Biomedical subjects
Publications and source records attributed to R D deShazo.
An apparent epidemic of fatal asthma has occurred despite ever-increasing expenditures for asthma medications. Atopy is the genetic predisposition toward responses that result in the formation of large quantities of allergen-specific IgE. Biotechnology has made it possible to manufacture proteins that regulate immune responses.
Maternal peripartum complications continue to be a significant problem in the United States, even among previously healthy women. The problems include peripartum bleeding, infection, hypertension, and thromboembolic disease. Primary care physicians are often called upon to treat these conditions. An awareness of the approach to diagnosis and management helps to ensure optimal outcome.
Stings by the imported fire ant almost always lead to dermal wheal and flare reactions followed by sterile pustules at sting sites. Less commonly, large local dermal reactions, pyoderma, anaphylaxis, or neuropathy may occur. Such reactions have previously been associated with contact with the insects out of doors. We present two previously unreported cases of indoor attacks on individuals by imported fire ants. One patient experienced a cerebrovascular accident in association with the attack, whereas the second patient had no obvious sequelae. With those two reports, a total of four such indoor massive sting episodes have appeared in the recent medical literature. Physicians and other individuals living in areas indigenous to the fire ant should be aware that infestation of buildings with fire ants may be associated with attacks on human beings indoors. Individuals with cognitive dysfunction seem to be especially at risk for attacks by fire ants.
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Patients are unhappy with the way physicians treat them, not so much medically, as personally. If public opinion is correct, recent medical graduates are less able to win the favor of their patients than previous ones. This article outlines a series of practical strategies for improving doctor-patient relationships. Sooner or later, most physicians learn these strategies by role-reversal. Perhaps a discussion of these with physicians in training (and others) will save some time, generate some goodwill, and improve outcomes for patients and physicians alike.
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Many syndromes of lung injury are associated with accumulation of neutrophils within the pulmonary parenchyma. These neutrophils have the capacity to produce lung injury by products including proteases and reactive oxygen species (ROS). We examined the ability of activated neutrophils to solubilize human alveolar extracellular matrix (ECM), and by use of scavengers and inhibitors, evaluated the role of ROS and proteases in this process. Supernatants of phorbol myristate acetate-activated neutrophils routinely solubilized 10.2% +/- 0.8% (n = 30) of collagen in human alveolar ECM, as measured by hydroxyproline release. Scavengers of ROS had no significant effect on ECM solubilization. Inhibitors of metalloproteases partially inhibited ECM solubilization (38.5% +/- 4.6% inhibition by ethylenediaminetetraacetic acid [n = 6], and 37.0% +/- 14.7% by 1,10-phenanthroline [n = 6]; p less than 0.05). Inhibitors of the neutrophil serine proteases, elastase and cathepsin G, markedly inhibited ECM solubilization (100.9% +/- 3.7% by alpha 1-protease inhibitor [alpha 1-PI] [n = 6] and 81.9% +/- 0.1% by soybean trypsin inhibitor [n = 6]; p less than 0.01). Since alpha 1-PI completely inhibited solubilization, metalloprotease activity appeared to be related to serine protease activity. This finding was confirmed by the observation that addition of a metalloenzyme activator, p-aminophenylmercuric acetate, in the presence of alpha 1-PI, restored solubilization to the same level as that inhibited by metal chelators. We conclude that human neutrophil metalloproteases and serine proteases directly solubilize human alveolar ECM. Furthermore, neutrophil serine proteases activate latent metalloproteases. However, ROS were not demonstrated to play a major role in ECM solubilization in our system.
Chronic fatigue syndrome (CFS) is a multi-faceted disorder for which no etiology has been determined. This paper discusses the implications of the new clinical case definition of CFS on previous and future studies of this illness. The authors' own management approach is also discussed.
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To understand better the effects of HIV infection on pregnancy, a group of 16 HIV seropositive pregnant patients was evaluated prospectively. Complications and results of pregnancy in these individuals were compared with those of 1,906 births at Charity Hospital, New Orleans during the time of the study. A subgroup of five patients underwent immunologic testing prenatally and postpartum. Thirty-one percent of HIV seropositive subjects had premature labor and low birth weight infants. Only 3.1% of the controls had premature labor and low birth weight infants (p less than or equal to .05). The percentage of C-sections was lower in the study group (12.5% versus 31.3%, p less than .10). All patients remained free of HIV-related disease through the postpartum period. Mean CD4 percentages were lower postpartum (21.9 +/- 3.4) than prepartum (45.1 +/- 6.7) in all five patients studied, although proliferative responses to the mitogens phytohemagglutinin and pokeweed were unchanged during the study period. One of the five seropositive patients who underwent immunologic testing with a CD4:CD8 ratio of less than 1.0 prepartum, had a progressive fall in CD4 percentages from 30% to 11% during the course of the study. HIV-I core antigen was not detected in the serum of any of the five patients during pregnancy or postpartum. Thus, HIV-I infection influenced both the course and outcome of pregnancy in the population studied. Further studies are indicated to assess the effects of pregnancy on the progression of HIV-related immunodeficiency in this population.
