PubMed Health⌕ Search

Biomedical subjects

G Parra

Publications and source records attributed to G Parra.

At least 37 records · Page 2Linked to original sources
PubMed1993

[Seropositive polyarthritis as a presentation form of angioimmunoblastic lymphadenopathy].

We present a 59-year-old male who was admitted due to fever and generalized lymphadenopathy. The patient had polyclonal hypergammaglobulinemia, Coombs-positive anemia, positive rheumatoid factor (latex 1:1280-SCAT 1:128), hypocomplementemia, negative LE cells and FAN negative. He had a 2 months history of a rheumatoid arthritis-like polyarthritis with poor response to non-steroid antiinflammatory drugs. On physical examination a mild symmetrical polyarthritis of small and large joints was seen. A lymph node biopsy showed architectural effacement, absence of germinal centers, arborization of postcapillary venules and a polymorphonuclear infiltrate that included immunoblasts. Thus, this patient fulfills the morphologic criteria of angioimmunoblastic lymphadenopathy (AILD) (Fig. 1 and 2). Our purpose was to describe the association of seropositive polyarthritis with AILD as a presentation sign. Whether this represents a case of a rheumatoid arthritis with AILD or the polyarthritis which has been described as part of the clinical picture or AILD is difficult to say due to the short time evolution of the disease.

Arthritis↗
PubMed1992

Increased urinary excretion of prostaglandin E2 in patients with idiopathic hypercalciuria is a primary phenomenon.

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P less than 0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean +/- SEM) was 11.62 +/- 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 +/- 0.48 nmol/day in the control subjects (P = 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.

Adolescent↗
PubMed1992

Myocardial cell hypertrophy after myocardial infarction with reperfusion in dogs.

BACKGROUND: The potential role of myocardial cell hypertrophy in the ischemic zone in the mechanism of late recovery of regional contractile function after myocardial infarction followed by reperfusion has not been examined. METHODS AND RESULTS: Eight chronically instrumented, conscious dogs were subjected to 90-120 minutes of circumflex coronary artery occlusion followed by reperfusion. The thickness and function of the anterior (AT) and posterior (PT) walls was measured by ultrasonic gauges at control, during occlusion, and after reperfusion. After 3 weeks, cross-sectional areas of surviving cells were determined from subepicardial (epi), midwall (mid), and subendocardial (endo) regions in six dogs and compared with those from six animals without infarction, including three sham-operated control dogs. PT systolic wall thickening showed dyskinesia during occlusion but recovered after reperfusion to 48% of control at 1 week and 67% at 3 weeks. End-diastolic thickness of the PT wall increased markedly after reperfusion, but AT and PT walls were only slightly thicker (p = NS) than in control dogs at 3 weeks. Cross-sectional areas of reperfused dogs in the infarct region averaged 279 (PTepi), 291 (PTmid), and 317 microns 2 (PTendo) and were significantly larger than in control animals (237 [PTepi], 241 [PTmid], and 233 microns 2 [PTendo]). PT cell areas were significantly larger than AT cells, ENDO cell areas were larger than EPI cells (both p < 0.05), and ENDO cells of the AT wall were larger than those of noninfarcted dogs (p < 0.05). CONCLUSIONS: In dogs with myocardial infarction followed by reperfusion, the cross-sectional areas of cells in the infarcted PT wall were larger than those in the noninfarcted AT wall, and within both the infarcted and noninfarcted zones, cell areas were larger in the endocardial than the epicardial region. In all regions of the infarcted wall and in the ENDO region of the noninfarcted wall, cell areas were generally larger than those of control dogs without infarction, and the control dogs showed no transmural differences in cell areas. The mechanisms responsible for this significant remodeling of the reperfused infarcted zone, which involves myocardial cellular hypertrophy, are unknown, but it is possible that hypertrophy of surviving regions of the infarcted wall played a role in the late recovery of regional function that accompanied this hypertrophic response.

Animals↗
PubMed1992

Acute serum sickness in normal and C6 deficient rabbits: role of membrane attack complex.

