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Biomedical subjects

A Jara

Publications and source records attributed to A Jara.

48 records · Page 3Linked to original sources
PubMed1992

[Miliary tuberculosis as a complication of BCG immunotherapy in cancer of the bladder. Case report].

Intravesical administration of BCG may be used as an ancillary immunotherapy after endoscopic resection for cancer of the bladder. Local side effects are usually mild. Here is reported a patient who developed miliary tuberculosis after this form of therapy. Radiologic studies of the thorax and liver biopsy confirmed the diagnosis. The patient recovered after treatment with anti-tuberculosis drugs (TA-81 scheme). Epithelial trauma may be invoked as an alteration facilitating this complication. Although it develops infrequently, patients with bladder cancer treated with BCG must be monitored for this complication.

BCG Vaccine↗
PubMed1990

[Human recombinant erythropoietin (rH-EPO) in chronic hemodialysis patients].

We studied 7 patients on chronic hemodialysis before and after 12 weeks of therapy with human recombinant erythropoietin. The drug was administered intravenously, 3 times a week at doses increasing from 50 to 125 U/kg. Dialysis was performed for 4 hr, 3 times a week and no blood transfusions were used during the study. An increased tolerance to daily physical activities was observed in all patients. Hematocrit increased from 19 +/- 3.4 to 28 +/- 4.1 and hemoglobin from 6.7 +/- 1.3 to 9.4 +/- 1.5, p less than 0.01. No changes were detected in blood pressure, weight, liver function tests and nutritional values. No patient developed either absolute (ferritin less than 30 ng/ml) or relative iron deficiency (transferrin saturation less than 20%) during the study. Efficiency of dialysis remained unaltered. No secondary effects from the drug were observed. Thus, this study confirms the clinical usefulness of human recombinant erythropoietin in patients with chronic renal failure and anemia on chronic dialysis.

Adult↗
PubMed1990

[IgA nephropathy (Berger's disease). Our experience in 78 cases].

We studied 78 patients with a diagnosis of IgA nephropathy. Renal biopsy was indicated in 69 patients by the presence of macroscopic hematuria (52%), microhematuria or proteinuria (22%), nephrotic syndrome (10%), severe hypertension with microhematuria or renal failure (14%) or nephritic syndrome (1%). Nine were healthy subjects being studied as live kidney donors. An association with IgG and/or IgM was present in 92% of patients. Serum IgA was elevated in 36% of patients. Hypertension was present in 30% and decreased renal function in 29%. Patients with serum creatinine above 1.5 mg/dl tended to be older (33.8 vs 28.7 years) and to have hypertension (52% vs 19%). Among 25 patients followed for more than 12 months renal function remained stable in 44%, deteriorated in 20% and 36% developed renal failure. The latter was associated to older age, hypertension, absence of macroscopic hematuria and nephrotic syndrome. The 9 live donors had no clinical manifestations of renal disease. Thus, IgA nephropathy is a highly variable clinical entity, both in its manifestations and its prognosis. An asymptomatic course is demonstrated in some subjects.

Adolescent↗
PubMedDate not supplied

Y chromosome sequences in Turner's syndrome: association with virilization and gonadoblastoma.

UNLABELLED: The presence of Y chromosome fragments in patients with Turner's syndrome is known to increase the risk of gonadoblastoma and virilization. Y chromosome material is detected in up to 6% of patients with Turner's syndrome by karyotype. By DNA analysis, Y chromosome sequences have been reported in 0-60% of patients. The putative gonadoblastoma gene has been mapped to the pericentromeric region of the Y chromosome increasing the interest in studying these sequences. AIMS: 1. To determine the frequency of occult Y chromosome sequences in patients with Turner's syndrome. 2. To analyze the clinical implications of Y sequences detected by karyotype and occult Y sequences. STUDY DESIGN: Cross-sectional study of 58 patients with Turner's syndrome (30 45,X; two with structural anomalies; 26 mosaic [two of whom were 45,X/46,XY]). SRY, TSPY and DYZ3 sequences were amplified by PCR using genomic DNA from peripheral blood. RESULTS: All three Y chromosome sequences were found in one out of 56 patients whose karyotype was not suggestive of having Y chromosome material and in one patient with 45,X/46,Xr(X) karyotype. The patients with the ring chromosome and 45,X/46,XY karyotype underwent surgery and were found to have a gonadoblastoma and dysgerminoma. The four patients with Y chromosome material had non-virilized female genitalia. CONCLUSIONS: Analysis by PCR was more sensitive in detecting Y chromosome sequences than conventional karyotype. The presence of Y material was not associated with virilization. We confirmed the association of Y fragments and gonadoblastoma at an early age.

Adolescent↗
PubMedDate not supplied

Catastrophic antiphospholipid syndrome associated with crescentic glomerulonephritis: a clinicopathologic case.

The association of renal failure with catastrophic antiphospholipid syndrome has been reported in the context of microvascular occlusions and/or malignant hypertension. We describe a 36-year-old woman who died of multiorgan failure with the laboratory, clinical and histopathological characteristics of catastrophic antiphospholipid syndrome associated with a crescentic glomerulonephritis and renal failure.

Adult↗
PubMedDate not supplied

[Utero-inguinal hernia].

A ten year old boy was operated for left inguinal hernia at age four years. Male gender was confirmed by sex chromatin. Y corpuscle and male genotype in chromosomal studies, and testicular function was tested by normal testosterone serum levels before and after parenteral human chorionic gonadotropin stimulus. On a second operation, two structurally normal testes and was deferens coexisted with Müllerian structures (rudimentary uterus and two Fallopian tubes of normal histological features) were found. A diagnosis of uterus-inguinalis hernia was made. Deficiencies at Müllerian inhibiting factor's secretion, activity or receptors have been postulated to explain this anomaly.

Child↗