Abnormal antibody responses to insulin in diabetic patients have been associated with syndromes of insulin hypersensitivity and abnormal insulin pharmacokinetics. In this study, we evaluated total and IgG subclass antibody responses to insulin in 70 diabetic subjects on insulin distributed into five clinical groups, and in two control groups using ELISAs with CDC/WHO recommended monoclonal antibodies. As expected, levels of total IgG insulin antibody were greater in diabetic patients treated with insulin than in the control group of diabetic patients on oral agents or nondiabetic controls. Insulin antibody responses of the IgG2 subclass were negligible to absent in all groups. Adult diabetic patients on insulin without complications and those with insulin associated anaphylaxis had mean values of IgG1, IgG3, and IgG4 insulin antibodies no different from those of controls. Patients with local hypersensitivity had elevated IgG1 responses. Type I diabetic patients had elevated IgG3 responses. A group of Type II diabetic patients selected for high levels of total IgG insulin antibodies had elevated levels of IgG1, IgG3, and IgG4 antibody responses. Thus, the IgG subclass response to insulin primarily involves IgG subclasses 1, 3, and 4 and varies with the type of diabetes and complications of insulin therapy.
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To understand better the mechanism of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema, we studied the effects of ACE-inhibitor treatment on wheal-and-flare responses to histamine, codeine, and bradykinin in 10 normal subjects. No change in the size of wheal-and-flare reactions to histamine occurred, but the size of wheal reactions to codeine and bradykinin increased in all study subjects after ingesting the ACE inhibitor, captopril. Five of 10 study subjects developed flushing reactions after ACE-inhibitor treatment. We conclude that inhibition of bradykinin metabolism by ACE inhibitors is the probable cause of ACE inhibitor-related angioedema and that substance P is not the predominant mediator in this process.
Sinusitis may present as an indolent infection, without the classic symptoms and signs commonly expected, and will probably be missed in children who have only cough and persistent rhinorrhea unless this diagnosis is kept in mind. Plain radiography is the most commonly used diagnostic procedure for sinusitis, but computed tomography may be more sensitive. The contribution of sinusitis to the induction and exacerbation of asthma is still unresolved. The existence of a nasobronchial reflex is not clearly supported by available data, although it is a likely explanation for the observed relationship between the two processes. However, sinusitis appears to be an important underlying trigger for some cases of asthma and, therefore, should be suspected any time that acute or chronic asthma is difficult to control.
PURPOSE: Although clusters of individuals infected with the human T-cell lymphotrophic virus type I (HTLV-I) have been identified in the United States, no systematic evaluation of the immunologic status of these persons has been reported. We therefore studied a group of 11 HTLV-I-infected former intravenous drug abusers who were long-term participants in a methadone maintenance program in New Orleans, Louisiana, to determine the effects of HTLV-I and chronic opiate use on immunity. PATIENTS AND METHODS: Mitogenic responses and results of serologic studies, cell phenotype analysis, and cytotoxicity assays were compared to those in two other HTLV-I seronegative groups: a similar group of 17 methadone users and 15 healthy age-, sex-, and race-matched control subjects. All study participants were seronegative for human immunodeficiency virus type 1. RESULTS: Percentages and numbers of total T lymphocytes (CD2+,CD3+), T-suppressor/cytotoxic lymphocytes (CD8+), cytotoxic lymphocytes (Leu7+, Leu11+, NKH-1+) and B lymphocytes (B4+) were similar among the study groups. Although percentages and numbers of total T-helper lymphocytes (CD4+) were also similar among the groups, HTLV-I-infected subjects had higher percentages and proportions of helper/inducer cells (CD4:4B4+) than did HTLV-I seronegative methadone users. Both methadone using groups had decreased percentages and numbers of suppressor/inducer T lymphocytes (CD4:2H4+). Major histocompatibility complex unrestricted T-cell cytotoxicity (lectin-dependent cellular cytotoxicity), natural killer cell function, and mitogenic responses to the T-cell mitogen phytohemagglutin were similar among the three study groups. Pokeweed mitogen responses were severely depressed in the HTLV-I-infected population. CONCLUSIONS: We conclude that HTLV-I infection is associated with abnormalities in T-cell-dependent B-cell proliferative responses. Furthermore, both long-term methadone use and HTLV-I infection are associated with abnormalities in the distribution of CD4+ cell subpopulations. The increase in the helper/inducer and T-cell cell populations and decrease in the pokeweed mitogenic response noted in HTLV-I-infected subjects appear to be markers for infection with this retrovirus.
We evaluated the ability of mononuclear cell populations from 56 hemophiliac subjects, 69 homosexuals, and 32 control subjects to proliferate spontaneously in vitro. Levels of spontaneous proliferation (SP) were not significantly different among homosexuals or hemophiliac subjects when they were grouped as asymptomatic human immunodeficiency virus (HIV) seronegative, asymptomatic seropositive, persistent generalized lymphadenopathy, acquired immunodeficiency syndrome-related complex, or acquired immunodeficiency syndrome groups. There was, however, a stepwise increase in levels of SP corresponding with progression of disease in both patient groups. No correlations were noted between SP and CD8+ cell populations or mitogenic responses in study subjects, but SP correlated inversely to percentages and numbers of CD4+ lymphocytes. Depletion of CD4+ cells from mononuclear cell populations of HIV-infected subjects decreased SP. Thus, in HIV-1-infected subjects, SP increases as HIV-1-related disease progresses and appears to be CD4 dependent.
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