Acute serum sickness was induced in New Zealand White (NZW) and in C6 deficient (C6D) rabbits, to compare the histology, immunofluorescence, especially distribution of poly C9 (MAC), and electron microscopic characteristics of the disease in each strain. Glomerulonephritis and albuminuria of comparable extent occurred in 13/17 NZW and 4/8 C6D rabbits. In NZW rabbits with albuminuria an early intense glomerular infiltration by mononuclear cells was associated with focal small fine granular glomerular basement membrane (GBM) deposits of IgG and BSA and more diffuse and larger deposits of C3 and MAC. After the disappearance of monocytes and decrease in mesangial cell proliferation, development of large subepithelial GBM deposits rich in all immune reactants was observed in NZB rabbits. In C6D rabbits with albuminuria a similar monocytic infiltrate occurred, but no association with IgG and C3 GBM immune deposits was noted. No deposits of MAC and no large subepithelial GBM 'humps' were observed in C6D rabbits. We conclude that the exudative (monocytic) phase of glomerular injury and albuminuria in acute serum sickness nephritis are not dependent upon terminal complement components, but the subsequent formation of large subepithelial GBM deposits does not occur in this model in the absence of MAC.

Albuminuria↗
PubMed1991

Atrial natriuretic peptide levels in brain venous outflow during cardiopulmonary bypass in humans: evidence for extracardiac hormonal production.

Atrial natriuretic peptide (ANP) is a hormone with an important role in the regulation of extracellular fluid volume. The ANP gene is not only expressed in the heart, but the high concentration of ANP in cardiac blood makes it difficult to demonstrate extraatrial hormonal secretion in vivo. This issue was addressed during complete cardiopulmonary bypass (CPB) in 13 patients undergoing elective cardiac surgery in whom ANP concentrations were followed in the internal jugular vein, representing largely brain venous outflow, as well as a peripheral vein and radial artery, after the heart and lungs were excluded from circulation. Plasma ANP levels in the peripheral venous circulation showed no significant changes during extracorporeal circulation, although they tended to decrease (from 6.75 +/- 2.16 fmol/mL to 4.76 +/- 0.69 fmol/mL; P greater than 0.05). ANP levels in the radial artery decreased significantly after the exclusion of the heart (from 16.84 +/- 3.51 fmol/mL to 6.83 +/- 0.97 fmol/mL; P less than 0.01). In contrast, ANP concentration in the internal jugular vein increased in 12 of 13 patients during the first 15 minutes of CPB (from 9.49 +/- 1.96 fmol/mL to 15.96 +/- 2.8 fmol/mL; P less than 0.01) and remained above the levels found simultaneously in other sampling sites during CPB. High-performance liquid chromatography analysis of plasma extracts showed multiple peaks of ANP, but the elution patterns of peripheral venous blood and brain outflow were similar. One of the immunoreactive peaks was located at the position of standard human ANP (Ser99-Met110-Tyr126).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Ultrasound study of acute appendicitis in children with emphasis upon the diagnosis of retrocecal appendicitis.

Acute appendicitis in children frequently presents equivocal clinical manifestations. Delay of the proper diagnosis and unnecessary laparotomies are common. Abdominal ultrasound has proved to be useful in the diagnosis of acute appendicitis in adults. We have performed a preoperative ultrasound study in 368 children with acute appendicitis. Among the, 92 had a retrocecal appendicitis. Ultrasound established the correct diagnosis in 92.6% of patients, and in 94.5% of those with a retrocecal appendicitis. At our institution an abdominal sonography is performed on any child with a doubtful clinical diagnosis of acute appendicitis, helping the surgeon to take the decision to perform a laparotomy.

Acute Disease↗
PubMed1990

Fish oil dietary supplementation reduces Ia expression in rat and mouse peritoneal macrophages.

Preliminary studies suggest that administration of fish oil fatty acids may be beneficial in several immunological diseases; therefore, we studied the effect of fish oil dietary supplementation on the expression of Ia in stimulated murine peritoneal macrophages. Rats (n = 19) and mice (n = 27) on standard rodent feeding were separated in experimental (E) and control (C) groups that received fish oil or saline solution, respectively, daily for 4 weeks by esophageal gavage. Cholesterol serum levels were significantly lowered by fish oil (E vs C, P less than 0.01). E and C groups were injected intraperitoneally with Listeria monocytogenes (LM) and peritoneal cells were harvested 4 and 7 days after infection. Decreased expression of Ia induced by LM was found in rats (C = 49.68 +/- 5.09%, E = 16.95 +/- 4.3%, P less than 0.01) and mice (C = 47.38 +/- 7.63%, E = 26.66 +/- 1.92%, P less than 0.01). Animals with a more pronounced depression of serum cholesterol (reduction of 44.04 +/- 1.52% of baseline levels) had more depression of Ia expression (6.47 +/- 1.22%, P less than 0.001 vs control). Reduction of Ia expression was not related to PGE2 production by peritoneal cells. Reduction of Ia expression by fish oil could induce down-regulation of antigen presentation and alloreactivity.

