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Nutrition and COPD
Findings support bacterial role in COPD flare-ups
Theophylline shows anti-inflammatory effects in COPD

NUTRITION AND COPD
Evidence for a role of diet in chronic obstructive pulmonary disease (COPD) has been accumulating rapidly over the past decade. Weight loss and muscle wasting commonly occur in patients with COPD. A decreased dietary intake and elevated energy requirements underlie the weight loss. Disturbances in intermediary metabolism caused by anabolic and catabolic mediators such as hormones, cytokines and growth factors, resulting in disproportionate muscle wasting have been described. Low body weight is associated with an impaired pulmonary status reduced diaphragmatic mass lower exercise capacity higher mortality rate Nutritional supplementation in combination with an anabolic stimulus (eg. exercise) has been shown effective in improving functional capacity, health status and mortality in most depleted patients. Sufficient protein, 1.0-1.5 gram/kg body weight, is necessary to maintain or restore lung and muscle strength, as well as promote immune function. A balanced ratio of protein (15 to 20% of calories) with fat (30 to 45% of calories) and carbohydrate (40 to 55% of calories) is important to preserve a satisfactory respiratory quotient (RQ) from substrate utilization. Repletion, but not overfeeding, is the hallmark of nutritional care. Vitamins C, E and beta-carotene are antitoxidant vitamins and may protect the lungs from oxidative damage by smoking or air pollution. Observational studies have shown repeatedly that the intake of vitamin C and of fruits rich in vitamin C is positively related to lung function. The role of minerals, such as magnesium and calcium, in muscle contraction and relaxation may be important for people with COPD. Intakes at least equivalent to the recommended dietary allowance (RDA) should be provided.
Adverse effects of lung disease on nutritional status
Increased energy expenditure Increased work of breathing Chronic infection Medical treatments (e.g. bronchodilators, chest physical therapy)
Insufficient intake
Anorexia due to chronic disease Difficulty chewing and swallowing from dyspnea Decreased oxygen saturation when eating Fluid restriction Gastrointestinal distress and vomiting
Other problems
Constipation from low-fiber food selections Diarrhoea from impaired peristalsis secondary to lack of oxygen to the GI tract.
Additional limitations
Difficulty preparing food due to fatigue Lack of interest in food preparation
Suggestions for increasing energy intake
Include foods of high-energy density: milk and dairy products, gram (channa), til laddoo, peanuts other nuts, dry fruits, soya products, chicken, fish and eggs. Include snacks regularly, especially before bedtime Serve snacks at least 2 hours before the next meal Keep foods readily accessible for snacking : high-fibre biscuits, chana (gram), laddoos, thick buttermilk, fruit juice. Soft foods and beverages may be easier to eat when there is shortness of breath: fruit, milkshakes, jelly with custard, thick lassi Add supplements to the normal foods to increase the calorie density: skimmed milk powder to milk, soups, sugar to fruit juice, butter, jam on bread Do not offer low calorie foods-water, dal / moong clear / soups Serve small portions Rest before meals Plan expectorant medication usage apart from mealtimes Pay attention to appearance, texture, and aroma of the foods offered.
References
Respir Res 2001; 2(5): 261-264 Ferreira IM, Brooks D, Lacasse Y, Goldstein RS, White J, Nutritional supplementation for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2002; (1). Curr Opin Pulm Med 2000; 6(2): 110-5 Clin Chest Med 2000; 21(4): 753-62 M. Kathleen and E. Sylvia. Kraus’s Food, Nutrition and Diet Therapy. W. B. Saunder’s company 2000, pg. 817, 825-8
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Findings support bacterial role in COPD flare-ups
Chronic obstructive pulmonary disease (COPD) flare-ups are more likely to be diagnosed at clinic visits when new bacterial strains are isolated than at visits when no new organisms are identified, according to a recent report. The issue of whether bacterial pathogens play a role in COPD exacerbations is controversial, according to study author Dr. Timothy F. Murphy, from the State University of New York. Dr. Murphy’s team analyzed sputum samples from 81 COPD patients. The samples were obtained at each monthly clinic visit and whenever an exacerbation occurred. Molecular typing was performed on each sample to determine not only the bacterial species present, but also the strain. A total of 1975 clinic visits occurred during the 56-month study period, 374 of which were made for disease flare-ups. Disease exacerbations were more than twice as likely to correlate with a clinic visit in which a new organism was identified than with a visit in which the bacterial environment had not changed. In particular, isolation of new strains of Haemophilus influenzae, Moraxella catarrhalis, and Streptococcus pneumoniae were associated with a significantly increased risk of a disease flare-up. ”COPD is associated with significant morbidity and mortality and much of this is due to the exacerbations that characterise the disease,” Dr. Murphy said. ”Without performing molecular typing, past researchers were unable to see the bacterial changes that may have been occurring with COPD exacerbations,” Dr. Murphy noted. ”As it turns out, there really is a dynamic turnover of bacterial strains in the respiratory tracts of COPD patients.” These findings provide ”strong evidence for a causative role of bacteria in COPD exacerbations and provide a rationale for treating these flare-ups with antibiotics,” Dr. Murphy said. ”Also, and more importantly, the results provide an impetus for developing vaccines for COPD patients,” he noted. Ref.: N Engl J Med 2002;347:465-471.
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Theophylline shows anti-inflammatory effects in COPD
According to a report from UK based researchers, low-dose theophylline shows anti-inflammatory effects in patients with chronic obstructive pulmonary disease1. 25 COPD patients received theophylline 150-300 mg twice daily and placebo, for 4 weeks each in a crossover fashion. Each treatment phase was separated by a two-week washout period. Sputum samples were evaluated from all 25 patients. Following theophylline administration, significant reductions from baseline were observed in total inflammatory cell counts and in the absolute number of neutrophils (by approximately 21 and 22%, respectively). Furthermore, sputum levels of interleukin-8, myeloperoxidase and lactoferrin were significantly reduced from baseline by a mean of 24%, 31% and 10%, respectively. The researchers believe that the above-mentioned study adds to the current literature and addresses the urgent clinical question of how to deal with inflammation in COPD2. However, long-term studies are now required, in order to demonstrate that low-dose theophylline is clinically superior to other therapies in the treatment of COPD.
References
American Journal of Respiratory and Critical Care Medicine 165: 1371-1373, 15 May 2002 American Journal of Respiratory and Critical Care Medicine 165: 1351-1352, 15 May 2002

