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Biomedical subjects

H Patrick

Publications and source records attributed to H Patrick.

At least 19 recordsLinked to original sources
PubMed2000

Treatment of gram-positive nosocomial pneumonia. Prospective randomized comparison of quinupristin/dalfopristin versus vancomycin. Nosocomial Pneumonia Group.

Nosocomial pneumonia is a frequent complication in hospitalized patients. Gram-positive pathogens, particularly Staphylococcus aureus, are responsible for the increasing frequency of nosocomial pneumonia. To evaluate the efficacy and safety of intravenous quinupristin/dalfopristin (Synercid) in the treatment of nosocomial pneumonia caused by gram-positive pathogens we conducted a prospective, randomized, open-label, international, multicenter, comparative clinical trial. Two hundred ninety-eight patients with nosocomial pneumonia were enrolled in 74 active centers in five countries: a subgroup of 171 (87 quinupristin/dalfopristin-treated and 84 vancomycin-treated patients) were evaluable for the major efficacy end points. One hundred fifty received 7.5 mg/kg of quinupristin/dalfopristin every 8 h; 148 patients received 1 g of vancomycin every 12 h. Aztreonam at a dose of 2 g every 8 h could be administered in both groups for coverage of gram-negative organisms, and tobramycin was added for coverage against Pseudomonas aeruginosa. The primary efficacy end point was the clinical response between the seventh and the thirteenth day after the end of treatment in clinically evaluable patients with documented causative pathogen(s) at baseline (bacteriologically evaluable population). Therapy was clinically successful (cure or improvement) in 49 (56.3%) of patients receiving quinupristin/dalfopristin and 49 (58.3%) patients receiving vancomycin (difference, -2.0% [95% CI, -16.8% to 12.8%]) in the bacteriologically evaluable population. Equivalent clinical success rates were also observed in the all-treated population (n = 298), and in the bacteriologically evaluable patients intubated in baseline (39/72 [54%] compared with 36/67 [54%]). The by-pathogen bacteriologic response was similar in both treatment groups, with equivalent clinical success rates for Streptococcus pneumoniae, Staphylococcus aureus, and methicillin-resistant Staphylococcus aureus. Adverse events (venous and nonvenous) were equally distributed between groups; 15.3% of quinupristin/dalfopristin patients and 9.5% of vancomycin patients discontinued therapy because of an adverse clinical event. In this study quinupristin/dalfopristin was shown to be equivalent to vancomycin in the treatment of nosocomial pneumonia caused by gram-positive pathogens. Quinupristin/dalfopristin merits further evaluation for the treatment of nosocomial pneumonia caused by methicillin-resistant S. aureus.

Adult↗
PubMed1999

Pulmonary hypertension in patients with myelofibrosis secondary to myeloproliferative diseases.

We examined the clinical characteristics of six patients with myelofibrosis secondary to myeloproliferative diseases whose clinical courses were complicated by pulmonary hypertension to determine possible causal links between the two disorders. Six patients (four male, two female), with diagnoses of myeloproliferative disease, myelofibrosis (one with polycythemia vera, three with agnogenic myeloid metaplasia, one with unclassified myeloproliferative syndrome, one with essential thrombocytosis), and pulmonary hypertension are presented. Measurement of the pulmonary artery pressure was performed by Doppler echocardiography in all patients and by right sided heart catheterization in four patients. The range of resting pulmonary artery systolic pressure was 35 to 47 mmHg above the mean right atrium by echocardiography. One patient had autopsy evidence of pulmonary myeloid metaplasia and interstitial fibrosis; another had acute leukemic infiltration of the lung parenchyma. All patients had thrombocytosis; symptomatology in one patient with marked thrombocytosis improved with plateletpheresis. Two patients suffered systemic thrombosis. All patients had severe hepatomegaly. Two patients had evidence of left ventricular dysfunction. The interval between the development of dyspnea and death was less than seven months in five of the patients. A causal link between pulmonary hypertension and myelofibrosis secondary to myeloproliferative diseases is suggested for each patient. Hematopoietic infiltration of the pulmonary parenchyma, portal hypertension, thrombocytosis, hypercoagulability, and left ventricular failure may account in part for the development of pulmonary hypertension in these patients. Patients with myelofibrosis and dyspnea should have Doppler echocardiography to evaluate pulmonary artery pressures.

Adult↗
PubMed1997

Outcome in sarcoidosis. The relationship of relapse to corticosteroid therapy.

