Clinical ecologists propose the existence of a unique illness in which multiple environmental chemicals, foods, drugs, and endogenous C. albicans have a toxic effect on the immune system, thereby adversely affecting other bodily functions. The proposal uses some concepts that superficially resemble those that apply to clinical allergy and toxicology and others that are novel. Review of the clinical ecology literature provides inadequate support for the beliefs and practices of clinical ecology. The existence of an environmental illness as presented in clinical ecology theory must be questioned because of the lack of a clinical definition. Diagnoses and treatments involve procedures of no proven efficacy. Case reports by clinical ecologists and evaluation of these patients by other physicians indicate that this diagnosis is applied most frequently to persons with symptoms of physiologic (somatic) or psychologic dysfunction, or both. Proof of cause-effect relations between environmental factors and symptoms of "environmental illness" is particularly difficult because clinical ecologists implicate such a broad range of agents, including chemicals, foods, hormones, and microorganisms. Most patients are believed to react to multiple environmental substances by any route of exposure, and some are said to be intolerant to the entire environment, the so-called "total allergy syndrome." The principal method of proof cited by clinical ecologists for the existence of "environmental illness" is the symptom-provocation test used in diagnosis of individual cases after the condition is suspected because of a history of symptoms and suspected causes. Published studies on the provocation test employed widely different subject-selection methods and outcome-measurement criteria. All were seriously flawed by the absence of matched patient-control groups, absence or inadequacy of the placebo, and failure to achieve or document randomness of trials. Not surprisingly, therefore, the conclusions from these studies are conflicting. Those studies reporting results of immunologic tests are insufficient to address theories of environmental illness; the number of cases is small and selection criteria are not clear. Enumeration of lymphocyte subsets and quantitation of serum immunoglobulin and complement levels in patients with "environmental illness" have not yielded clear-cut evidence of immunologic abnormality. Clinical ecologists use a treatment program that includes avoidance of environmental chemicals, rotation of foods in the diet, and neutralization of symptoms with injected or sublingual extracts. Except for small-dose oral nystatin, which is used for treatment of patients with the candida hypersensitivity syndrome, drug therapy is intentionally avoided, although some clinical ecologists recommend mineral salts, oxygen, vitamins, minerals, and antioxidants for relief of symptoms.(ABSTRACT TRUNCATED AT 400 WORDS)

To review the various rheumatologic manifestations of human immunodeficiency virus (HIV) infection and to discuss their potential pathogenic mechanisms.

Idiopathic inflammatory myopathy, a category encompassing polymyositis, dermatomyositis, and a number of other disorders, is very uncommon, but has been the focus of intense study in the Arthritis and Rheumatism Branch of the National Institute of Arthritis and Musculoskeletal and Skin Diseases for the past several years. We describe the clinical picture, stressing the need for biopsy to ensure correct diagnosis. It is especially important to recognize the treatment-resistant variant, inclusion body myositis. The extraskeletal manifestations, particularly the cardiopulmonary, oropharyngeal, gastrointestinal, and endocrine involvement, are described. The cardiopulmonary involvement, especially interstitial lung disease, arrhythmias, and cardiac failure, may dominate the clinical picture. The known causes are varied, and include drugs, toxins, and some infectious agents, however, in most cases a cause cannot yet be identified. Circumstantial evidence suggests that picornaviruses may initiate some cases in humans, and a very similar disease in mice caused by a picornavirus is actively under study. Studies of autoantibodies and cellular immune function support a central role for disordered immunity in the pathogenesis. The myositis-specific autoantibodies, especially those directed at certain enzymes important in protein synthesis (the aminoacyl-transfer RNA synthetases), are found in a clinically distinct subset of patients. Although most patients respond initially to corticosteroids, cytotoxic drugs are sometimes added when steroid toxicity or refractoriness develops. We describe several newer therapies under study for such cases and outline future directions in research.

This revision of the "General Recommendations on Immunization" updates the 1983 statement. Changes or new sections include 1) listing of vaccines available in the United States by type and recommended routes, 2) updated schedules for immunizing infants and children, 3) clarification of the guidelines for spacing administration of immune globulin preparations and different vaccines, 4) an updated table of recommendations for routine immunization of children infected with human immunodeficiency virus, 5) listing of conditions that are often inappropriately considered contraindications to immunizations, and 6) addition of information on the National Childhood Vaccine Injury Act of 1986 and the National Vaccine Injury Compensation Program. These recommendations are not comprehensive for each vaccine: Immunization Practices Advisory Committee (ACIP) recommendations on each vaccine should be consulted for more details.

