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Biomedical subjects

L A Laitinen

Publications and source records attributed to L A Laitinen.

At least 37 records · Page 2Linked to original sources

Sleep-related disordered breathing during pregnancy in obese women.

STUDY OBJECTIVES: This study was designed to evaluate sleep-related disordered breathing in obese women during pregnancy. Obesity is known to predispose to sleep-related breathing disorders. During pregnancy, obese mothers gain additional weight, but other mechanisms may counteract this effect. DESIGN: A case-control study to compare sleep-related breathing in obese pregnant women (mean prepregnancy body mass index [BMI] > 30 kg/m(2)) with pregnant women of normal weight (mean BMI, 20 to 25 kg/m(2)). SETTING: University teaching hospital with a sleep laboratory. PARTICIPANTS: We recruited 11 obese women (BMI, 34 kg/m(2); mean age 31 years) and 11 control women (BMI, 23 kg/m(2); mean age 32 years). INTERVENTIONS: Overnight polysomnography was performed during early (after 12 weeks) and late (after 30 weeks) pregnancy. MEASUREMENTS AND RESULTS: During pregnancy, obese mothers gained 13 kg and control women gained 16 kg. Sleep characteristics did not differ between the groups. During late pregnancy, the women in both groups slept more poorly and slept in supine position less. During early pregnancy, their apnea-hypopnea indexes (1.7 events per hour vs 0.2 events per hour; p < 0.05), 4% oxygen desaturations (5.3 events per hour vs 0.3 events per hour; p < 0.005), and snoring times (32% vs 1%, p < 0.001) differed significantly. These differences between the groups persisted in the second polysomnography, with snoring time further increasing in the obese. Preeclampsia and mild obstructive sleep apnea were diagnosed in one obese mother. One obese mother delivered a baby showing growth retardation (weight - 3 SD). CONCLUSIONS: We have shown significantly more sleep-related disordered breathing occurring in obese mothers than in subjects of normal weight, despite similar sleeping characteristics.

Adult↗

Extrafine beclomethasone dipropionate breath-actuated inhaler (400 micrograms/day) versus budesonide dry powder inhaler (800 micrograms/day) in asthma.

Hydrofluoroalkane-134a beclomethasone dipropionate extrafine aerosol breath-actuated inhaler (Qvar Autohaler; BDP-AH) provides an alternative to chlorofluorocarbon metered dose inhalers or dry powder inhalers (DPIs). The aim of this six-week, open-label study was to determine whether BDP-AH demonstrates equivalent asthma control to twice the dose of budesonide (BUD)-DPI (Pulmicort Turbuhaler). Adults with symptomatic asthma inadequately controlled on BUD-DPI 400 micrograms/day and beta-agonist were enrolled. Patients (n = 193) were randomised to receive 400 micrograms/day BDP-AH (n = 98) (two puffs of 100 micrograms/actuation inhaler twice daily) or 800 micrograms/day BUD-DPI (n = 95) (two puffs of 200 micrograms/actuation inhaler twice daily). Both groups showed a statistically significant change from baseline in morning (a.m.) peak expiratory flow (PEF) at weeks 5-6 (p < 0.01), indicating study treatment improved a.m. PEF over prestudy 400 micrograms/day BUD. Changes from baseline in a.m. PEF at weeks 5-6 were 15.9 l/min for BDP-AH and 14.2 l/min for BUD-DPI; the groups were statistically equivalent (90% CI -7.02-10.44; p < -0.001 [equivalence = within +/- 25 l/min]). Other efficacy assessments (evening PEF, FEV1, asthma symptoms, beta-agonist use) confirmed the treatments were clinically equivalent. Thirty-nine (40%) patients on BDP-AH and 35 (37%) on BUD-DPI experienced at least one adverse event (p = 0.767). Four (4%) patients on BDP-AH and 3 (3%) on BUD-DPI reported increased asthma symptoms. BDP-AH at half the daily dose provided equivalent asthma control to BUD-DPI; both treatments were well tolerated.

