News about Medicine - Part 3
Stroke is the leading cause of serious long-term disability in adults. In the United States, > 700,000 people experience a stroke annually, and approximately 4 million Americans are currently alive after experiencing a cerebrovascular event. Two thirds of individuals require rehabilitation, and the majority of stroke survivors have residual disability, with equal proportions having mild, moderate, or severe impairment.
All stroke survivors expect to receive appropriate interventions directed at improving outcomes and preventing a recurrent event. In addition to addressing hypertension, predisposing cardiac conditions, and hypercoagulable states, secondary prevention should be directed toward improving other risk factors that contribute to the development of atherosclerosis, including lifestyle modifications. Over the past 2 decades, exercise capacity and activity status have become well-established predictors of cardiovascular and overall mortality.2’ In both healthy subjects and those with cardiovascular disease, peak exercise capacity is a stronger predictor of an increased risk of death than other clinical variables or established risk factors. In one trial, the risk of death from any cause in subjects whose exercise capacity was < 5 metabolic equivalents was roughly double that of subjects whose exercise capacity was > 8 metabolic equivalents.
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Population of Patients
The population under study consisted of 55 patients homozygous for hemoglobin S and 17 patients with hemoglobin SC; there were 43 male and 29 female patients. The mean age was 28 ±9 years (range, 10 to 60 years), and eight patients (11 percent) were more than 40 years of age. The mean hematocrit reading of the 72 patients was 28 ±5 percent (range, 15 to 44 percent). The mean age of hemoglobin SS patients was 29 ± 9 years and that of hemoglobin SC patients 26 ± 8 years (difference not significant; two-tailed Students f-test applied to unequal sample sizes). The mean hematocrit reading of hemoglobin SS patients was 26 ±3 percent and that of hemoglobin SC patients 35 ±4 percent (p<0.001).
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In 1979, Hunninghake and Fauci in their review entitled “Pulmonary Involvement in the Collagen Vascular Disorders,” suggested that this involvement is frequent in Sjögren s syndrome and can be manifested as pleurisy, interstitial fibrosis, desiccation of the tracheobronchial tree, and lymphoid interstitial disease. They also stated that the first two could be manifestations of the concomitant rheumatic disorder and that only desiccation of the tracheobronchial tree and lymphoid interstitial fibrosis are “specific” for Sjogren’s syndrome.
There have been several articles on the lungs and Sjogren’s syndrome since then. Only two deal with large populations of patients with primary Sjogren’s syndrome. Oxholm et al reported in their large series of 46 such patients that the most common functional abnormality was reduced pulmonary diffusing capacity. We have reported in a previous study of 22 patients with primary Sjogren’s syndrome that there are two distinct forms of respiratory involvement, ie, (1) “xerotrachea” manifested only by dry cough without any roentgenologic or functional abnormality, and (2) diffuse interstitial pulmonary disease. Pulmonary function in that study was evaluated only with spirometry and arterial blood gas levels. Three other studies deal with small numbers of patients with both primary and secondary Sjogren’s syndrome and stress airways obstruction as the most common abnormality. In this study, based on clinical, roentgenologic, functional, and histologic data, we suggest that primary Sjogren’s syndrome can frequently (75 percent) involve the respiratory system from the trachea and large airways to the small airways, pulmonary parenchyma, and pulmonary interstitium.
Involvement of the trachea and large airways results in their desiccation and presents with dry cough that can, at times, be very annoying. We had patients treated for “asthma,” “chronic bronchitis,” or even “tuberculosis” because of this cough before Sjogren’s syndrome was diagnosed. We can attribute this isolated symptom of dry cough that was the only abnormal respiratory manifestation in six of our patients (17 percent) to desiccation of the tracheobronchial tree (“xerotrachea”), since no other cause for the cough was found, and the desiccation of the airways was documented bronchoscopically. This has also been documented by other investigators in the past who have shown bronchial mucosal infiltration with mononuclear cells in similar patients. It is interesting that this group of patients cannot be detected with functional criteria, and therefore clinical evaluation is very valuable in their case.
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Eosinophils as Effector Cells in Inflammatory and Immune Reactions
The list of human disorders associated with an excess of eosinophils in the blood, tissues and secretions includes diseases characterized by IgE-mediated hypersensitivity, such as allergen-induced bronchial asthma, allergic rhinitis and allergic bronchopulmonary aspergillosis, infections with metazoan parasites, certain drug reactions, a number of connective tissue diseases as well as various solid tumors and lympho-proliferative and lymphoreticular disorders. Although it is universally accepted that eosinophils have a specialized role in host defense against parasites, just as neutrophils destroy and kill various bacteria, their functions in the inflammatory reactions associated with malignant or immune diseases are not completely understood. In this context, a wide variety of solid and hematologic cancers are occasionally accompanied by eosinophilia, but the mechanisms underlying this relationship remain obscure. Read the rest of this entry »
Although eosinophils are common components of a variety of inflammatory and immune-mediated responses, which role they may play in many pulmonary and pleural diseases is unclear. However, since these diseases often are characterized by injury to parenchymal cells and since eosinophils, when activated, can secrete a variety of cytotoxic products, it is reasonable to hypothesize that eosinophils may be involved in processes leading to the derangement of the normal tissue components. The present study demonstrates the following: (a) Human peripheral blood eosinophils, like peripheral blood neutrophils, possess an intense oxidative metabolic burst which can be induced by soluble membrane activators, such as PMA. (b) In addition to PMA, physiologic stimuli such as IgG and, to a lesser extent, IgE immune complexes, can activate human eosinophils to release considerable amounts of H202. Read the rest of this entry »
Ability of Catalase to Inhibit Eosinophil and Neutrophil Cytotoxic Activity
To demonstrate that the cytotoxic damage induced on Cr-labeled Raji cells by stimulated eosinophils and neutrophils was mostly related to the generation of H202, various numbers of peripheral blood or pleural fluid leukocytes were cocultured with the target cells in the presence of PMA, IgG IC and Agg IgE and with or without the H202 specific scavenger. When peripheral blood eosinophils were stimulated with PMA, a cytotoxicity index of 59 ± 9 percent at an effector-to-target ratio of 30:1 was generated while the addition of catalase virtually completely inhibited PMA-induced cytotoxicity (11 ±3 percent; p<0.001) (Fig 4,A). Read the rest of this entry »
Cytotoxic Activity of Peripheral Blood Eosinophils and Neutrophils from Control Subjects
Peripheral blood eosinophils and neutrophils from control subjects exhibited a very low spontaneous cellular cytotoxicity for Cr-labeled Raji cells after 4 h incubation (Fig 2). In contrast, stimulation of the cells with PMA induced a detectable eosinophil- and neutrophil-mediated killing which increased directly, for both eosinophils and neutrophils, with increasing effector-to-target cell ratio. Significant cytotoxicity was present for eosinophils at an effector-to-target ratio of 4:1 and for neutrophils at an effector-to-target ratio of 7.5:1. The cytotoxic activity of PMA-stimulated eosinophils was higher than the cytotoxic activity of PMA-stimulated neutrophils at an effector-to-target cell ratio of 15:1 (p<0.05) and of 30:1 and 60:1 (p<0.01). Read the rest of this entry »