A vaccine against asthma could be ready for trials in just three years. In a major breakthrough, scientists have discovered the active part of the virus that is thought to be behind a third of all asthma cases. The respiratory syncytial virus (RSV) inflames the inside of the lungs, weakens the immune system and produces mucus that obstructs the airways. Scientists at the Imperial College School of Medicine in London and American experts at the National Institute of Health believe they have identified the protein, which causes the inflammation. It was found that only a small amount of the G protein was necessary to damage the immune system of mice.

The National Institute in Washington hopes to develop a vaccine, which could be tested on humans within three years. But it may not all be plain sailing as earlier trials of a vaccine for RSV led to hospitalisation of some children following exposure to the virus.

http://news.bbc.co.uk/1/hi/health.

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SALMETEROL IMPROVES PULMONARY FUNCTION IN HEART PATIENTS

Inhaled salmeterol, a long acting 2 agonist used in asthma, has been found to improve pulmonary function in heart patients.

Investigators from the Department of Pharmacy Practice and Internal Medicine at the University of Utah Health Sciences Center, U.S. conducted a prospective, randomised, double-blind, 14-day cross over study to determine the effect of inhaled salmeterol on pulmonary function. Inhaled salmeterol (84 g) was administered every 12 hours for 14 days to 8 symptomatic heart failure patients with left ventricular ejection fraction (LVEF) < 40% and FEV1 < 80%.

Results showed that the therapy led to a significant 6% improvement in FEV1 2.46 litres compared to 2.33 litres with placebo. Rate pressure product also increased by 5% with salmeterol. However, there was no increase in plasma norepinephrine, epinephrine, plasma renin activity or ventricular ectopy. Thus, the study revealed that inhaled salmeterol improved FEV1 without producing measurable effects on neuroactivation or ventricular ectopy. The clinical significance of the minor increase in rate-pressure product remains to be determined.

J. Cardiovasc. Pharmacol 2002; 40(1): 140-145

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ROFECOXIB IN ASPIRIN-SENSITIVE ASTHMA

Aspirin-induced asthma (AIA) is an airway mucosa inflammatory disease that combines with the precipitation of asthma and attacks of rhinitis and is triggered by the ingestion of aspirin and most nonsteroidal anti-inflammatory drugs (NSAIDs). AIA affects about 10% of adults with asthma. These asthmatic attacks usually occur within 3 hours after ingestion of aspirin or an NSAID. The attacks are often severe and in many cases life-threatening, requiring emergency mechanical ventilation. AIA is a crucial problem since drugs for the management of common medical conditions such as pain, fever and inflammation are commonly required. Therefore, it is important to choose an alternative anti-inflammatory agent for vulnerable asthma patients. Cyclooxygenase (COX) enzymes, which appear to be central to the mechanism of aspirin sensitivity, exist in at least two isoforms, COX-1 and COX-2. Most NSAIDs inhibit both isoforms, although at different intensities. The anti-inflammatory effects are due to COX-2 inhibition and adverse effects are due to COX-1 inhibition. Rofecoxib is a selective COX-2 inhibitor, used as an analgesic in patients with primary dysmenorrhoea and post-operative dental pain. It has very little or no effect at all on gastric mucosa.

A study was conducted to demonstrate the safety of rofecoxib in asthma patients suffering from AIA or other NSAID- induced asthma. The study covered 40 patients, all of whom experienced asthma induced by at least two different NSAIDs. Out of the 40 patients, 77.5% had moderate asthma and 12.5% had severe asthma. The patients were challenged in a single-blind manner with different doses of rofecoxib on 3 different days (1st day- 6.25 mg, 2nd day - 12.5 mg, 3rd day - 25 mg), until either the therapeutic dose of 25 mg or intolerance was reached. Each patient was again challenged with 25 mg of rofecoxib 7 days later if no evidence of intolerance had been observed before.

At the end of the challenge procedure, all the patients tolerated the 25 mg dose of rofecoxib well, without any signs of immediate or delayed reactions. The mean PEF variation before the provocation test was 11.20% and afterwards 11.38%. There were no significant differences between PEF variations before and after the administration of rofecoxib. Thus the study demonstrated that a 25 mg dose of rofecoxib was well tolerated in all 40 patients with AIA and NSAID- induced asthma.

Chest 2002; 121: 1812-1817

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