Animals↗
PubMed1990

Atrial natriuretic factor in the acute nephritic and nephrotic syndromes.

Because the role of systemic hormones in the pathophysiology of edema in acute renal disease remains incompletely understood, we compared the levels of atrial natriuretic factor (ANF) and plasma renin activity (PRA) in patients with acute glomerulonephritis (AGN), nephrotic syndrome (NS), and normal individuals during salt deprivation and salt loading. Sixteen patients with AGN (10 males) and nine patients with NS and hypoalbuminemia (7 males) were studied on admission, and after recovery (12 AGN patients) or remission (4 NS patients). Eighteen normal controls were each studied after five days on a low (20 mEq Na/day), regular (120 mEq Na/day) and high (300 mEq Na/day) dietary salt intake. Patients with AGN and NS had comparable edema (AGN 2.8 +/- 0.53 kg; NS 3.36 +/- 0.47 kg; SE) and urinary Na excretion (mean +/- SEM: AGN 0.97 +/- 0.11 mEq/hr; NS 1.06 +/- 0.16 mEq/hr), but AGN patients had five times higher ANF (AGN 27.2 +/- 4.06 fmol/ml; NS 5.51 +/- 1.02 fmol/ml; P less than 0.001) and six times lower PRA ng/liter.sec levels (AGN 0.187 +/- 0.047; NS 1.144 +/- 0.222; P less than 0.001) than NS patients. The degree of edema was correlated with ANF levels in AGN patients (P less than 0.001) but not in NS patients. There was a strong exponential negative correlation (r = -0.773, P less than 0.0001) between ANF and PRA, in which AGN patients and Na-restricted controls were located in the opposite ends of the volume sensing-response, and NS patients in the middle, alongside controls with regular Na intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1990

Migration inhibition factor in acute serum sickness nephritis.

Monocytes have been demonstrated to play an important role in acute serum sickness (AcSS) nephritis. Because accumulation of monocytes within the glomeruli could be the result of local lymphokine production, we studied migration inhibition factor (MIF) activity in supernatants from glomerular cultures, analyzed its temporal relationship with monocyte and lymphocyte accumulation, and tested the effect of anti-T lymphocyte monoclonal antibody on local MIF production. AcSS was induced in 12 rabbits, and one additional rabbit had antigen elimination without proteinuria. Single nephrectomy was performed at the time of antigen elimination in all animals; the remaining kidney was removed four days (4 rabbits) or 14 days afterwards (5 rabbits). In glomerular cross sections (gcs), lymphocytes were identified using monoclonal antibody M108, and monocytes by nonspecific esterase stain (ES). MIF activity was determined in supernatants of cultures of isolated glomeruli by the agarose microdroplet method. Peak of MIF activity (84.3 +/- 2.6%, SEM) was observed the first day of proteinuria in association with peak of lymphocyte infiltration (1.15 +/- 0.1 lymphocytes/gcs) and monocyte infiltration (2.4 +/- 0.3 mean ES score/gcs). MIF activity diminished by day 4 (66.0 +/- 6.3%) and reached control levels by day 14 (12.8 +/- 3.2%). There was a significant correlation between lymphocyte infiltration and MIF activity (r = 0.776, P less than 0.0001) as well as between MIF activity and monocyte accumulation (r = 0.858, P less than 0.0001). In five additional rabbits with AcSS, glomeruli were isolated, treated successively with M108 and normal rabbit serum, and supernatants harvested from 24-hour cultures were tested for MIF activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Atrial natriuretic factor increases after a protein meal in man.

