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Biomedical subjects

R Escamilla

Publications and source records attributed to R Escamilla.

At least 19 recordsLinked to original sources
PubMed2006

Pneumocystis jirovecii genotypes and granulomatous pneumocystosis.

This study describes the initial data concerning molecular typing of Pneumocystis jirovecii in a patient having developed granulomatous Pneumocystis pneumonia (PCP). Three types, B(1)a(3), B(1)a(4), B(1)b(2), were identified. All three had been described in reports concerning patients with common diffuse alveolar PCP. The present data show that identical microorganisms can be involved in both granulomatous PCP and diffuse alveolar PCP and that the pathogenesis of the granulomatous response to P. jirovecii may more likely be related to host factors.

Bacterial Typing Techniques↗
PubMed2004

[Granulomatous pneumocystis pneumonia].

INTRODUCTION: Granulomatous pneumocystis pneumonia (PCP) is a rarity whose presentation may be misleading. CASE REPORT: We report the case of a patient suffering from chronic lymphatic leukaemia presenting with acute respiratory insufficiency, with a fatal outcome, due to granulomatous PCP. Broncho-alveolar lavage (BAL) remained negative and the diagnosis could only be made later by open lung biopsy. CONCLUSION: Although infrequent, granulomatous PCP should be recognised because in this situation the standard investigation (BAL) may be negative. New, more sensitive, methods of investigation such as the polymerase chain reaction (PCR) may permit earlier diagnosis.

Biopsy↗
PubMed2003

[Intra-vascular lymphoma presenting with respiratory symptoms].

INTRODUCTION: Intra-vascular large cell lymphoma is a rare disease characterised by the proliferation of malignant cells within small blood vessels. CASE REPORT: We report a case of intra-vascular lymphoma presenting with unexplained dyspnoea, hypoxaemia and associated neurological symptom. The diagnosis was made by liver biopsy but the patient ultimately died. CONCLUSIONS: Earlier diagnosis with transbronchial biopsy might have improved the prognosis by allowing more prompt treatment.

Aged↗
PubMed2001

Estradiol decreases the acetylcholine-elicited airway reactivity in ovariectomized rats through an increase in epithelial acetylcholinesterase activity.

Estrogen replacement therapy (ERT) is frequently prescribed for postmenopausal women. Epidemiological data suggest that sex hormones may play a role in the expression of asthma, but the mechanism(s) whereby this influence is mediated remain(s) unclear. To better understand the role of physiologic doses of estrogens in airway function, we tested the hypothesis that 17beta-estradiol (E(2), 10 microg/kg per d for 21 d) given to oophorectomized female rats modifies airway responsiveness to cholinergic agonists, compared with oophorectomized rats given placebo. In vivo, the concentration of inhaled acetylcholine (ACh) required to double pulmonary resistance (EC(200)RL) in anesthetized spontaneously breathing tracheotomized rats was calculated as an index of airway responsiveness. E(2)-treated rats were less responsive to ACh than placebo-treated rats (EC(200)RL, 9.40 +/- 1.48 vs. 1.52 +/- 0.85 mg. ml(-1), respectively). Ex vivo airway responsiveness was evaluated with the cumulative concentration-response curve (CCRC) of isolated tracheal segments. Compared with placebo, E(2) treatment significantly increased the EC(50) of ACh (p = 0.01) but did not alter the CCRC to carbachol. Removing the epithelium or treatment with physostigmine abolished the difference in EC(50) of ACh between the groups. Acetylcholinesterase (AChE) activity of homogenized whole trachea was 1.4-fold greater in the E(2)-treated group compared with placebo (p = 0.02), whereas no difference was found in homogenized epithelium-free trachea. We conclude that E(2) treatment decreases airway responsiveness to ACh in ovariectomized rats at least in part by increasing AChE activity dependent on the presence of the epithelium.

Acetylcholine↗
PubMed2001

[Acquired right-to-left shunt with normal right heart pressure].

Intracardiac right-to-left shunting through a patent ovale foramen (POF) despite normal right-sided pressures is an uncommon cause of dyspnea with posture worsening in adults. We report herein 6 cases which sum up etiological circumstances, diagnostic workup and management of this syndrome. The main reported etiopathologic mechanism is consistent with a change in the internal configuration of the right atria leading to preferential blood flow from inferior vena cava through patent foramen ovale. The treatment lies on surgical closure of the septal defect, which can now be performed using a noninvasive percutaneous procedure.