Administration, Inhalation↗

Rebirth of the university hospital: the Finnish strategy.

Like the academic hospitals worldwide, the Finnish university hospitals are under increasing economical pressures seeking ways to re-assess their traditional missions. It is strongly felt that new solutions within the field of evaluative sciences could bring added value to university hospitals. In this vein, university hospitals must take a leading position in assessing efficacy, (cost-)effectiveness and, ultimately, cost-utility of both traditional and emerging clinical technologies. This will affect the research culture of university hospitals both profoundly and permanently.

Cost-Benefit Analysis↗

Laminin alpha1-chain shows a restricted distribution in epithelial basement membranes of fetal and adult human tissues.

Two novel monoclonal antibodies were raised and used to study the expression of laminin (Ln) alpha1-chain in developing and adult human tissues. In both fetal and adult kidney, a distinct immunoreactivity was seen in basement membranes (BM) of most proximal tubules but not in the distal tubular or glomerular BM or in the basal laminae of blood vessels. Immunoprecipitation of metabolically labeled cultured human renal proximal tubular cells showed an abundant production and deposition of Ln alpha1-chain to the extracellular matrix, suggestive of an epithelial origin of kidney Ln-1. Quantitative cell adhesion experiments with JAR choriocarcinoma cells showed that purified human Ln-1 is a good substrate for cell adhesion that it is differently recognized by integrin receptors when compared to mouse Ln-1. In fetal and adult testes immunoreactivity was solely confined to BM of the seminiferous epithelium. In the airways BM-confined reaction was only seen in fetal budding bronchial tubules (16-19 weeks) at the pseudoglandular stage of development. In the skin a distinct immunoreactivity was confined to BM of developing hair buds but not in epithelial BMs of adult epidermis or of epidermal appendages. In other adult tissues, immunoreactivity was found in BMs of thyroid, salivary, and mammary glands as well as in BMs of endometrium and endocervix, but not of ectocervix or vagina. No immunoreactivity was found in BMs of most of the digestive tract, including the liver and pancreas, except for BMs of esophageal submucosal glands and duodenal Brunner's glands. In fetal specimens, BMs of the bottoms of the intestinal and gastric glands were positive. Basal laminae of blood vessels were generally negative for Ln alpha1 chain with the exception of specimens of both fetal and adult central nervous system in which immunoreactivity for Ln alpha1 chain was prominently confined to capillary walls. The results suggest that outside the central nervous system, Ln alpha1 chain shows a restricted and developmentally regulated expression in BMs of distinct epithelial tissues.

Adult↗

Histopathologic features of early and progressive asthma.

During the last decade, morphologic studies on bronchial biopsy specimens have led to our present understanding of asthma as an inflammatory airways disease. However, little knowledge exists about the sequence of cellular events during the disease or of possible mucosal changes early in asthma. So far the primary cause, the site of damage, and the mechanisms inducing the inflammatory reaction remain to be elucidated. A multifactorial genetic susceptibility may be important for the development of asthma. Suggested factors that may trigger changes in the cells' morphologic and functional phenotype are viral infections, allergen exposure, maternal factors, diet, and smoking. Current evidence has implied that interactions between epithelial cells and the subepithelial connective tissue in the mucosa are important for normal homeostatic balance. Changes in airway epithelial phenotype possibly resulting from altered gene expression in its lining cells may be very important even as a first line change in asthma.

Animals↗

Early interventions in asthma with inhaled corticosteroids.

We have earlier shown epithelial damage in the airway mucosa in patients with asthma. Later other structural changes have been recognized in asthma, such as deposition of collagen and tenascin in the subepithelial basement membrane and changes in the laminin subchain composition. These processes are modified by an inflammatory process in the airways. Both the United States National Institutes of Health and the British Thoracic Society guidelines on the management of asthma emphasize the need for early use of anti-inflammatory drugs. Many clinical studies that used airway biopsy specimens have shown a decrease in airway inflammatory cell numbers after inhaled corticosteroid therapy. However, there is very little information on the effects of asthma medication on the structural components of the airways. Both the synthesis and degradation of many extracellular matrix components may be affected by the disease process and the drugs resulting in altered remodeling and gene expression in the airways. Because there are only a few studies that try to identify early changes in asthma, it is not known whether the anti-inflammatory treatment of asthma proposed by the guidelines is started early enough.