STUDY OBJECTIVE: To determine the demographic, clinical, and radiographic characteristics of corticosteroid-treated patients with sarcoidosis who developed relapse following a period of clinical stability lasting longer than 1 month, and to compare these characteristics with those of a group of patients with sarcoidosis who were not treated. DESIGN: Historic, concurrent and prospective, nonrandomized, observational study. SETTING: Ambulatory sarcoidosis clinic in a university city hospital. PATIENTS: Over a 4-year calendar period, 337 patients with sarcoidosis were prospectively enrolled in a registry. One hundred eighteen patients were assigned to a spontaneous remission group when symptoms resolved without treatment, and 103 were assigned to an induced remission group when symptoms resolved following corticosteroid therapy and successful discontinuation. In 116 patients assigned to a recalcitrant group, therapy could not be stopped for 1 month or more owing to severity of symptoms or lack of compliance. We defined relapse as a recurrence of symptoms of sufficient severity to warrant treatment with corticosteroids, following a remission without treatment lasting greater than 1 month. INTERVENTION: Patients who were judged to be sufficiently symptomatic to preclude observation without treatment or who failed to respond to conservative treatment with topical or inhaled corticosteroids or nonsteroidal anti-inflammatory agents were treated with systemic corticosteroids at a target dose of 20 mg prednisone per day for 1 year. MEASUREMENTS AND RESULTS: We observed a 74% relapse rate in the induced remission group, but only an 8% relapse rate in the spontaneous remission group (p < 0.01). Relapse occurred with similar frequency in whites and African-Americans (20% vs 28%), despite a lower treatment rate in white patients than in African-Americans (43% vs 76%; p < 0.01). White patients maintained a sustained remission with twice the frequency of African-Americans (58% vs 29%; p < 0.01). During relapse, 40% of chest radiographs showed no change in type, but there was a significant increase in interstitial profusion (p < 0.05). Initial presentation with asymptomatic chest radiographic abnormalities, erythema nodosum, or peripheral adenopathy portended a favorable prognosis, with sustained remission in 60% of such patients lasting 130 +/- 226 months from time of diagnosis. In contrast, patients who presented with musculoskeletal complaints were nine times, and those with symptoms from hepatic involvement were three times more likely to suffer relapse than to sustain remission without receiving corticosteroids. Most relapses (50%) occurred between 2 and 6 months after discontinuing steroid therapy, but late relapse was not unusual, occurring more than 12 months after discontinuing steroid therapy in 20% of patients with induced remission. CONCLUSIONS: Relapse occurred frequently in patients with sarcoidosis who had been treated with corticosteroids, and rarely occurred in patients who had not been treated with corticosteroids in the past. The striking difference in relapse rate between treated and untreated patients suggests that patients with disease that would later be severe and protracted were almost unerringly identified early in their course. One explanation is that severe presenting symptoms portend a protracted and recurrent course; an alternative explanation is that corticosteroids contributed to the prolongation of the disease by delaying resolution.

Adult↗
PubMed1995

Chronic cough.

Chronic cough is a common symptom presenting to all clinicians. Every effort should be made to determine the cause(s) of cough because specific therapy has a higher likelihood of success than empiric therapy. Evaluation begins with a complete history, physical examination, routine health screen laboratory testing, chest film, and pulmonary function testing. Further investigation should be guided by the response to treatment of the most likely diagnostic possibilities: postnasal drip, cough-variant asthma, gastroesophageal reflux, chronic bronchitis, bronchiectasis, and ACE inhibitor induced. The majority of each patient's workup can be performed and ordered by the primary care physician.

Ambulatory Care↗
PubMed1994

Care of the elderly and occupational health for staff in local nursing homes: quality issues.

Describes a questionnaire sent to 11 of the 66 nursing homes in the Brighton Health Authority to compare the quality of care provided. These homes care for 242 patients (representing 13 per cent of the 1,728 places in Brighton nursing homes). Questions dealt with residential environment, occupational health, care and control of medicines, clerical services, procedures for prevention and control of infection, etc. Results are discussed and recommendations for further improvements made.

Aged↗
PubMed1991

Whole-body gallium 67 scans. Role in diagnosis of sarcoidosis.