Aged↗
PubMed2000

[Pulmonary hypertension in patient with beta-thalassemia major].

We report a case of pulmonary hypertension (PH) in a 35-year old patient with beta-thalassemia major; he had commenced blood transfusions after the age of 4 years and had been splenectomised at the age of 6 years. PH clinical presentation was not uncommon. Hemodynamic study revealed precapillary PH with high cardiac output; vasodilators agents led to significant pulmonary responsiveness. In beta-thalassemia, whereas congestive heart failure is common and due to cardiac hemosiderin deposition, PH appears to be non rare but its etiopathogenic mechanism remain unclear and probably non univoqual. Hypoxemia as well as hemodynamic changes related to chronic anemia including increased pulmonary flow might play an important role. Management should include blood transfusions to correct anemia, the indication and the choice of vasodilator agents need to be evaluated.

Adult↗
PubMed1998

[Pulmonary artery hypertension in HIV seropositive drug addicts. Apropos of 10 cases].

Pulmonary hypertension (PH) is a classic complication associated with intravenous drug addiction. Various pathogenic mechanisms may be involved but HIV infection now appears to be the main etiologic factor. We report herein 10 case of PH occurred in HIV+ intravenous drug abusers. Each patient had several pathogenic factors: HIV infection, pills crushed and intravenously injected (6 cases), heavy and repeated consumption of amphetamines and cocaine (6 cases), cirrhosis with portal hypertension (2 cases), anticardiolipid antibodies (2 cases). The clinical findings were similar to those reported for PH in HIV seronegative patients; however, in 5 cases, opiates could have alleviated dyspnea, which became perceptible only at the time of drug withdrawal. Because drug addicts usually exhibit a weak support for medical prescriptions, long term therapy needing regular follow-up such as anticoagulation appears to be hazardous and even dangerous. The prognosis remains poor, since the progression of PH led to the death of one third patients within the year following the diagnosis.

Adult↗
PubMed1998

Surfactant changes during experimental pneumocystosis are related to Pneumocystis development.

Pneumocystosis-related surfactant changes have been reported in both humans and corticosteroid-treated experimental hosts. As corticosteroids induce an increase in pulmonary surfactant, some findings could be considered as controversial. The aim of this study was to investigate whether the surfactant composition changes during experimental pneumocystosis were related to the Pneumocystis development. In this work two corticosteroid-untreated animal models were used: rabbits, which develop spontaneous pneumocystosis at weaning; and severe combined immunodeficiency mice, which were intranasally inoculated with Pneumocystis carinii. Surfactant phospholipid and protein content was explored by bronchoalveolar lavage. The in vitro effect of surfactant on P. carinii growth was also explored. In the two models, the surfactant phospholipid/protein ratio was significantly increased, whereas parasite rates were low. This ratio decreases with the slope increase of the parasite growth curve. These early surfactant changes suggested that Pneumocystis proliferation requires alveolar lining fluid changes, and that normal surfactant is not suitable for parasite development. In this way, in vitro experiments presented here have revealed an inhibitory effect of synthetic or seminatural surfactants on the P. carinii growth. Further studies are needed to determine how Pneumocystis induces the reported early modifications of the surfactant, and why the parasite development is inhibited by pulmonary surfactant.

Animals↗
PubMed1997

Guanidinium restores the chromophore but not rapid proton release in bacteriorhodopsin mutant R82Q.

Replacement of the Arg residue at position 82 in bacteriorhodopsin by Gln or Ala was previously shown to slow the rate of proton release and raise the pK of Asp 85, indicating that R82 is involved both in the proton release reaction and in stabilizing the purple form of the chromophore. We now find that guanidinium chloride lowers the pK of D85, as monitored by the shift of the 587-nm absorbance maximum to 570 nm (blue to purple transition) and increased yield of photointermediate M. The absorbance shift follows a simple binding curve, with an apparent dissociation constant of 20 mM. When membrane surface charge is taken into account, an intrinsic dissociation constant of 0.3 M fits the data over a range of 0.2-1.0 M cation concentration (Na+ plus guanidinium) and pH 5.4-6.7. A chloride counterion is not involved in the observed spectral changes, as chloride up to 0.2 M has little effect on the R82Q chromophore at pH 6, whereas guanidinium sulfate has a similar effect to guanidinium chloride. Furthermore, guanidinium does not affect the chromophore of the double mutant R82Q/D85N. Taken together, these observations suggest that guanidinium binds to a specific site near D85 and restores the purple chromophore. Surprisingly, guanidinium does not restore rapid proton release in the photocycle of R82Q. This result suggests either that guanidinium dissociates during the pump cycle or that it binds with a different hydrogen-bonding geometry than the Arg side chain of the wild type.

