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Biomedical subjects

C Campo

Publications and source records attributed to C Campo.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Fournier's gangrene. A study of 12 patients and a review].

We present the clinicoepidemiological and therapeutic characteristics of 12 patients with Fournier's gangrene. The mean age of the patients was 66 years and all had a known predisposing factor for the disease. In all cases there was a predominance of mixed flora (four Gram-positive cocci, nine Gram-negative bacilli and ten anaerobic pathogens), with only one case of bacteremia reported. Initial surgery was conducted and was complemented by antimicrobial administration (imipenem, cefotaxime, clindamycin, penicillin and gentamicin alone and in combination) and local treatment with sugar and povidone-iodine. Hyperbaric oxygen was not used in any cases. At the end of treatment a mesh graft could be applied in 11 patients, all of whom showed an excellent functional and aesthetic recovery. The mean time of hospital stay was lengthy (49 days). The good evolution of the lesions after starting the local treatments with the sugar povidone-iodine combination should be emphasized.

Administration, Topical↗
PubMed1999

Effects of acid suppression and bismuth medications on the performance of diagnostic tests for Helicobacter pylori infection.

OBJECTIVE: This study was designed to investigate whether acid suppression and bismuth medications interfere with the performance of diagnostic tests for Helicobacter pylori (H. pylori) infection. METHODS: Sixty patients with previous diagnoses of atrophic gastritis and H. pylori infection made in gastric biopsies taken at Hospital Departmental, Pasto, Colombia, were enrolled in the study. 13C breath urea test (UBT) and stool antigen test (HpSA) were performed simultaneously. Two baseline tests were performed: one 7 days before and another the day before starting medications. A total of 20 patients received for 2 wk one of the following treatments: a) ranitidine; b) lansoprazole; or c) bismuth subsalicylate. The tests were repeated while the patients were on the prescribed medication on days 7 and 14 and then 2 wk after finishing the medication. RESULTS AND CONCLUSIONS: Utilizing standard cut-off values for the tests, our results indicate that in the case of the 13C UBT test, ranitidine does not interfere with the results, whereas lansoprazole and bismuth may be expected to yield a significant proportion of false negative results (30-40% for lansoprazole and 45-55% for bismuth). In the case of the HpSA test, ranitidine does not interfere, whereas lansoprazole and bismuth may be expected to yield a nonsignificant proportion of false negative results (15-25% for lansoprazole and 10-15% for bismuth). Absolute values for both tests may be used to study the effects of the pharmacological agents on the characteristics of the infection.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1999

Molecular-weight-dependent effects of nonanticoagulant heparins on allergic airway responses.

We have hypothesized that antiallergic activity of inhaled heparin is molecular weight dependent and mediated by "nonanticoagulant fractions" (NAF-heparin). Therefore, we studied comparative effects of high-, medium-, and ultralow-molecular-weight (HMW, MMW, and ULMW, respectively) NAF-heparins on acute bronchoconstrictor response (ABR) and airway hyperresponsiveness (AHR) in allergic sheep. Specific lung resistance was measured in 23 allergic sheep, before and immediately after challenge with Ascaris suum antigen, without and after pretreatment with inhaled NAF-heparins. Airway responsiveness was estimated before and 2 h postantigen as the cumulative provocating dose of carbachol in breath units, which increased specific lung resistance by 400%. NAF-heparins attenuated ABR and AHR in a molecular-weight-dependent fashion. HMW NAF-heparin (n = 8) was the least effective agent: it attenuated ABR [inhibitory dose causing 50% protection (ID50) = 4 mg/kg] but had no effect on AHR. MMW NAF-heparin (n = 8) showed intermediate efficacy (ABR ID50 = 0.8 mg/kg, AHR ID50 = 1.4 mg/kg), whereas ULMW NAF-heparin (n = 7) was the most effective agent (ABR ID50 = 0.4 mg/kg, AHR ID50 = 0.2 mg/kg). ULMW NAF-heparin was 3.5 times more potent in attenuating antigen-induced AHR when administered "after" antigen challenge and failed to inhibit the bronchoconstrictor response to carbachol and histamine. In 15 additional sheep, segmental antigen challenge caused a marked increase in histamine in bronchoalveolar lavage fluid that was not prevented by any of the inhaled NAF-heparins. These data indicate that antiallergic activity of inhaled heparin is independent of its anticoagulant action and resides in the <2,500 ULMW chains. The antiallergic activity of NAF-heparins is mediated by an unknown biological action and may have therapeutic potential.