1. The renal function changes induced by dietary protein are thought to result from the activity of hormonal factors that remain as yet undefined. Since a meat meal and high dose atrial natriuretic factor (ANF) infusions have similar effects on glomerular filtration rate, natriuresis and kaliuresis, we decided to investigate the possibility that a protein meal could stimulate ANF activity. 2. We studied 10 normal volunteers who had a fixed protein and sodium intake for 7 days before the experiments. The subjects received a meat meal (1-1.5 g of protein/kg) and, on a separate occasion, a carbohydrate meal that had a similar caloric, sodium and potassium content. Diuresis was stimulated with water ingestion, and urine collections were obtained before the meals (baseline) and after the meals for a period of 3 h. Blood samples were obtained 30 min and 5 min before the meals and every hour for 3 h in the period after the meal. 3. The protein meal, but not the carbohydrate meal, was associated with parallel increments in plasma immunoreactive ANF (i-ANF), natriuresis, kaliuresis and glomerular filtration rate (estimated from creatinine clearances) which reached peak values 2-3 h after the meal. The mean increment of plasma i-ANF after the protein meal represented a twofold increase over baseline levels. 4. We conclude that ANF may participate in the physiological response to an oral protein load.

Atrial Natriuretic Factor↗
PubMed1988

Increased urinary excretion of prostaglandin E in patients with idiopathic hypercalciuria.

1. Because urinary prostaglandin excretion could play a role in idiopathic hypercalciuria (IH), we studied the excretion of prostaglandin E (PGE), calcium and sodium at various urine flows in 21 patients (14 males) with urolithiasis and IH, seven stone formers (five males) with normal calciuria and 20 controls (11 males). Dietary composition was comparable and sodium intake was restricted to 100-120 mmol/day. 2. Analyses were performed on 30 min urine collections obtained after overnight water deprivation and during water diuresis. Male IH patients had increased levels of urinary PGE at all ranges of urine flow. PGE excretion correlated directly with urine flow in patients and controls, but the slope of this relationship in individual IH male patients was steeper than in controls (P less than 0.01). Calciuria correlated directly with urine output in patients with IH but not in controls. Calcium and sodium excretion were directly correlated (P less than 0.0001) in patients and controls. There were no significant differences between absorptive IH (seven patients) and renal IH (eight patients). There were no significant differences between stone formers with normocalciuria and control subjects. 3. The findings suggest that increased urinary PGE could play a role in the hypercalciuria syndrome, possibly by promoting natriuresis.

Adolescent↗
PubMed1988

Urinary prostaglandin E and kallikrein activity in glomerular hyperfiltration induced by a meat meal in man.

Because renal vasodilator systems may be involved in the physiologic response to a protein meal, we studied the relationship of prostaglandin E (PGE) and kallikrein (KE) activity to the renal hemodynamic changes induced by a meat meal. Ten normal subjects on a maintenance diet providing 1 g protein per kg and 100 mmol Na daily were studied before and after a meal of 86 g of meat protein, once without medication, and again after treatment with indomethacin (150 mg daily for 3 days before and 50 mg the morning of the test). A carbohydrate meal of similar caloric, Na and K content was used in control studies. Glomerular filtration rate (GFR, inulin clearance), renal blood flow (RBF, para-aminohippurate [PAH] clearance), PGE and kallikrein urinary excretion were determined. All studies were performed during water diuresis to avoid bladder catheterization. The protein load induced an increase in GFR (ml/min, mean +/- s.e.m.: baseline 107.2 +/- 6.05, peak postmeal 146.4 +/- 6.79, p less than 0.01) and RBF (baseline 529.7 +/- 42.9, postmeal 678.9 +/- 61.9, p less than 0.05). Renal hemodynamic changes were unrelated to changes in urinary PGE and KE excretion. Indomethacin treatment inhibited PGE excretion by 73% during the test meal but did not modify the protein-induced hyperfiltration. Our results suggest that these renal vasodilator systems are not primarily responsible for the hyperfiltration response. In addition, the data show that inhibition of prostaglandin synthesis is not a practical approach to prevent glomerular hyperfiltration in clinical practice.

Adult↗
PubMed1988

Short-term treatment with captopril in hypertension due to acute glomerulonephritis.

