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Biomedical subjects

P Diaz

Publications and source records attributed to P Diaz.

64 records · Page 4Linked to original sources
PubMed1981

Corticosteroid resistance in chronic asthma.

Fifty-eight patients with chronic asthma in whom airflow obstruction was relieved by bronchodilator aerosols but not by oral corticosteroids were compared with 58 other chronic asthmatics who responded equally well to both treatments. The two groups were matched for age and sex. The only significant clinical differences between the two groups were that in the "corticosteroid-resistant" patients there was a more frequent family history of asthma and a longer duration of symptoms. Resistant patients also had a relatively lower peak expiratory flow rate in the morning than later in the day and a greater degree of bronchial reactivity to methacholine. Such features, however, may not be specific criteria of corticosteroid resistance since they were also observed in untreated asthmatics who subsequently responded well to corticosteroids. The failure of prednisolone to inhibit a monocyte-mediated bronchial reaction may explain why some chronic asthmatics do not respond to corticosteroids. Patients with corticosteroid-resistant asthma should be recognised at an early stage so that regular treatment with oral corticosteroids may be withdrawn. Failure to do this results in needless exposure to the risk of developing serious side effects.

Adrenal Cortex Hormones↗
PubMed1981

Corticosteroid-resistant chronic asthma and monocyte complement receptors.

Monocyte complement receptors (MCR) and enhancement of MCR by a monocyte chemotactic factor (casein) (CRE) were measured in corticosteroid-resistant and corticosteroid-responsive chronic asthmatics. In newly-diagnosed patients who subsequently responded to corticosteroids, the percentage of MCR and CRE was lower after taking oral prednisolone for 7 days and returned to pretreatment values when prednisolone was withdrawn. MCR and CRE in corticosteroid-responsive asthmatics receiving prednisolone were significantly lower than in corticosteroid-resistant asthmatics taking prednisolone. However, there was no significant difference in MCR and CRE between non-responders taking prednisolone and non-responders receiving other forms of therapy. These results suggest that one of the effects of systemic corticosteroids in asthmatics who respond to this form of treatment is a decrease in both MCR and the degree of CRE. Since these changes were not found in corticosteroid-resistant chronic asthmatics such patients may have a defect in the expression and mobilization of complement receptors on the monocyte cell membrane.

Asthma↗
PubMed1979

Echocardiographic assessment of left ventricular function in patients with chronic uremia.

Cardiac function was determined non-invasively in 7 patients (average age 24 years) with chronic uremia. Each was on maintenance hemodialysis. Echocardiograms and carotid pulse tracings were recorded 30 minutes prior to dialysis, and again 30 minutes, 24 and 48 hours following hemodialysis. End-diastolic and end-systolic diameters averaged 5.4 +/- 0.2 and 3.4 +/- 0.1 cm, respectively before and 5.0 +/- 0.2 and 3.2 +/- 0.1 cm immediately after hemodialysis (P less than 0.05 for both). Calculated stroke volume fell from 92.1 +/- 8.8 to 76.7 +/- 10.5 ml (P less than 0.025). Heart rate increased minimally, and average cardiac output was not significantly increased. Following dialysis, body weight and systolic and diastolic blood pressures fell significantly. Thus preload as well as afterload declined. Because of the fall in both stroke volume and end-diastolic volume, a shift along the ventricular function curve downwards and to the left occurred implying diminished cardiac pumping function. Nonetheless the indices of myocardial contractility were normal and showed no change from pre-dialysis value. During the 48 hour interval following hemodialysis all measured and calculated values returned to pre-dialysis levels. Thus organic heart disease as evaluated by non-invasive techniques does not appear to be a necessary sequel to kidney failure, at least in young patients in a hemodialysis program. Gross abnormalities of myocardial function may be absent for at least seven years after the onset of chronic uremia.

Adolescent↗
PubMedDate not supplied

Managing rapid metabolizers of antidepressants.

Depressed patients who rapidly metabolize antidepressants may be common, and may not respond to even high doses of antidepressants if subtherapeutic plasma levels are produced. Rapid metabolizers (RMs) are identifiable if patients are on tricyclic antidepressants (TCAs), and TCA plasma levels (commonly available) are monitored. Strategies to achieve therapeutic levels in RMs include: (1) megaprescribing, or (2) inhibiting the metabolism of the parent drug. Megaprescribing TCAs runs the risk of markedly elevating levels of potentially toxic hydroxy metabolites. In this study twelve depressed, non-responding RMs were identified while taking the TCA, desipramine. Fluoxetine or paroxetine, selective serotonin re-uptake inhibitors (SSRIs) known to potently inhibit cytochrome P450 2D6 (the isoenzyme responsible for desipramine metabolism), was then added to continuing desipramine. Therapeutic range desipramine levels were achieved in ten patients, and seven of the ten achieved excellent or good sustained responses. The combination SSRI and TCA therapy was well tolerated. Whether response primarily reflected the TCA at therapeutic range levels, or a synergistic serotonin-noradrenaline interaction between the respective antidepressants, requires further clarification. The results of this open study suggest the need for controlled trials of antidepressant metabolism inhibition in RMs.

Adult↗
PubMedDate not supplied

Long-term survival of free fat grafts in muscle: an experimental study in rats.

In this study, we showed both macroscopically and microscopically the viability of the autotransplanted fat placed intramuscularly in long-term follow-up. The study was performed on 120 Wistar rats during a 12-month period. The fat grafts were obtained from either the inguinal region or preurinary bladder cavity. Rats were divided into six groups. In group 1, the fat was injected in thin rolls in the frontal subcutaneous layer. In group 2, the fat was injected in thin rolls in the gluteus superficialis, biceps femoris, gastrocnemius, and semitendinosus muscles. In group 3, 6 mm x 2 mm fat strips were placed subcutaneously in the frontal region. In group 4, the same dimension of fat strips were placed in the gluteus superficialis and biceps femoris muscles. In group 5, large cystic spaces of fat were injected subcutaneously in the frontal region, and in group 6, large cystic spaces of fat were injected intramuscularly. Rats at 3, 6, 9, and 12 months after fat grafting were sacrificed in order to carry out the macroscopic observations. The results showed clinical and microscopic success in groups 2 and 4, and problems and failure with the remaining groups.

Adipocytes↗