Early studies of 67gallium (67Ga) scanning in sarcoidosis focused on the lungs as a measure of disease activity, likelihood of progression, and the advisability of corticosteroid therapy. The predictive value of pulmonary uptake proved to be limited, but there has been renewed interest in 67Ga scanning as a diagnostic aid with special attention to characteristic extrapulmonary uptake patterns. Review of whole-body 67Ga scans in 172 patients with sarcoidosis, 21 with lymphoma, and 51 with other disorders demonstrated distinctive cranial, mediastinal, and hilar uptake patterns in sarcoidosis patients. Bilateral hilar uptake occurred in 81 sarcoidosis patients (47%) but in no lymphoma cases. Increased lacrimal and/or salivary gland uptake was observed in 47.5% but lacked specificity. Uptake in peripheral lymph nodes was infrequent in sarcoidosis (5%) but common in lymphoma (57%). 67Ga scans are especially valuable in patients with uveitis and liver granulomas whose chest radiographs are normal or equivocal. 67Ga scans, unnecessary in typical cases of sarcoidosis, have an important diagnostic role by reducing the need for invasive biopsy procedures in asymptomatic patients.

Citrates↗
PubMed1990

Inhibition and recovery of mammalian respiratory ciliary function after formaldehyde exposure.

Formaldehyde (HCHO) has been reported to impair mucociliary clearance. The present investigation using rabbit and porcine tracheal explants in vitro examined (1) the impairment of ciliary activity, an essential component of mucociliary clearance; (2) the reversibility of ciliary dysfunction after HCHO exposure; and (3) the mechanism by which ciliary activity is reduced by HCHO. HCHO treatment of rabbit tracheal rings significantly decreased zones of active ciliated epithelium in direct proportion to concentration and exposure duration. There was also a significant concentration-dependent reduction of ciliary beat frequency. Removal of HCHO permitted recovery of zones of ciliary activity to normal beat frequencies; greater inhibitory concentrations of HCHO required greater time for return of function. Treatment of porcine tracheae with increasing concentrations of HCHO for time periods inhibitory to rabbit ciliary activity correspondingly reduced the yield of cilia extractable from treated epithelium. Furthermore, the specific activity of ATPase of extracted ciliary axonemes was diminished with increasing HCHO concentration, indicating loss of function. A recovery period following identical exposures of the porcine tracheae to the lower HCHO concentrations resulted in normal yields of functionally intact ciliary axonemes. Similarly, a recovery period after the highest HCHO concentration produced more functional axonemes than obtained from exposed tracheae without a recovery period, although less than normal yields. Therefore, ciliary dysfunction elicited by a defined range of HCHO concentrations is reversible. The yield and functional integrity of ciliary axonemes from epithelium exposed to HCHO with a recovery period are significantly greater than those without such a recovery period, suggesting an alteration and subsequent repair of epithelial surface components following HCHO exposure.

Adenosine Triphosphatases↗
PubMed1983

Computed tomographic diagnosis of pulmonary varix.

A solitary pulmonary nodule was shown by dynamic computed tomography to be vascular, to be enhanced during the pulmonary venous phase, and to be in continuity with the left inferior pulmonary vein. The diagnosis of pulmonary varix was confirmed by pulmonary angiography, an invasive procedure that can be avoided in the future.

Female↗
PubMed1982

Polymorphonuclear leucocytes release a factor(s) that induces platelet aggregation and ATP release after interaction with insoluble and surface-fixed immune complexes.

We have found that human polymorphonuclear leucocytes (PMN) can be stimulated by large aggregates (heat-aggregated IgG, chemically polymerized IgG, heavily aggregated human immune complexes) and by surface-bound immune complexes (IC) to release enzymes (lysozyme, beta glucuronidase) and a factor(s) able to induce platelet aggregation and ATP release from the platelets. Surface-bound IC were most effective in stimulating the release of this factor(s). We used several substrates for their preparation: plastic-adsorbed antigen. Sepharose-coupled antigen and polymerized antigen. The platelet-aggregating factor(s) released by IC-stimulated PMN and zymosan-stimulated PMN were compared for their susceptibility to inhibition by indomethacin. Both induced a first phase of platelet aggregation that was resistant to indomethacin, but the second phase of aggregation and the release of platelet ATP were inhibited to a variable degree, more pronounced in the case of the factor(s) released after PMN-IC interaction. The lack of inhibition of the early phases of aggregation induced by our factor(s) when platelets were simultaneously exposed to indomethacin suggests that the classical, phospholipid PAF is released under these experimental conditions. Although, further experiments will be necessary to fully characterize the factor(s) involved, our observations suggest a complex interrelationship between human PMN and platelet activation, which may play an important role in the sequence of events that mediate the tissue deposition of IC and appearance of inflammatory changes.

Adenosine Triphosphate↗