Administration, Inhalation↗

Safety of sputum induction in chronic obstructive pulmonary disease.

The aim of the present study was to evaluate the safety of sputum induction in patients with varying severity of chronic obstructive pulmonary disease. The subjects were 28 smokers with baseline forced expiratory volume in one second (FEV1) of (mean and range) 1.8 (0.8-2.9) L that is 53 (28-69)% of the predicted and reversibility of 2.5 (-7.4-9.9)%. Sputum was induced after premedication with 200 microg salbutamol at increasing concentrations (0.9, 3, 4, and 5%) of hypertonic saline nebulized by an ultrasonic nebulizer. The procedure was well tolerated, and none of the patients reported major side-effects. However, the mean change from prebronchodilator FEV1 during induction was -8.5 (-23-11)%, p=0.001, and from postbronchodilator FEV1 -10.7 (-25-5)%, p<0.0001. Three (11%) of the patients had a fall in FEV1 from the prebronchodilator baseline of >20%, and a further 10 (36%) had a fall of 10-20%. Patients with greater reversibility in airway obstruction seemed to get the best benefit from the bronchodilator pretreatment, since there was an inverse relationship between reversibility in FEV1 and fall in FEV1 during induction (r=-0.4, p=0.03). It is concluded that sputum induction by hypertonic saline inhalation can cause meaningful bronchoconstriction in patients with chronic obstructive pulmonary disease, despite pretreatment with an inhaled beta2-agonist. The results highlight the importance of monitoring spirometry during sputum induction to detect bronchoconstriction.

Aerosols↗

The IL9R region contribution in asthma is supported by genetic association in an isolated population.

Interleukin 9 (IL9) is involved in mast cell maturation and the enhancement of IgE production by B cells. Furthermore, linkage data in human and mice have suggested that IL9 may contribute to asthma. Since our genetic analysis of the 5q cytokine cluster did not support a genetic role for the IL9 gene, we became interested in the IL9 receptor gene (IL9R) in the pseudoautosomal region. We genotyped markers sDF2 and sDF1 close to the IL9R gene among 289 affected and 368 family-based controls. The results were studied by using linkage, transmission disequilibrium, association and homozygosity analyses. Linkage analyses remained negative, presumably because of our low power for linkage study. However, all the other analyses yielded evidence that the IL9R gene region may have a role in the development of asthma. The sDF2*10 allele was more frequently transmitted than untransmitted to asthmatic offspring (34 vs 16, pchi2 < or = 0.01), and it was found homozygotic among asthma patients more often than expected (Psimul2 = 0.009). Also, a specific X chromosomal haplotype, sDF2*10-sDF1*6 associated with asthma (40 vs 7, Pchi2 < 0.005, Psimul1 = 0.04).

Alleles↗

Perinatal risk factors for asthma in Finnish adolescent twins.

BACKGROUND: Previous studies have suggested that, in addition to genetic liability and environment in early childhood, intrauterine life also influences the risk for asthma beyond childhood. Low birth weight, prematurity, young maternal age, and maternal smoking have all shown an association with asthma. The effect of perinatal factors on the risk for asthma in relation to familial and social risk factors was studied in a nationwide population-based sample of adolescent twins. In addition to a distribution of birth characteristics among twins which differs from that of singletons, data on twins enable a distinction to be made between genetic and environmental sources of variation. METHODS: Questionnaires were sent to five consecutive birth cohorts of Finnish 16 year old twins born in 1975-9 and to their parents (3065 families). The outcome measure was life time prevalence of doctor-diagnosed asthma in these adolescents. The association between asthma and potential risk factors was assessed by multiple logistic regression and discordant twin pair analysis. RESULTS: Risk for asthma increased with increasing ponderal index (p for trend <0.01) and decreasing maternal age (p for trend <0.05). Among the 25% of twins with the highest ponderal index, the odds ratio for asthma was 1.82 (95% confidence interval 1.18 to 2.79) compared with those in the lowest 25%. Neither birth weight, gestational age, nor Apgar score was associated with asthma. When perinatal risk factors were combined with familial and social risk factors, ponderal index, maternal smoking, parental asthma, and sibship size were all significant independent determinants of asthma in these adolescents. CONCLUSIONS: The risk for asthma in adolescent twins increases with increasing ponderal index when adjusted for familial and social factors.