Animals↗
PubMed1998

Detection of a t(8;21)(q22;q22) in a case of M5 acute monoblastic leukemia.

Although the translocation (8;21) is the single most common structural rearrangement reported in acute myeloblastic leukemia (AML), it is rarely seen in AML FAB type M5. We describe a case of a 51-year-old male with a diagnosis of acute monoblastic leukemia (AML M5b with hemophagocytic component) whose karyotype showed at (8;21)(q22;22). To our knowledge, this is the first report of this translocation in an AML M5b. The t(8;21) has been associated with a good prognosis, but our patient suffered a fast and fatal evolution.

Chromosomes, Human, Pair 21↗
PubMed1998

Microalbuminuria in essential hypertension.

Microalbuminuria is frequently seen in patients with established essential hypertension, and is a predictor of a higher risk for cardiovascular and probably renal dysfunction. The presence of microalbuminuria has been shown to correlate with the other cardiovascular risk factors commonly seen in hypertensive patients. This fact indicates that the detection of an increased urinary albumin excretion could probably be the best index of an increased global cardiovascular risk in a given patient. Blood pressure control is accompanied by a fall in the content of albumin in urine. Agents with the capacity to block the renin-angiotensin system have shown a capacity to decrease urinary albumin excretion, which is independent of their ability to lower blood pressure. Whether or not a decrease in urinary albumin excretion is accompanied by an improved renal and cardiovascular prognosis in hypertensive patients remains to be elucidated.

Albuminuria↗
PubMed1998

Blood pressure control, proteinuria and renal outcome in chronic renal failure.

The presence of proteinuria has been shown to be an excellent predictor for a worse outcome of renal function. Both proteinuria and arterial hypertension often coexist in the same patient, and therapy must be directed at decreasing protein excretion in the urine as well as lowering the blood pressure. Any antihypertensive agent has the capacity to lower proteinuria simply by lowering blood pressure. Furthermore, the antiproteinuric capacity of angiotensin-converting enzyme inhibitors can be equalized by other agents or their combination, provided that the fall in blood pressure is great enough. For this reason studies are needed in which the strict control of arterial hypertension combined with a decrease in proteinuria are considered.

Antihypertensive Agents↗
PubMed1998

Inhibition of antigen-induced airway hyperresponsiveness by ultralow molecular-weight heparin.

Unfractionated heparin (UF-heparin) has been shown to prevent antigen-induced airway hyperresponsiveness (AHR), but it is ineffective when administered after the antigen challenge. We hypothesized that the failure of UF-heparin to modify postantigen AHR might depend on molecular weight. We therefore studied the effects of UF-heparin and three low-molecular-weight heparin fractions (medium-molecular-weight heparin [MMWH]; low-molecular-weight heparin [LMWH]; and ultralow-molecular-weight heparin [ULMWH]) on antigen-induced AHR and histamine release in bronchoalveolar lavage fluid (BALF). Specific lung resistance (SRL) was measured in 20 allergic sheep before, immediately after, and up to 2 h after challenge with Ascaris suum antigen. Airway responsiveness was expressed as the cumulative provocative dose of carbachol, in breath units, that increased SRL by 400% (PD400). PD400 was determined before and 2 h after antigen, both without and after treatment with aerosolized UF-heparin (1,000 U/kg) and various heparin fractions (0.04 mg/kg to 5 mg/kg) administered after the antigen challenge. Inhaled UF-heparin (n = 4), MMWH (n = 4), and LMWH (n = 6) failed to modify postantigen AHR when administered after the challenge. Only ULMWH (n = 6) inhibited postantigen AHR in a dose-dependent manner (percent protection ranged from 31% to 139%). In eight additional sheep, histamine in BALF was measured with a radioimmunoassay (RIA) before and after the segmental antigen challenge, without and after pretreatment with inhaled UF-heparin, LMWH, or ULMWH. Inhaled UF-heparin and LMWH inhibited antigen-induced histamine release as measured in BALF by 81% and 75%, respectively; whereas ULMWH was ineffective in this respect. We conclude that: (1) modification of antigen-induced AHR by fractionated heparins is molecular-weight dependent; and (2) only ULMWH attenuates AHR when administered after antigen challenge, via an unknown mast-cell-independent action.