Bacteriorhodopsins↗
PubMed1995

Pulmonary veno-occlusive disease in a HIV-infected intravenous drug abuser.

Pulmonary veno-occlusive disease (PVOD) is a rare cause of pulmonary hypertension. Its origin remains unknown but in some cases a viral aetiology has been suggested. Recently primary pulmonary hypertension has been increasingly observed in patients with human immunodeficiency virus (HIV) infection, but only one case of pulmonary veno-occlusive disease has so far been described. We report the case of a 27 year old male intravenous drug abuser with HIV infection and pulmonary hypertension. Open lung biopsy led to the diagnosis of pulmonary veno-occlusive disease. This second case of pulmonary veno-occlusive disease raises the question of a relationship between HIV infection and lesions involving the pulmonary veins. However, the pathogenesis of vascular changes remains to be elucidated.

Adult↗
PubMed1995

[Disseminated aspergillosis with pulmonary and cardiac localization in an HIV-infected patient].

The authors report a case of invasive aspergillosis with pulmonary and cardiac involvement revealed by a pericarditis in a seropositive patient (VIH1). Clinical findings, differential diagnosis and outcome underly the issues encountered in the management of aspergillosis in AIDS patients. Indeed, the low prevalence of aspergillosis in AIDS and the insidious features of aspergillosis locations make the early diagnosis difficult. It is though essential for a favourable outcome under specific treatment. The risk factors, clinical characteristics and diagnostic procedures are mentioned as well as the various available treatments.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Bronchoalveolar lavage phospholipid abnormalities in HIV-infected patients.

Our aim was to evaluate the quality of pulmonary surfactant, a nonspecific defence system, during the course of human immunodeficiency virus) infection. Protein and phospholipid composition were determined in 127 bronchoalveolar lavage (BAL) fluids from 89 HIV seropositive patients (54 acquired immune deficiency syndrome (AIDS), 35 non-AIDS) and 11 healthy controls. In all of the HIV BAL samples, biochemical abnormalities were found. In subjects with pulmonary infection or Kaposi's sarcoma, the phospholipid/protein ratio was decreased, mainly because of elevated protein levels (15.8 and 20, respectively, vs 7.2 mg.100 ml-1 for controls, p < 0.05). In subjects without obvious pulmonary involvement, phospholipid was decreased (1.3 +/- 0.2 vs 2.9 +/- 0.3 mg.100 ml-1 for controls, p < 0.001), whereas the protein was not altered. Phospholipid composition was also altered: the phosphatidylcholine percentage was decreased, whilst the other main phospholipids were increased. We conclude that the alveolar lining is altered, whatever the stage of HIV disease. In most patients, it results from an increase of vascular permeability, with an influx of serum proteins. However, changes in phospholipid composition suggest that, in some cases, surfactant is also altered.

Acquired Immunodeficiency Syndrome↗
PubMed1993

[Monotherapy using amoxicillin/clavulanic acid as treatment of first choice in community-acquired lung abscess. Apropos of 57 cases].