Adolescent↗

Placebo-controlled study of inhaled budesonide on indices of airway inflammation in bronchoalveolar lavage fluid and bronchial biopsies in cross-country skiers.

BACKGROUND: Asthma-like symptoms, methacholine hyperresponsiveness, use of inhaled steroids, airway inflammation, and increased tenascin expression in the reticular basement membrane have been reported in competitive cross-country skiers. OBJECTIVE: To investigate the effect of inhaled budesonide, 400 mug twice daily, on indices of airway inflammation in 'ski asthma', defined as asthma-like symptoms within the previous year and bronchial hyperresponsiveness to methacholine. METHODS: A randomised double-blind placebo-controlled parallel-group bronchial biopsy and bronchoalveolar lavage (BAL) study of 25 (19 male) competitive cross-country skiers (mean age 18 (16-20) years for a mean (range) treatment period of 22 (10-32) weeks over the competitive season. RESULTS: No changes were seen regarding cellular inflammation in the bronchial mucosa or tenascin expression. In the BAL fluid, both groups had a significant decrease in activated T-suppressor (CD8) lymphocytes and an increase in macrophages, with no differences across the groups. Within the budesonide group, there was a decrease in IL2 receptor-activated T-helper lymphocytes and an improvement in FEV(1). Asthma-like symptoms were unchanged in 17 (68%) skiers. Methacholine provocation test was negative in 15 subjects, and remained positive in 5 subjects in each group. The improvement in bronchial responsiveness occurred in both groups and was not accompanied by a decrease in cellular inflammation. CONCLUSIONS: We were unable to show any clear beneficial effect of budesonide in 'ski asthma'. As changes in training intensity probably accounted for the spontaneous improvement in bronchial responsiveness, more attention should be directed at reducing environmental stress to the airways than at attempting pharmacological modulation of induced inflammatory changes.

Administration, Inhalation↗

Association study of the chromosomal region containing the FCER2 gene suggests it has a regulatory role in atopic disorders.

On the basis of studies with animal models, the gene for the low-affinity receptor for immunoglobulin E (IgE) (FCER2, CD23) has been implicated as a candidate for IgE-mediated allergic diseases and bronchial hyperreactivity, or related traits. Given evidence for genetic complexity in atopic disorders, we sought to study two European subpopulations, Finnish and Catalonian. We studied three phenotypic markers: (1) total serum IgE level; (2) asthma; and (3) specific IgE level for a mixture of the most common aeroallergens in Finland. Altogether, eight polymorphic markers spanning a region of 10 cM around the FCER2 gene on chromosome 19p13 were analyzed in 124 families. The physical order of the markers and the location of the FCER2 gene were confirmed by using radiation hybrids. The allele and haplotype association study showed a suggestive haplotype association (significance of p </= 0.03 based on a permutation test) for a high serum IgE response. In a subset of chromosomes segregating with asthma in families with two or more affected members, a single haplotype was found to be highly enriched (p = 8.3 x 10(-6)). However, sequence polymorphisms, which would verify structural differences in the FCER2 gene, were not detected in the coding region of the receptor. Our results suggest that chromosome 19p13 might harbor a genetic determinant of IgE-related traits. Studies in other population samples are needed to verify this finding.

