Strategies for suppression, containment, and eradication of resurgent tuberculosis.

This review provides strategies for the suppression, containment, and eventual eradication of resurgent tuberculosis. Some ethnic minority communities are at greatest risk because of the prevalence of human immunodeficiency virus/acquired immunodeficiency syndrome, poverty and malnutrition, congregate living situations, aberrant lifestyles, illegal immigration, and underemployment among these populations. Proposed strategies include the education of the population at risk as well as health care providers to permit the optimization of preventive, diagnostic, and therapeutic technologies. Also necessary is the development of effective, safe, newer medications to enhance patient compliance and decrease drug resistance. Strategic planning embraces national socioeconomic policy to permit adequate resources to combat poverty and malnutrition, to rebuild the infrastructure of the public health system, and to improve access to health care among rural and urban dwellers. It is concluded that these efforts must continue to ensure the eradication of tuberculosis.

Primary care paradigm for management of sarcoidosis, Part 2.

Sarcoidosis is a systemic granulomatous disease of undetermined etiology in which the immune system is overstimulated. Management of the patient with sarcoidosis entails continuity of patient care far beyond disease, even into remission. Care is comprehensive, including all involved organ systems, coordination of specialty consultations and services, and includes diagnostic tests. Therapeutic decisions are the responsibility of the primary care practitioner. Prognosis of sarcoidosis is not uniformly good. Patients can die. Subacute sarcoidosis patients usually do not require pharmacologic therapy. Chronic sarcoidosis may require long-term treatment for years to indefinitely. Corticosteroids are still the drugs of choice and other therapy is now available. Health organizations and private nonprofit support groups are available for patient education and assistance. Close support must still come from the family unit. Sarcoidosis may occur in family members in different cohorts at all ages in life and in any racial or ethnic group. The second in a two-part series on management of the patient with sarcoidosis, this article describes coordination of care and considers community, prevention, and family aspects of the disease.

Primary care paradigm for management of sarcoidosis, Part 1.

Sarcoidosis is a systemic granulomatous disease of undetermined etiology in which the immune system is overstimulated. Management of the patient with sarcoidosis entails continuity of patient care far beyond disease, even into remission. Care is comprehensive, including all involved organ systems, coordination of specialty consultations and services, and diagnostic tests. Therapeutic decisions are the responsibility of the primary care practitioner. Prognosis of sarcoidosis is not uniformly good. Patients can die. Subacute sarcoidosis patients usually do not require pharmacologic therapy. Chronic sarcoidosis may require long-term treatment for years to indefinitely. Corticosteroids are still the drugs of choice and other therapy is now available. Health organizations and private nonprofit support groups are available for patient education and assistance. Close support must still come from the family unit. Sarcoidosis may occur in family members in different cohorts at all ages in life and in any racial or ethnic group. This article is the first in a two-part series on management of the patient with sarcoidosis in the 21 st century by the primary are provider. Applications of principles of family medicine are emphasized. Part 1 considers continuity, comprehensiveness, and coordination of care. Part 2 will complete coordination of care, and consider community, prevention, and family aspects of this disease.

Pulmonary disability in former Appalachian coal miners.

A prospective case-control study was undertaken to assess respiratory disability in 133 former coal miners who were claimants for "black lung" benefits. Consecutive assignment was made to either case or control group based on their chest radiograph having shown coal workers' pneumoconiosis or no coal workers' pneumoconiosis. A respiratory occupational survey was completed with physical examination that placed special emphasis on the cardiorespiratory systems. Subjects underwent pulmonary function testing while 92 of these also received arterial blood gases to assess respiratory disability and pulmonary insufficiency. Arterial blood gases were superior to spirometry in assessment of pulmonary insufficiency/disability. Smoking interacts with coal workers' pneumoconiosis to cause pulmonary insufficiency. The most frequent spirometric pattern was obstructive. Disability was caused by occupational injuries and comorbidities, both of which occurred with greater frequency in miners with coal workers' pneumoconiosis than in controls. Pulmonary insufficiency appears to be a better discriminator than respiratory disability in coal miners, suggesting that arterial blood gases replace spirometry in their evaluation. Greater emphasis on smoking intervention among coal miners should be given.

Smoking is a factor in causing acute chest syndrome in sickle cell anemia.

A link between cigarette smoking and "acute chest syndrome" in sickle cell anemia is suggested. Acute chest syndrome in the patient with sickle cell anemia is characterized by fever, leukocytosis, cough, chest pain, and pulmonary infiltrates in the chest radiograph. This article describes the results of a study of 69 adolescent and young adult sickle cell anemia patients. Twenty-nine of these patients were smokers, three were former smokers, and 37 were nonsmokers. Patients completed respiratory questionnaires that focused on smoking habits and included a history of chest syndrome. Information obtained was confirmed by review of clinical records. The chi-square test demonstrated a strong relationship between cigarette smoking and chest syndrome in sickle cell anemia. All 29 smokers had a history of chest syndrome, but only 24 of 37 nonsmokers had such a history. Although the exact mechanism of the relationship between smoking and the development of acute chest syndrome remains speculative, cigarette smoking joins infection, hypoxia, acidosis, infarction, dehydration, and analgesics as a causative factor in adolescent and adult patients with sickle cell anemia. Behavioral modification of the smoking habit in patients with sickle cell anemia may decrease the frequency of acute chest syndrome and sequelae of sickle cell lung disease.

Short-term effects of smoking cessation: benefit or penalty?

Eight of ten cigarette smokers successful in a smoking cessation group therapy program were examined, initially, and at six and 12 months postcessation. Examination included completion of a respiratory questionnaire and selective pulmonary function testing that included maximum expiratory flow volume curves, slope of phase 3 alveolar plateau, and closing volume. Two symptomatic subjects became symptom-free within six months postcessation. Results indicate a mean weight gain of 4.1 kg within 12 months (P less than 0.01), deterioration in mean forced expiratory volume in one second as percent of forced vital capacity (P less than 0.05), and deterioration in mean forced expiratory volume in three seconds as percent of forced vital capacity postcessation (P less than 0.05). Other tests derived from the maximum expiratory flow-volume curve, slope of phase 3, or closing volume showed no change. These results may be explained by a number of factors and may have implications for future studies.

Lung function in sickle cell hemoglobinopathy patients compared with healthy subjects.

Previous studies of lung function tests performed on patients with sickle cell disease have shown a restrictive ventilatory defect, usually a diffusion defect, and mild hypoxia at rest. The present study was undertaken to explain the pathophysiology of these changes and to extend these studies to include functional measurements not reported previously.Lung function studies were performed at rest and during treadmill walking on 66 patients with sickle cell anemia and on 16 healthy control subjects. Patients had restrictive ventilatory defects, decreased lung compliance, and uneven ventilation-perfusion ratios. These abnormalities caused an increased alveolar-arterial oxygen tension difference that caused hypoxemia. The diffusion defects were because of the sickle cell disease.Carboxyhemoglobin levels were increased in patients with sickle cell disease. This increase may be caused by a combination of factors, including increased cigarette smoking, hemolysis, and preferential survival of red blood cells that contain carbon monoxide and which do not sickle. During treadmill walking, the patients with sickle cell disease showed a decreased work tolerance caused by impaired oxygen delivery. The anaerobic threshold is reached sooner in patients with sickle cell disease and may also account for the limitations in work capacity of these patients.