123rc/medical_text huggingface dataset:
The association of selected cancers with service in the US military in Vietnam. III. Hodgkin's disease, nasal cancer, nasopharyngeal cancer, and primary liver cancer. The Selected Cancers Cooperative Study Group As part of a series of investigations into the health of Vietnam veterans, we conducted case-control studies involving 310 men with Hodgkin's disease, 48 with nasal carcinoma, 80 with nasopharyngeal carcinoma, 130 with primary liver cancer, and 1776 controls between 1984 and 1988. All men born between 1929 and 1953 and diagnosed in an area covered by eight cancer registries were considered eligible as cases; controls were recruited by random-digit dialing. Whereas the study had excellent power (96%) to detect a twofold increase in risk for Hodgkin's disease among Vietnam veterans, its ability to detect a similarly elevated risk in the other cancers was limited, ranging from 38% (nasal carcinoma) to 75% (primary liver cancer). Analyses showed that risks among Vietnam veterans relative to other men were 1.1 (Hodgkin's disease), 0.7 (nasal carcinoma), 0.5 (nasopharyngeal carcinoma), and 1.2 (primary liver cancer). None of these relative risks was significantly different from 1.0. Similar results were obtained if Vietnam veterans were compared with (1) other veterans or (2) men who never served in the military. An examination of several attributes of military service in Vietnam (eg, branch, duration of service, and other characteristics that may have been associated with the use of Agent Orange) failed to identify any groups of veterans who were at increased risk for Hodgkin's disease. Small numbers limited further analyses of nasal, nasopharyngeal, and liver cancer. These results provide no evidence that, 15 to 25 years following service in Vietnam, the risk of these malignant neoplasms is higher among veterans.
Evidence of serum-protein leakage across the blood-brain barrier in the acquired immunodeficiency syndrome. Lesions of the central nervous system (CNS) in 23 patients with the acquired immunodeficiency syndrome (AIDS) were compared with control cases for the presence of serum protein by immunoperoxidase staining. A sensitive immunostaining kit in conjunction with rabbit antisera to human serum, albumin, immunoglobulins and complement component 3c was used to demonstrate specific immunoreactivity in paraffin-embedded sections. Most AIDS patients with CNS lesions had serum protein immunoreactivity in some neurons, glial cells (including astrocytes), gliomesenchymal cell nodules, vascular endothelial cells, inflammatory cells or microvascular walls. Cases with the most necrosis tended to have the least immunostaining. Immunoreactivity for IgG and fixed complement in anatomically intact or morphologically altered neural cells may indicate cellular lesions and potential cellular necrosis beyond the damage indicated by routine studies alone. Part of this immunoreactivity might represent a humoral autoimmune response.
Endoprosthetic reconstruction after bone tumor resections of the proximal tibia. The advent of successful adjuvant chemotherapy and radiation therapy protocols for primary malignant tumors and the development of custom-designed metallic endoprostheses has now made possible a successful limb salvage procedure for malignancies of the proximal tibia. Use of the transposed medial gastrocnemius flap, as proposed by Dr. Jean Duboussett of Paris, has been critical to the soft-tissue reconstruction that routinely permits an excellent active and passive range of motion for these patients. This article describes the operative techniques and technical considerations necessary for a successful proximal tibial endoprosthesis reconstruction.
Chronic blood hyperviscosity in subjects with acute stroke, transient ischemic attack, and risk factors for stroke. The origin and significance of blood hyperviscosity in subjects with acute stroke has been controversial. It has been argued that viscous abnormalities simply reflect either elevated hematocrit or an acute-phase response to the stroke itself. To address these issues, we measured the factors that determine blood viscosity in a cross-sectional study of 430 subjects, including 135 with acute stroke, 89 with acute transient ischemic attacks of the brain, 115 with recognized risk factors for stroke, and 91 healthy controls. The at-risk group was balanced with the acute stroke group for types of risk factors and medication usage, and all four groups were balanced for age. The viscosity of whole blood at low rates of shear and the plasma viscosity were significantly elevated in both groups with cerebrovascular symptoms and in the at-risk group compared with the healthy controls. The severity of hyperviscosity was stroke group greater than transient ischemic attack group greater than at-risk group greater than healthy controls. Increased viscosity of whole blood was associated with an elevated plasma fibrinogen concentration and with a decreased albumin/globulin ratio. This study provides evidence that blood hyperviscosity is present not only in subjects with acute brain infarction, but also in those with risk factors for stroke, and that these abnormalities are, to a considerable degree, chronic.