Adult↗

Evidence of airway inflammation and remodeling in ski athletes with and without bronchial hyperresponsiveness to methacholine.

Asthma-like symptoms, methacholine hyperresponsiveness, and use of asthma medication are prevalent in elite cross-country skiers. We quantitated mucosal inflammatory cell infiltration and tenascin expression in the subepithelial basement membrane in endobronchial biopsy specimens of the proximal airways from 40 elite, competitive skiers (mean: 17.5; range: 16 to 20 yr) without a diagnosis of asthma, in 12 subjects with mild asthma, and in 12 healthy controls, through immunohistochemistry and indirect immunofluorescence, respectively. All of the subjects were nonsmokers. T-lymphocyte, macrophage, and eosinophil counts were, respectively, greater by 43-fold (p < 0.001), 26-fold (p < 0.001), and twofold (p < 0.001) in skiers, and by 70-fold (p < 0.001), 63-fold (p < 0.001), and eightfold (p < 0.001) in asthmatic subjects than in controls. In skiers, neutrophil counts were more than twofold greater than in asthmatic subjects, and mast cell counts were not significantly different than in controls. Tenascin expression (as measured through the thickness of the tenascin-specific immunoreactivity band in the basement membrane) was increased in skiers (median: 6.7 microm; interquartile range [IQR]: 5.3 to 8.5 microm, p < 0.001) and asthmatic subjects (mean: 8.8 microm; IQR: 7.2 to 10.8 microm, p < 0. 001) compared with controls (mean: 0.8 microm; IQR: 0 to 3.1 microm) and did not correlate with inflammatory cell counts. Inflammatory changes were present irrespective of asthmalike symptoms, hyperresponsiveness, or atopy. Prolonged repeated exposure of the airways to inadequately conditioned air may induce inflammation and remodeling in competitive skiers.

Adolescent↗

Endothelial sulfated sialyl Lewis x glycans, putative L-selectin ligands, are preferentially expressed in bronchial asthma but not in other chronic inflammatory lung diseases.

Lymphocyte infiltrate is a hallmark of inflammatory responses. We have previously shown that de novo-induced endothelial sialyl Lewis x (sLex) expression guides lymphocytes in an L-selectin-dependent manner to sites of acute organ transplant rejections. In this research, we have analyzed five groups of chronic lung inflammations to determine the presence of properly glycosylated, i.e., sulfated, sLex-decorated, L-selectin ligands. Two anti-sLex (2F3 and HECA-452) and one anti-6- and/or 6'-sulfated and/or 6,6'-bisulfated (MECA-79) monoclonal antibodies (mAbs) were used. The control lung specimens did not express L-selectin ligands on endothelium. In contrast, the endothelial staining intensity and the number of positive peribronchial venules and capillaries with mAbs 2F3, HECA-452, and MECA-79 were significantly greater in bronchial biopsies from patients with asthma compared with normal specimens (P<0.003). However, no significant increase of peribronchial endothelial reactivity with these antibodies was observed in adult respiratory distress syndrome, chronic bronchitis, fibrosing alveolitis, and granulomatous inflammation compared with controls. These data suggest that sulfated sLex glycans, acting putatively as ligands for L-selectin, could be instrumental in lymphocyte extravasation into human peribronchial lung tissue during asthma, but not so important in several other inflammatory lung diseases.

Adult↗

Long-term treatment with inhaled budesonide in persons with mild chronic obstructive pulmonary disease who continue smoking. European Respiratory Society Study on Chronic Obstructive Pulmonary Disease.