Barriers frequently develop in physician-patient encounters. If they go unrecognized, they can severely limit the therapeutic potential of the doctor-patient relationship. Because barriers are not always explicit, a strategy is presented for recognizing implicit signs such as verbal-nonverbal mismatch, cognitive dissonance, unexpected resistance, and physician discomfort. Once a potential barrier is identified, its source can be defined and explored using standard clinical reasoning techniques such as hypothesis generation and testing. Patients can often share in the process of generating hypotheses about the nature and sources of barriers. Once defined and understood, most barriers can be lessened and sometimes resolved using the basic communication skills of acknowledgment, exploration, empathy, and legitimation. When conflict exists, common interests and differences must be clarified. Conflict might involve disagreement about the presence of a barrier, its nature or source, its relevance to the physician-patient relationship, or about strategies for approaching it. Negotiation need not be limited to the initial positions, but can include creative solutions whereby both parties gain. The decision to confront a barrier depends on both doctor and patient readiness, as well as how critical the barrier is to the therapeutic process, and how amenable it is to change. By effectively uncovering and addressing barriers, the physician can often turn roadblocks to effective communication into means for enhancing the therapeutic relationship.

Experimental findings in animals and epidemiologic studies in humans provide strong evidence that hypertension promotes the onset and progression of atherosclerosis. However, effective antihypertensive therapy has not consistently reduced the incidence of cardiac events in the major trials of treatment for mild hypertension. In reviewing these trials and the recent data on the pathophysiologic interrelationships among hypertension, atherosclerosis, and myocardial ischemia, two factors stand out: First, the power of these trials to produce a positive result was limited because of their size, entry criteria, duration, and other considerations; second, autopsy and epidemiologic data suggest that some patients in these trials probably had advanced coronary artery disease at the time of entry. Because these patients probably developed symptomatic coronary artery disease by virtue of this pre-existing disease, the failure of antihypertensive therapy alone to prevent cardiac events in trials of relatively short duration should not be construed as evidence against its value as a long-term therapy.

To evaluate the transmission of infectious agents from organ donors to transplant recipients, and to assess risk factors for transmission, primarily in recipients of kidney, cornea, and heart allografts.

Stroke is a major cause of morbidity and mortality in the United States with 250,000 cases per year. Cerebral ischemia is the largest category of stroke with cardiac arrest, profound hypotension, and vascular occlusion the principal causes. Traditional approaches to the treatment of ischemic stroke focus on maintaining cardiac output, blood pressure, cerebral blood flow, and on preventing thrombosis. Recently, attention has been focused on developing new therapies that are directed toward abnormal biochemical events at excitatory synapses. Ischemia causes impairment of brain energy metabolism and the release of excessive amounts of glutamate into the extracellular space. This process secondarily excites neurons and further depletes energy stores. The excitotoxic hypothesis of brain injury proposes that glutamate is a principal cause of damage in ischemia. Three components of this hypothesis have been tested and largely proved in experimental studies in tissue culture and in animal models of stroke. First, elevated concentrations of glutamate cause excessive excitation at a subset of glutamate receptors, the N-methyl-D-aspartate (NMDA) receptor. Second, excitation at this receptor leads to excessive influx of sodium chloride and water which causes acute neuronal damage, and calcium which causes delayed and more permanent damage. Third, pharmacologic blockade at the NMDA receptor-ion channel complex prevents ischemic neuronal damage. Studies using specific pharmacologic compounds that block glutamate's action hold particular promise for treating stroke in humans, including competitive antagonists at the NMDA glutamate binding site (for example, 2-amino-5-phosphonovalerate, AP5), noncompetitive antagonists at the calcium channel (for example, MK-801, dextromethorphan, ketamine), and agents that might be directed at the glycine, zinc, and magnesium sites.

To synthesize and analyze new information on the epidemiology, pathophysiology, and management of hypertension in the elderly to guide physicians making treatment decisions.

Research in cognitive science, decision sciences, and artificial intelligence has yielded substantial insights into the nature of diagnostic reasoning. Many elements of the diagnostic process have been identified, and many principles of effective clinical reasoning have been formulated. Three reasoning strategies are considered here: probabilistic, causal, and deterministic. Probabilistic reasoning relies on the statistical relations between clinical variables and is frequently used in formal calculations of disease likelihoods. Probabilistic reasoning is especially useful in evoking diagnostic hypotheses and in assessing the significance of clinical findings and test results. Causal reasoning builds a physiologic model and assesses a patient's findings for coherency and completeness against the model; it functions especially effectively in verification of diagnostic hypotheses. Deterministic reasoning consists of sets of compiled rules generated from routine, well-defined practices. Much human problem solving may derive from activation and implementation of such rules. A deeper understanding of clinical cognition should enhance clinical teaching and patient care.