Clinical value of magnetic resonance imaging for cervical myelopathy. The magnetic resonance imaging (MRI) findings in 115 cases of cervical myelopathy, 121 cases of cervical radiculopathy, and 64 cases of neck pain with no neurologic deficit were prospectively studied to investigate the clinical value of MRI for cervical myelopathy. The MRI findings in the T1-weighted sagittal projection were classified into four groups according to the degree of the compressed deformities of the cervical cord. The degree of compression of the cervical cord on MRI findings showed a significant correlation with the severity of myelopathy, the anteroposterior diameter of the spinal column, and the degree of compression of the dural tube in the myelograms (P less than 0.01). Fifty-one patients of cervical myelopathy had undergone both preoperative and postoperative MRI. Of these, the spinal canal of 47 patients that was well decompressed was recognized according to plain computed tomography (CT). However, 24 (51%) of these 47 patients showed on MRI a deformity in the spinal cord amounting to cord atrophy. The correlation between the clinical function of the spinal cord and the recovery of the cord deformity on MRI at the operative levels was accurately investigated in 34 patients who had no cord deformities in the adjacent intervertebral levels. Twenty patients with cord atrophy had slightly poor clinical results, although no significant difference was found between these 20 and 14 patients with recovery in the cord deformities. From these results, it was evident that T1-weighted MRI is useful in the accurate diagnosis of compression myelopathy, in accurately deciding the level of the disease focus, and in the accurate assessment of the surgical results.
Corticosteroid use and peptic ulcer disease: role of nonsteroidal anti-inflammatory drugs. OBJECTIVE: To estimate the relative risk for peptic ulcer disease that is associated with the use of oral corticosteroids. DESIGN: A nested case-control study. SETTING: Tennessee Medicaid program. PARTICIPANTS: The case patients (n = 1415) were hospitalized between 1984 and 1986 for gastric or duodenal ulcer or for upper gastrointestinal hemorrhage of unknown cause. The controls (n = 7063) were randomly selected from Medicaid enrollees not meeting the study criteria for inclusion as case patients. MEASUREMENTS AND MAIN RESULTS: The estimated relative risk for the development of peptic ulcer disease among current users of oral corticosteroids was 2.0 (95% CI, 1.3 to 3.0). However, the risk was increased only in those who concurrently received nonsteroidal anti-inflammatory drugs (NSAIDs); these persons had an estimated relative risk associated with current corticosteroid use of 4.4 (CI, 2.0 to 9.7). In contrast, the estimated relative risk for those corticosteroid users not receiving NSAIDs was 1.1 (CI, 0.5 to 2.1). Persons concurrently receiving corticosteroids and NSAIDs had a risk for peptic ulcer disease that was 15 times greater than that of nonusers of either drug. CONCLUSION: Discrepant findings among earlier studies regarding steroids and the risk for peptic ulcer disease could in part be due to differences in the use of NSAIDs among study participants. The high risk for peptic ulcer disease associated with combined use of NSAIDs and corticosteroids indicates the need to prescribe this drug combination cautiously.
Dexamethasone as an adjunct in oropharyngeal obstruction in a patient with leukemia. Incipient airway obstruction due to fulminating bacterial infection of pharyngeal tissues requires prompt and definitive intervention. A case is presented in which dexamethasone was a key adjunct to antibiotic therapy in averting this problem in a severely neutropenic patient with acute leukemia.