We report that the inhibition of the angiotensin converting enzyme is an effective short-term treatment of low-renin hypertension in acute glomerulonephritis (AGN). We treated 9 patients who had AGN with moderate to severe hypertension and suppressed plasma renin activity with 25-50 mg of captopril per os every 6-8 hours. Control of blood pressure was achieved in 1-2 hours and maintained thereafter. Captopril therapy was associated with an increase in plasma renin activity, a decrease in plasma aldosterone and an increase in the urinary excretion of prostaglandin E2 and kallikrein, independent of changes in urine output. Creatinine clearance increased 39.6 +/- SE 15.2% with captopril and decreased in the postcaptopril period, suggesting that captopril exerted a reversible effect on glomerular filtration rate, possibly modifying intrarenal vasoconstriction. Our study shows that rapid control of hypertension in AGN may be obtained with oral inhibition of the angiotension converting enzyme. Stimulation of PGE2 and kinins, as well as angiotensin II blockade appear to contribute to the hypotensive effect of the drug; by inference, the suppressed activity of vasodilator systems seems to play a significant role in the hypertension of AGN.

Acute Disease↗
PubMed1984

Cell populations and membrane attack complex in glomeruli of patients with post-streptococcal glomerulonephritis: identification using monoclonal antibodies by indirect immunofluorescence.

Poststreptococcal glomerulonephritis (PSGN) had been thought to arise from renal deposition of immune complexes and as such is analogous to acute serum sickness. Recent studies of acute serum sickness in animals and PSGN in humans, however, have suggested a pathogenetic role for cellular immunity. To enlarge on these observations, cellular components of glomeruli were characterized by indirect immunofluorescence in 11 tissues from individuals with PSGN using monoclonal antibodies. These studies demonstrate infiltration of glomeruli by monocytes, granulocytes, and lymphoid cells. Focal accumulations of T lymphocytes were also observed adjacent to Bowman's capsule. Analysis of glomerular T-cell subpopulations revealed a predominance of cells reactive with OKT4 early and with OKT8 later in the course of disease. Proliferation of parietal and visceral epithelial cells was associated with increased binding of BA-1 and J5, respectively. The presence of the membrane attack complex of complement was demonstrated by glomerular reactivity with a monoclonal antibody (poly-C9 MA) which recognizes a neoantigen present in poly-C9. Fluorescence was present along the glomerular basement membrane early and within the mesangium late in the course of disease, a distribution similar to that observed for C3 and C5. These observations suggest that immune cells as well as terminal components of complement either provoke or mark tissue injury in PSGN.

Adolescent↗
PubMed1981

Skin window immune response to normal human IgG in patients with rheumatoid arthritis and acute poststreptococcal glomerulonephritis.

The skin window technic was utilized to determine the reactivity of patients with rheumatoid arthritis (RA) and acute poststreptococcal glomerulonephritis (APSGN) to human IgG (H-IgG). The response to H-IgG was compared in nine patients with RA, 20 patients with APSGN, and 10 normal individuals. All subjects were tested concomitantly with the saline solution used as solvent for H-IgG. The normal controls and five patients were challenged, in addition, with diphtheria-tetanus-pertussis antigen (DPT) to which they had previous prophylactic exposure. The following results were obtained: 1) Four patients with RA and nine patients with APSGN responded with increased lymphocyte migration (more than 2 SD above the normal mean level) at nine and 12 hours. 2) The mean estimated immunogenic lymphocytosis (calculated subtracting the lymphocyte counts of the saline skin windows) of both patient groups was significantly higher than that of controls at the same time intervals. 3) The response of normal individuals and patients to DPT was comparable in time of appearance and intensity to the response of patients to H-IgG. Our studies that patients with RA and APSGN respond to H-IgG in a manner comparable to that observed with a known antigenic stimulus and support a clinical role for antiglobulin reactivity.

Adolescent↗
PubMed1977

Congenital total hemihypertrophy and carcinoma of undescended testicle: a case report.

The first case of germinal cell tumor of the testis in a patient with congenital total hemihypertrophy is reported. The literature is discussed with emphasis placed on the frequent association of hemihypertrophy with oncogenesis and teratogenesis. We conclude that because of the high incidence of malignancy in the undescended testis prophylactic orchiectomy should be considered in a patient with hemihypertrophy and cryptorchidism.

Cryptorchidism↗