis, the responsible microorganisms and to describe the predisposing and prognostic factors. METHODS: A retrospective analysis was conducted of 85 episodes of bacteremia occurred from 1979-1994; the episodes involved 71 patients (male/female ratio: 27/44) with a mean age of 58 years (29-80). RESULTS: Eighty-seven microorganisms were recovered, which included 61 grampositive cocci (67% Staphylococcus aureus), 25 gramnegative bacilli (52% Escherichia coli) and 1 anaerobe. The mean incidence was 3.1/100 patients on hemodialysis/year (range: 1.1-8.3), higher in patients with interstitial and cystic renal disease. In 52% of cases an intravascular source was detected, associated with vein access for hemodialysis (in 91% there were inflammatory signs at the fistula). In 16 cases (19%) no portal of entry was detected and in the remaining patients the portal of entry had an extravascular origin. Eighty patients received antibiotic therapy and 35 patients required the substitution of the vein access. Thirteen patients died (15%) as a result of bacteremia. The mortality rate was higher among patients developing shock (50%), endocarditis (75%) and in those who had remained for longer than 1,000 days on hemodialysis (45%). Bacteremia accounted for the third known cause of death on dialysis, and was responsible for 11% of deaths occurred during the time of the study. CONCLUSIONS: Bacteremia among hemodialysed patients was mainly associated with Staphylococcus aureus infections at the vascular access. Bacteremia was the direct responsible for 11% of deaths occurred on dialysis.

Adult↗

Cytomegalovirus preemptive therapy with ganciclovir in renal transplant patients treated with OKT3.

In an attempt to decrease the prevalence and severity of cytomegalovirus (CMV) disease, preemptive therapy with ganciclovir was administered to all renal transplant patients treated with OKT3 between February 1993 and December 1994 (26 patients). The results were compared with those of a historical group treated with OKT3 but not with ganciclovir (29 patients). Both groups were similar in age, sex, number of previous transplants, number of rejections, serological status of donor and recipient and OKT3 dose. Ganciclovir was administered during the period of treatment with OKT3. Only 2 (7.7%) treated patients developed CMV disease versus 11 (37.9%) of the control group (p = 0.01). In the control group the intensity of the disease was severe in 7 (63.6%) cases, whereas in the treated patients it was always of slight intensity (p = 0.01). In conclusion, preemptive therapy with ganciclovir during treatment with OKT3 decreases the prevalence and severity of CMV disease.

Acyclovir↗

Cytomegaloviraemia and T cell subpopulations in renal transplant patients.

We studied 54 consecutive recipients of renal transplants to evaluate their immunological responses to cytomegalovirus (CMV) infection. Forty-three (79.6%) patients developed CMV infection, and all of them subsequently recovered. Fourteen of these infected patients (32.6%) developed viraemia during the infectious process, four of whom then manifested the disease. The number of lymphocytes and their main subpopulations was normal before the appearance of CMV infection. During the infection there was a significant growth (P < 0.001) in the CD8+DR+ subset, corresponding to activated T suppressor/cytotoxic lymphocytes, whereas the natural killer measured subsets remained within normal limits during the whole infectious process. As all viraemic patients recovering from the infection developed CD8+DR+ activation, we conclude that this recovery is associated with the immunological activation.

Adult↗

DNA microsatellite analysis of families with autosomal dominant polycystic kidney disease types 1 and 2: evaluation of clinical heterogeneity between both forms of the disease.

We studied 17 large families affected by adult dominant polycystic kidney disease (ADPKD). Ultrasonographic analysis was performed on all the family members. DNA microsatellite markers closely linked to PKD1 on 16p13.3 were analysed, and linkage of the disease to this locus was determined. Families showing a negative linkage value were evaluated for linkage to the PKD2 locus on 4q. Five of the 17 families showed negative linkage for the 16p13.3 markers. In these families significant linkage to 4q was obtained. Renal cysts developed at an earlier age in PKD1 mutation carriers, and end stage renal failure occurred at an older age in people affected with PKD2. Analysis of large families with ADPKD in a Spanish population indicates that this is a genetically heterogeneous disorder, but mutations at only two loci are responsible for the development of the disease in most if not all the families. Clinicopathological differences between both forms of the disease occur, with subjects with ADPKD2 having a better prognosis than those with mutations at PKD1.

Adolescent↗

[Diagnosis of dominant renal polycystosis in adults by analysis of DNA polymorphism].

BACKGROUND: Adult renal polycystosis (ARP) is a dominant autosomic disease. The gene responsible for this disease in most families has been located on the short arm of chromosome 16 (16 p) by restriction analysis of the DNA polymorphisms (RFLP). METHODS: The existence of several polymorphic markers flanking this gene permits the diagnosis of any member of an affected family. A series of proximal and distal genetic markers have been used to study the segregation of the disease in a group of families with more than one affected member. RESULTS: The clinical and genetic results obtained from a study of 10 Spanish families with ARP have been reported. A high percentage of the members under 30 years of age (40%) did not present renal cysts. CONCLUSIONS: Restriction analysis of DNA are fundamentally for a disease in which a high percentage of carriers remain asymptomatic within the reproductive age.

Adult↗

Genetic and clinical studies in autosomal dominant polycystic kidney disease type 1 (ADPKD1).

Thirteen Spanish families with autosomal dominant polycystic kidney disease were studied. In one family the disease did not segregate with polymorphic markers around the PKD1 locus. All subjects over the age of 30 years carrying a mutation at the PKD1 locus showed renal ultrasonographic cysts, but 40% of carriers of the PKD1 mutation younger than 30 years did not have renal cysts. Hypertension was found to be more frequent in those with renal cysts. Recombinants between 16p polymorphic loci and the PKD1 locus are described.

Adult↗