BACKGROUND: Although patients with chronic obstructive pulmonary disease (COPD) should stop smoking, some do not. In a double-blind, placebo-controlled study, we evaluated the effect of the inhaled glucocorticoid budesonide in patients with mild COPD who continued smoking. After a six-month run-in period, we randomly assigned 1277 subjects (mean age, 52 years; mean forced expiratory volume in one second [FEV1], 77 percent of the predicted value; 73 percent men) to twice-daily treatment with 400 microg of budesonide or placebo, inhaled from a dry-powder inhaler, for three years. RESULTS: Of the 1277 subjects, 912 (71 percent) completed the study. Among these subjects, the median decline in the FEV1 after the use of a bronchodilator over the three-year period was 140 ml in the budesonide group and 180 ml in the placebo group (P=0.05), or 4.3 percent and 5.3 percent of the predicted value, respectively. During the first six months of the study, the FEV1 improved at the rate of 17 ml per year in the budesonide group, as compared with a decline of 81 ml per year in the placebo group (P<0.001). From nine months to the end of treatment, the FEV1 declined at similar rates in the two groups (P=0.39). Ten percent of the subjects in the budesonide group and 4 percent of those in the placebo group had skin bruising (P<0.001). Newly diagnosed hypertension, bone fractures, postcapsular cataracts, myopathy, and diabetes occurred in less than 5 percent of the subjects, and the diagnoses were equally distributed between the groups. CONCLUSIONS: In patients with mild COPD who continue smoking, the use of inhaled budesonide is associated with a small one-time improvement in lung function but does not appreciably affect the long-term progressive decline.

Administration, Inhalation↗

Regular albuterol or nedocromil sodium--effects on airway subepithelial tenascin in asthma.

Both albuterol and nedocromil sodium have been recognized to possess certain anti-inflammatory properties. However, there are no data on the impact of these drugs on the pathophysiology of the bronchial extracellular matrix in asthma characterized by enhanced tenascin (Tn) expression, known to occur proportional to the severity of asthma. This paper reports data from a morphometric study on the effects of regular treatment with inhaled albuterol or nedocromil sodium on the extent of bronchial subepithelial deposition of Tn, collagen types III, IV, and VII and mucosal infiltration with macrophages. Thirty-two patients (14 women) with chronic asthma, aged 38.7 years (median) with a median forced expiratory volume in 1 sec (FEV1) of 74.4% predicted, were selected to undergo fibre-optic bronchoscopy with bronchial biopsies before and after 12 weeks of treatment with either inhaled albuterol 0.2 mg or nedocromil sodium 4 mg four times daily according to a double-blind protocol. Cryostat sections of the biopsy specimens were studied by indirect immunostaining techniques using monoclonal antibodies and computer-assisted quantitative image analysis. Albuterol treatment significantly reduced the median thickness of subepithelial Tn expression from 9.7 to 6.3 microns (P = 0.023) and macrophage numbers in the epithelium (P = 0.034), lamina propria (P = 0.039) and entire mucosa (P = 0.033), whereas nedocromil sodium had no effect. Expression of the collagen types was not affected by either treatment. There was no identifiable statistical difference between the two treatments for any of the outcome variables measured. Nevertheless, the results demonstrate that even a short-acting beta 2-agonist may exert anti-inflammatory potential sufficient to interfere with the basic mechanisms of asthma as shown by reduction of subepithelial Tn content and mucosal macrophage count.

Adrenergic beta-Agonists↗

Increasing prevalence of asthma but not of chronic bronchitis in Finland? Report from the FinEsS-Helsinki Study.

To assess the prevalence of asthma, chronic bronchitis and respiratory symptoms, and to calculate risk factors for them, we performed a postal survey in Helsinki, the capital of Finland. During the spring of 1996, questionnaires were mailed to a random sample of 8000 individuals aged 20-69. The total response rate was 76%, with 6062 complete answers. The prevalence of having ever had asthma was 7.2%, physician-diagnosed asthma was 6.6% and physician-diagnosed chronic bronchitis was 3.7%. Asthma was significantly more common among women than men, but no gender differences existed in prevalence of chronic bronchitis. The most common respiratory symptom was sputum production when coughing, reported by 27%. During the previous 12 months, wheezing had occurred in 20% and attacks of shortness of breath in 13% of subjects. Generally, the prevalence of different respiratory symptoms were significantly higher among smokers. The most important risk factor for asthma was a family history of asthma (Odds ratio:OR 3.3). Multivariate analysis revealed that being a member of the socioeconomic group, manual workers, was associated with a significantly increased risk for chronic productive cough (OR 1.7), and for wheezing during the previous 12 months (OR 1.7). Manual workers of both genders had the highest prevalence of asthma, chronic productive cough and wheezing during the previous 12 months. The prevalence of asthma in Helsinki was higher than previously found in Finland, and was at a similar level to that of other Nordic countries. In contrast, prevalence of chronic bronchitis was lower than previously shown in Finland.