In a multicentre open prospective trial the effectiveness of AM-CA as first-line treatment of community-acquired lung abscess was evaluated in immunocompetent adult patients. AM-CA was administered intravenously in doses of 4 g/day for at least 7 days, then orally in doses of 2 g/day for at least 14 days. Radio-clinical and laboratory evaluations were made during treatment, and 30 and 60 days after it was discontinued. The results of this trial concerned 57 patients (48 men, 9 women; mean age 52 years). The facilitating factors were those usually found in lung abscess. Twenty-seven patients had previously received an antibiotic treatment which had failed. The clinical picture, built up gradually in 42/37 patients, consisted of infectious syndrome (52 cases), altered general condition (39 cases), purulent expectoration (47 cases), sometimes foetid (10 cases), and thoracic clinical abnormalities (57 cases. X-ray films of the chest showed round abscess images (44 cases) or looked like necrotizing pneumonia (13 cases) with pleural reaction (8 cases). Protecting bacteriological sampling by BFW brushing and transtracheal or transparietal sample collecting was performed in 41 of the 57 patients. The pathogens, isolated in 31 cases, were: S. pneumoniae 5; Streptococcus spp. 12; Staph. aureus 4; H. influenzae 7; Enterobacteriaceae 6; anaerobes 7. These organisms were associated in 8 cases. With the exception of Enterobacter cloacae, all were sensitive to AM-CA in-vitro. The outcome was satisfactory in 52 patients.

Adolescent↗
PubMed1992

Surfactant analysis during Pneumocystis carinii pneumonia in HIV-infected patients.

Pulmonary surfactant is altered in experimental Pneumocystis carinii pneumonia. Although P carinii is a major causative agent of pneumonia in immunocompromised patients, the pathophysiology of lung injury caused by this organism is poorly understood. Therefore, we studied bronchoalveolar lavage specimens obtained from 19 HIV-infected subjects with PCP compared with specimens from ten healthy control subjects. As iterative BAL was performed, 37 BAL specimens were analyzed for protein and phospholipid. The BAL samples were divided into two groups as follows: 22 BAL samples with the presence of P carinii and 15 BAL samples without P carinii. Compared to control subjects, HIV+ BAL presented a significant increase of PR and a decrease of total PL in both P carinii+ and P carinii- BAL, but in P carinii+ BAL, the fall of PL/PR ratio was significantly more pronounced compared to P carinii- (0.09 +/- 0.02 vs 0.19 +/- 0.04, p less than 0.02). The BAL performed during the recovery of PCP showed an improvement of initial biochemical abnormalities. Surfactant composition was also altered, with a phosphatidylcholine and phosphatidylglycerol drop and a sphingomyelin and lysophosphatidylcholine increase. The presence, even in P carinii- BAL, of less polar compounds of undetermined nature, was revealed. We concluded that in HIV+ patients, abnormalities of pulmonary surfactant were present before PCP, and that the development of PCP enhances these abnormalities. These surfactant alterations may contribute to the saprophyte-pathogen transformation of P carinii, but this hypothesis requires further investigation that is presently in progress.

Adult↗
PubMed1992

[Respiratory function in heroin addicts with or without HIV infection. Study of 107 cases with a 6-month follow-up of 36 subjects].

Both intravenous drug addiction (IVDA) and HIV infection can involve respiratory system. So, we have studied pulmonary function in 107 heroin abusers during deprivation to clarify the extent of these two factors respectively. Two groups were separated: 50 subjects without HIV infection (HIV-) and 57 seropositive subjects (HIV+) in early stage of the disease (mean CD4 lymphocytes: 457 +/- 61/mm3). 36 subjects have been investigated 6 months later to evaluate the reversibility of possible observed abnormalities. Altered pulmonary function was encountered similarly in HIV+ and HIV-. DLco was abnormal in 40% of cases both in HIV+ (mean DLco: 63.4 +/- 1.1% of predicted values) and HIV- (mean DLco: 65.4 +/- 1.5% pred); obstructive lung disease was present in 18% of HIV- (FEV1/VC: 63.8 +/- 2.5) and 9% of HIV+ (FEV1/VC: 61 +/- 3.6); restrictive lung disease was found more frequently (16% vs 10%) in HIV+ (FEV1/VC: 81.2 +/- 2.1, TLC: 72.4 +/- 3.6% pred) than in HIV- (FEV1/VC: 84.2 +/- 1.6, TLC: 71.2 +/- 0.9% pred). These abnormalities were not associated with significant arterial blood gas modifications. As a whole, DLco tend to improve in the two groups and this significantly for HIV+ (p less than 0.03). But for individuals initial DLco alteration was persistent in 68% of cases suggesting slow improvement. In conclusion, in this study HIV+ and HIV- IVDA were not different concerning pulmonary function. In this risk group, DLco itself had a poor specificity and only it follow-up may be of interest for pulmonary opportunistic infection screening.

Adult↗