Administration, Inhalation↗
PubMed1997

L-arginine reverses the antinatriuretic effect of cyclosporin in renal transplant patients.

BACKGROUND: Cyclosporin has been shown to facilitate renal vasoconstriction and to have an antinatriuretic effect. The existence of an interference of cyclosporin with the vasodilating properties of endothelium mediated by nitric oxide production could mediate these effects. On the other hand, the infusion of the nitric oxide precursor L-arginine has been shown to induce renal vasodilatation and to facilitate natriuresis in normal volunteers. We have investigated the renal effects of the administration of an infusion of L-arginine in renal transplant patients chronically treated with cyclosporin. To facilitate the analysis of the data the effects of the administration of a similar dose of cyclosporin on renal function during the infusion of a vehicle were also investigated during the administration of a vehicle of L-arginine. DESIGN: Ten male renal transplant patients, chronically treated with cyclosporin and with a stable renal function were studied during 2 consecutive days after the administration of the usual morning dose of cyclosporin. The first day they received an intravenous infusion of vehicle and the second the infusion of graded doses of L-arginine (50, 100, 150 mg/kg/h) during 3 consecutive h. RESULTS: The first day, after cyclosporin administration a significant fall (P < 0.01) was observed in natriuresis and kaliuresis in the absence of changes in renal plasma flow and glomerular filtration rate. After the administration of L-arginine significant (P < 0.01) increases of renal plasma flow, glomerular filtration rate, and natriuresis were seen. The increase in blood levels of cyclosporin after its administration did not differ between days 1 and 2. CONCLUSION: These results indicate that L-arginine facilitates renal vasodilatation and natriuresis in renal transplant patients. Furthermore, the observed increase in sodium excretion could indicate that L-arginine counteracts the antinatriuretic effect of cyclosporin.

Adult↗
PubMed1997

The natriuretic effect of nifedipine gastrointestinal therapeutic system remains despite the presence of mild-to-moderate renal failure.

BACKGROUND: Calcium channel blockers facilitate the renal excretion of sodium and this effect is maintained during chronic administration of these drugs. However, it is unknown whether this natriuretic effect remains despite the presence of a decreased renal function. OBJECTIVE: To compare the natriuretic capacity of nifedipine gastrointestinal therapeutic system (GITS) and lisinopril in patients with mild-to-moderate chronic renal failure. METHODS: An open-label, randomized, comparative study was conducted to compare the natriuretic capacity of nifedipine GITS and lisinopril in the presence of mild-to-moderate renal failure (creatinine clearance 30-80 ml/min). After a wash-out period of 4 weeks an intravenous saline infusion (30 ml/kg of body weight of isotonic saline in 4 h) was performed and repeated after 4 weeks of active therapy. Two sex- and age-matched groups of hypertensive patients (n = 25) were included in the study. Renal failure was diagnosed as secondary to nephrosclerosis in all the patients. RESULTS: A significant increase in the renal capacity to excrete the sodium load was observed in patients receiving nifedipine GITS (n = 11) but not in those taking lisinopril (n = 13). Both drugs controlled blood pressure to a similar extent. No changes were observed in body weight, glomerular filtration rate and renal plasma flow (measured as inulin and paraaminohippurate clearances). A significant drop was observed in urinary albumin excretion after lisinopril, but not after nifedipine. Heart rate was higher in nifedipine group. CONCLUSION: The natriuretic capacity of nifedipine GITS remains despite the presence of mild-to-moderate chronic renal failure. Such an effect takes place in the absence of changes in renal hemodynamics, suggesting that it is caused by a direct tubular effect.

Administration, Oral↗
PubMed1997

Inhibition of antigen-induced acute bronchoconstriction, airway hyperresponsiveness, and mast cell degranulation by a nonanticoagulant heparin: comparison with a low molecular weight heparin.