Adult↗

Chronic bronchitis and chronic obstructive pulmonary disease: Finnish National Guidelines for Prevention and Treatment 1998-2007.

1. A national recommendation for the promotion of prevention, treatment and rehabilitation in relation to chronic bronchitis and COPD from 1998 to 2007 has been prepared on the basis of extensive collaboration by order of the Ministry of Social Affairs and Health. The Programme needs to be revised as necessary, because of rapid developments in medical knowledge, and in drug therapy in particular. 2. COPD is a disease characterized by slowly progressing, irreversible airways obstruction. Over 5% of the population suffer from symptomatic forms of the disease. It is estimated that a further 5% of the population may suffer from latent COPD. Most patients (75%) suffer from mild forms of the disease. The disease is often preceded by chronic bronchitis. A total of 400,000 Finns suffer from chronic bronchitis or COPD. Occurrence of these diseases in future will be particularly affected by decreased smoking by men, increased smoking by the young and by women, and aging of the population. 3. In 1997, the annual treatment costs of chronic bronchitis and COPD were estimated to be FIM 1.5 thousand million, total costs FIM 5 thousand million. Without intensification of measures to prevent and treat the diseases, costs will rise significantly. Costs arising from severe COPD (5% of patients with COPD) account for roughly 65% of costs overall and are primarily related to hospitalizations. 4. The goals of the Programme for the Prevention and Treatment of Chronic Bronchitis and COPD are as follows: (a) to decrease the incidence of chronic bronchitis; (b) to ensure that as many patients as possible with chronic bronchitis recover; (c) to maintain capacity for work and functional capacity of patients with COPD; (d) to reduce the percentage of patients with moderate to severe COPD; (e) to decrease the number of hospitalization days of COPD patients by 25% overall; and (f) to decrease annual costs per patient. 5. The following means are suggested for achieving the goals: (a) reduction in smoking; (b) reduction in work-related and outdoor air pollutants and improvement of quality of indoor air; (c) enhancement of knowledge about risk factors and treatment of the diseases is in key groups; (d) promotion of early diagnosis and active treatment, in smokers in particular; (e) improvement of guided self-care; (f) early commencement of rehabilitation, individual planning and implementation, primarily as an element in treatment; and (g) encouragement of scientific research. 6. COPD and exacerbation of its symptoms can be prevented through choices relating to life habits, such as not smoking, maintaining good general condition, and protection against exposure to dusts. The Programme gives examples of such measures and appeals to various authorities and voluntary organizations to increase their cooperation. Preventive methods should be individualized, and based on due consideration. 7. Chronic bronchitis and COPD should be diagnosed at early stages, and treated appropriately from the outset. Treatment consists of: (a) treatment according to causes, such as stopping smoking and work hygiene; (b) early rehabilitation such as patient education and guided self-care: (c) drug therapy; (d) hospital treatment; and (e) rehabilitation. 8. The hierarchy of referrals in the treatment of COPD should be revised to accord a greater role to the primary health care sector. Good exchanges of information and cooperation between the primary health care and specialized medical care sectors will all be necessary if this hierarchial model is to have the desired effect. 9. Hospital districts and health centres should ensure that different levels of the health-care system are capable of fulfilling the tasks assigned to them appropriately. One specialist in each hospital district should be given charge of prevention and assembly of know-how relating to treatment, and of quality of treatment at regional level. (ABSTRACT TRUNCATED)

Bronchitis↗