Intravenous administration of recombinant human granulocyte-macrophage colony-stimulating factor causes a cutaneous eruption The intravenous administration of recombinant human granulocyte-macrophage colony-stimulating factor to three patients with leukemia who were receiving marrow aplasia-inducing chemotherapy resulted in the development of wide-spread erythematous macules and papules. The course of the eruption paralleled the time of infusion of the granulocyte-macrophage colony-stimulating factor. Skin biopsy specimens taken from two of the eruptions displayed characteristic changes consisting of a variable mixture of granulocytes and lymphocytes, increased number and size of dermal macrophages, mild to moderate epidermal exocytosis, intercellular edema, and rare dyskeratotic keratinocytes. Immunophenotypic analysis of one specimen was notable for keratinocyte intercellular adhesion molecule-1 expression. Administration of the recombinant human cytokine in pharmacologic doses is postulated to induce changes in the immunologic status of the skin, resulting in the expression of a cutaneous eruption.
Synergistic effect of murine cytomegalovirus on the induction of acute graft-vs-host disease involving MHC class I differences only. Analysis of in vitro T cell function. The development of acute graft-vs-host disease (GVHD) is a common outcome after the injection of fully MHC disparate parental T cells into unirradiated F1 mice. Murine cytomegalovirus (MCMV) infection has been previously shown to augment the development of acute GVHD in the parent-into-F1 (P----F1) model, such that 10-fold fewer parental cells are required. In the present study, we have investigated the effect of MCMV infection on the induction of non-lethal GVHD that occurs in P----F1 combinations involving MHC class I only or class II only differences. Using P----F1 combinations involving either an H-2K only difference or an H-2D only difference, MCMV infection of F1 mice 3 days before the injection of parental spleen cells led to a profound T cell immunodeficiency that strongly resembled that observed in acute GVHD. Further studies examining the H-2K disparate P----F1 combination, C57Bl/6---- (C57Bl/6xB6.C-H-2bm1) F1 and combined MCMV infection showed that the immunodeficiency is characterized by a profound loss of in vitro Th cell production of IL-2 and an intrinsic defect in T effector function as shown by an inability of rIL-2 to restore defective CTL responses. Additional experiments in these mice revealed the presence of suppressor cells as well as significant parent-anti-F1 CTL activity possibly accounting for the suppressor effect. This pattern of immunodeficiency was not seen after the administration of either MCMV or MHC class I disparate parental cells alone. MCMV infection did not detectably alter the immunodeficiency observed in a P----F1 combination involving a MHC class II difference only. These results indicate that MCMV infection can alter the pattern of GVHD in the setting of an MHC class I disparity, but not in the setting of class II disparity, such that it resembles acute GVHD. These results may have relevance to the human transplant setting where intercurrent CMV infection has been associated with an adverse clinical outcome.