Inhaled heparin prevents antigen-induced bronchoconstriction and inhibits anti-IgE-mediated mast-cell degranulation. We hypothesized that the antiallergic action of heparin may be dependent on molecular weight and related to its nonanticoagulant properties. Therefore, in the present investigation we studied the effects of a nonanticoagulant fraction of heparin (LA-heparin) on antigen-induced bronchoconstriction, airway hyperresponsiveness (AHR), and mast-cell degranulation, and compared its antiallergic activity with that of a low molecular weight heparin (LMW-heparin, fragmin). Specific lung resistance (SRL) was measured in 15 sheep before, immediately after, and serially for as long as 2 h after airway challenge with Ascaris suum antigen, without and after pretreatment with inhaled fractionated heparins at doses of 2.5 and 5 mg/kg. Airway responsiveness was estimated before, and 2 h after antigen as the cumulative provocating dose (PD400) of carbachol in breath units, which increased SRL by 400% (one breath unit was defined as one breath of 1% carbachol solution). LA-heparin caused a dose-dependent inhibition of antigen-induced bronchoconstriction, and a 5-mg/kg nebulized dose caused a 67% inhibition of allergic bronchoconstriction, whereas a 2.5-mg/kg dose was ineffective (20% inhibition). Inhaled fragmin was more potent than LA-heparin, as shown by 84% (2.5 mg/kg) and 82% (5 mg/kg) inhibition of allergic bronchoconstriction. Fragmin (5 mg/kg) also attenuated the postantigen AHR, whereas LA-heparin was ineffective. In vitro, preincubation with both LA-heparin and fragmin inhibited the anti-IgE-induced degranulation of rat peritoneal mast-cells in a dose-dependent fashion. LA-heparin was fourfold more potent than fragmin, with IC50 of 80 and 320 microg/ml, respectively. These data suggest that: (1) fractionated heparins attenuate antigen-induced acute bronchoconstriction, (2) nonanticoagulant fractions mediate the antiallergic activity of inhaled heparin, and (3) antiallergic activity of nonanticoagulant heparin and LMW-heparin may be related to prevention of mast-cell degranulation.

Acute Disease↗
PubMed1996

Aging abolishes the renal response to L-arginine infusion in essential hypertension.

A defect in the endothelium-dependent vasorelaxation could contribute to the development of arterial hypertension through the facilitation of renal vasoconstriction and sodium retention. In this study, we tested the hypothesis that aging impairs kidney function in essential hypertension through a derangement of nitric oxide-dependent renal mechanisms. To this end, we compared the renal response to an intravenous infusion of the precursor of nitric oxide synthesis, L-arginine, in young and aged essential hypertensives. In young hypertensives, L-arginine induced a significant increase in renal plasma flow, glomerular filtration rate, natriuresis and kaliuresis, without changes in filtration fraction. These effects were not observed in aged hypertensives. Neither PRA nor PA were affected by L-arginine infusion in any group. These results indicate that aging produces a derangement of endothelial function in essential hypertension.

Adult↗
PubMed1994

Relationship between blood pressure and renal function.

RENAL DAMAGE CAUSED BY HYPERTENSION: Renal vasoconstriction seems to be a key factor in the origin of arterial hypertension and accounts for the decrease in renal blood flow commonly observed in patients with hypertension. An inverse correlation has been found between renal blood flow and clinic blood pressure levels in established hypertension. Other features of renal damage attributable to high blood pressure have also been correlated with clinic blood pressure levels. Microalbuminuria is a good example of an alteration in renal function that depends in part on blood pressure levels. EFFECTS OF ANTIHYPERTENSIVE AGENTS: Antihypertensive agents can prevent or ameliorate renal vascular damage secondary to arterial hypertension, including renal failure. Ambulatory blood pressure monitoring is an excellent method of studying blood pressure levels in relation to end-organ damage and the blood pressure response to antihypertensive agents. Preliminary studies using this technique indicate that changes in renal function are closely correlated with the average daily blood pressure in arterial hypertension. CONCLUSIONS: Further studies are needed on the mechanisms of renal deterioration and on how to preserve renal function in arterial hypertension.

Antihypertensive Agents↗
PubMed1994

[Bone marrow aplasia and gold salts. Review of the literature apropos of 2 cases].

Bone marrow aplasia remains the most serious adverse effect with gold therapy. Its prevalence is still a controversial issue and at present it is not possible to give accurate figures on its frequency. Two patients diagnosed of rheumatoid arthritis are reported. They underwent chrysotherapy and developed bone marrow aplasia within a 2-month period of therapy. The pathogenic mechanism of blood dyscrasias secondary to gold salts is still unknown. The best available method in the prevention of this serious condition is the periodical obtention of complete blood counts.

Anemia, Aplastic↗