Treatment of decompensated chronic obstructive pulmonary disease in the emergency department--correlation between clinical features and prognosis. STUDY OBJECTIVE: Patients with decompensated chronic obstructive pulmonary disease (COPD) are at high risk of relapse after treatment in an emergency department. The purpose of this study was to determine if the risk of relapse correlates with the clinical features of the disease. PATIENTS: Three hundred fifty-two patients with documented COPD who were treated for dyspnea in the ED of the Albuquerque Veterans Administration Medical Center over a three-year period. METHODS: We reviewed the clinical features and pulmonary function tests of the patients, who were considered to have COPD if the baseline prebronchodilator one-second forced expiratory volume (FEV1) was less than 80% predicted, and less than 80% of the forced vital capacity and inhaled bronchodilators failed to increase the FEV1 to levels of more than 80% predicted. Visits for pneumonia, pneumothorax, pleural effusion, or pulmonary emboli were excluded. A relapse was defined as an unscheduled revisit to the ED within 14 days of initial treatment. Data were entered into a microcomputer data base and analyzed by a commercial statistical package. RESULTS: Of 877 visits in which the patient was treated and released from the ED, 281 (32.0%) resulted in relapse and were considered unsuccessful Compared with successful visits, unsuccessful visits were characterized by a shorter duration of dyspnea (P = .002), a lower entry FEV1 (P = .027), a lower discharge FEV1 (P = .040), a greater number of treatments with nebulized bronchodilators (P = .009), more frequent use of parenteral adrenergic drugs (P = .006), and less frequent use of oral prednisone on discharge (P = .016). Patients with one or more relapse visits during the study period (relapsers) differed from nonrelapsers in several respects. Relapsers had a greater bronchodilator response on baseline FEV1 than nonrelapsers (P = .047). Nevertheless, relapsers required more bronchodilator treatments in the ED (P less than .001); were treated more frequently with parenteral adrenergic drugs (P less than .001), IV glucocorticoids (P less than .001), and oral prednisone (P less than .001); and recovered less of their baseline FEV1 (P less than .014). CONCLUSION: Bronchodilator response on baseline pulmonary function testing appears to identify patients with COPD who have a poor prognosis after emergency treatment. Their poor response to intensive bronchodilator treatment suggests that loss of bronchodilator response may be involved in the pathogenesis of respiratory decompensation.
Efficacy of interferons on bowenoid papulosis and other precancerous lesions. Preliminary results of an open randomized trial of recombinant interferon gamma in patients suffering from bowenoid papulosis are described. Recombinant interferon gamma was given subcutaneously to 12 patients at a daily dose of 4 X 10(6) I.U. by injection. Four patients each were assigned to one of three treatment groups consisting of continuous therapy (group A) with three subcutaneous injections per week for 13 weeks; intermittent block therapy (group B) with four six-week cycles consisting of five injections on days 1, 3, 5, 7, and 9 of each cycle; and intermittent single-dose therapy (group C) with six four-week cycles consisting of only one subcutaneous injection on day one of each cycle. At the twenty-sixth week after onset of therapy, complete responses were seen in three of four patients of treatment group A, whereas in the treatment groups B and C only one patient, respectively, responded partially. These results suggest that in contrast to condylomata acuminata bowenoid papulosis lesions respond better to continuous than to intermittent interferon gamma injections.
Paralysis of saccades and pursuit: clinicopathologic study. We report a 73-year-old patient with an eye movement disorder characterized by paralysis of saccades and pursuit. At autopsy, there were small cortical lesions in the middle frontal gyrus immediately anterior to the precentral gyrus and in the inferior parietal lobule on both sides.
Prevalence of hemodynamically significant stenosis of the carotid artery in an asymptomatic veteran population. The results of previous studies have suggested that significant stenosis of the carotid artery occurs in less than 6 per cent of asymptomatic patients. However, some populations studied were not representative of those seen by most vascular surgeons. Accordingly, we examined two cohorts of patients at the Veterans Administration Medical Center using Duplex scanning. There were 153 volunteers in group 1, all more than 50 years of age, who were being treated at our outpatient department for nonvascular problems. There were 116 patients of similar age in group 2 but who were known to have significant arterial occlusive disease of the lower extremity. The majority of patients were men with a mean age of 64.4 years. Risk factors in the total population included hypertension, diabetes mellitus, coronary arterial disease, peripheral vascular disease and smoking. Over-all, significant (greater than 50 per cent diameter) stenosis of the carotid artery was discovered in 25 of 269 patients. The prevalence for those in group 1 was 6.5 per cent versus 12.9 per cent for those in group 2 (p = 0.058). The prevalence in patients with cardiac disease was 15.2 per cent compared with 6.8 per cent in those without cardiac disease (p = 0.032). Smoking was associated with a 10.6 per cent rate of significant disease compared with a 2.3 per cent rate in nonsmokers (p = 0.065). Hypertension and diabetes were not significant risk factors. Significant stenosis of the carotid artery was found in seven of 40 patients in whom coronary arterial disease, peripheral vascular disease and smoking were all present.
Epidemiologic risk factors for children with acute lower respiratory tract infection in Buenos Aires, Argentina: a matched case-control study. The risk factors that predisposed 516 hospitalized and 154 ambulatory patients to acute lower respiratory tract infection (ALRI) are examined in a matched case-control study. The control group was selected from children attending immunization and well-baby clinics at the same institution that was treating the children with ALRI. Sex, age, nutritional status, socioeconomic level, as well as season and place of residence were used as matching criteria. Because of their distinct profiles, hospitalized and outpatient groups were analyzed separately. However, the four variables with the highest odds ratios (incidence ratios or relative risk) were found to be the same for both groups. These variables were related to the host's condition (bronchial hyperreactivity, presence of persistent symptoms of the upper respiratory tract), family (presence of acute respiratory tract disease in household members), and environment (indoor contaminants).
Beta-lactam resistance mechanisms of methicillin-resistant Staphylococcus aureus. In vitro and in vivo activity of amoxicillin and penicillin G alone or combined with a penicillinase inhibitor (clavulanate) were tested against five isogenic pairs of methicillin-resistant Staphylococcus aureus (MRSA) producing or not producing penicillinase. Loss of the penicillinase plasmid caused an eight times or greater reduction in the MICs of amoxicillin and penicillin G (from greater than or equal to 64 to 8 micrograms/ml), but not of the penicillinase-resistant drugs methicillin and cloxacillin (greater than or equal to 64 micrograms/ml). This difference in antibacterial effectiveness correlated with a more than 10 times greater penicillin-binding protein 2a affinity of amoxicillin and penicillin G than of methicillin and a greater than or equal to 90% successful amoxicillin treatment of experimental endocarditis due to penicillinase-negative MRSA compared with cloxacillin, which was totally ineffective (P less than .001). Amoxicillin was also effective against penicillinase-producing parent MRSA, provided it was combined with clavulanate. Penicillinase-sensitive beta-lactam antibiotics plus penicillinase inhibitors might offer a rational alternative treatment for MRSA infections.
Effects of indomethacin on hepatogenic pulmonary angiodysplasia. A patient had liver cirrhosis associated with marked hypoxemia. With administration of indomethacin (75 mg/day for six days), PaO2 was elevated up to 50 mm Hg from 44 mm Hg. At that time, dynamic pulmonary perfusion imaging revealed a plateau time course curve of MAA uptake in the lungs, as compared with findings obtained during the state of severe hypoxemia without indomethacin. These observations suggest that part of hepatogenic pulmonary angiodysplasia is a functional vasodilatation that is presumably modulated by vasoactive substances, such as prostaglandins and/or other eicosanoids.
Complications of extracorporeal membrane oxygenation in neonates. In cases of severe respiratory failure, cardiopulmonary bypass has been used as support until cardiac and pulmonary recovery occurs. We report the Wilford Hall USAF Medical Center experience with extracorporeal membrane oxygenation (ECMO) and its associated complications. From July 1985 to March 1989, 57 neonates were placed on membrane oxygenators. The overall survival was 79%. Technical complications encountered included catheter-related problems, mechanical complications of the pump apparatus, and hemorrhage. Hemorrhagic complications were the most frequent and devastating complications encountered. Intracranial hemorrhage accounted for six deaths associated with bypass. Extracorporeal membrane oxygenation is successful in significantly improving survival of neonates whose predicted mortality approaches 100% with conventional treatment. The rate of infant mortality using the membrane oxygenator is not affected by technical complications related to catheter position, mechanical problems with the circuit, or hemorrhage, excluding intracranial hemorrhage. The major cause of death of infants receiving extracorporeal membrane oxygenation is the underlying disease process leading to cardiopulmonary failure.
Structural alterations of nerve during cuff compression. Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure- and time-related structural changes observed in the present study under the cuff were (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (ii) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement of layers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.