Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “COUGH”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 469 records · Page 26Linked to original sources
PubMed1997

Double-blind comparison of losartan, lisinopril, and metolazone in elderly hypertensive patients with previous angiotensin-converting enzyme inhibitor-induced cough.

This study compared the incidence of cough with the angiotensin-converting enzyme (ACE) inhibitor lisinopril and the diuretic metolazone with angiotensin II receptor antagonist losartan in elderly hypertensive patients with previous histories of ACE inhibitor-induced cough. A randomized, double-blind, stratified, parallel-group comparison of lisinopril at 10 mg, losartan at 50 mg, and metolazone at 1 mg, each given once daily for a maximum of 10 weeks, was performed in four hypertension clinics in four centers in two countries. Cough was detected by a questionnaire (the primary end point) given to elderly patients with hypertension, and the cough frequency was quantified by a visual analog scale (a secondary end point). A total of 84 elderly patients with hypertension, all who were nonsmokers with ACe inhibitor-induced cough and were confirmed by lisinopril rechallenge then placebo dechallenge, were randomized to the three treatment groups. The incidence of cough with losartan (18%) was significantly lower than with lisinopril (97%) and similar to that for metolazone (21%). Cough frequency evaluated by the visual analog scale was significantly lower for losartan than for lisinopril and similar to that for metolazone. The specific, selective angiotensin II receptor antagonist losartan is associated with a decrease in the incidence of cough in patients with previous ACE inhibitor-induced cough.

Aged↗
PubMed1998

Cough-challenge trial with a new angiotensin-converting enzyme inhibitor, imidapril.

This study was conducted to examine whether imidaprilat, an active diacid of the angiotensin-converting enzyme (ACE) inhibitor imidapril, preferentially inhibits angiotensin I degradation rather than bradykinin degradation, and whether imidapril is less active than other ACE inhibitors in inducing cough in patients with hypertension. The effect of imidaprilat on the inhibition of pressor response to angiotensin I and augmentation of depressor response to bradykinin was compared with that of enalaprilat and captopril in anesthetized rats. To determine the incidence of cough associated with imidapril, patients with a history of ACE inhibitor-induced dry cough were enrolled in a randomized, open-labeled, crossover trial with two 6-week periods to be treated with imidapril or amlodipine, a calcium-channel blocker. The recurrence of cough was assessed during both treatments. In the animal study, there were no significant differences in the ratio of inhibition of pressor response to angiotensin I and the augmentation of depressor response to bradykinin among the ACE inhibitors. In the cough-challenge trial, a total of 60 patients with hypertension were enrolled in the study. Cough and cough related symptoms recurred in 98.3% of the patients (59/ 60) during imidapril therapy. In contrast, only two patients reported cough during treatment with amlodipine. These results indicate that imidapril has no selectivity in inhibiting angiotensin I- and bradykinin-degradation in rats, and that clinically it is not different from other ACE inhibitors in inducing cough in patients with hypertension.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

Role of substance P in cough.

The sensory neuropeptide, substance P (SP), is present in human airway nerves, beneath and within the epithelium where the condensed localization of neutral endopeptidase (NEP), the major enzyme degrading SP, is observed. To test the hypothesis whether SP stimulates the cough reflex and NEP modifies the cough reflex, we studied the cough response to various stimuli in awake guinea-pigs. Inhibition of NEP with phosphoramidon caused cough, which was inhibited by systemic capsaicin treatment and by aerosols of a specific NK1 receptor antagonist FK 888. Aerosols of FK 888 also inhibited cough induced by bronchoconstricting agents such as acetylcholine and histamine in non-sensitized animals and by ovalbumin antigen in animals sensitized to ovalbumin. The number of coughs induced by histamine aerosols was inhibited by systemic capsaicin treatment and enhanced by pretreatment with a NEP inhibitor phosphoramidon. Likewise, FK 888 inhibited the augmented cough response to aerosolized capsaicin in female guinea-pigs treated with a long-term medication of an angiotensin-converting enzyme inhibitor, cilazapril. In humans, aerosols of SP did not cause cough in normal subjects, whereas it did in patients with common colds. The SP fragment a major metabolite of SP produced by NEP, was less effective compared with SP in these patients, suggesting that damaged epithelium may facilitate the penetration of SP. These findings suggest that SP released from sensory nerves in response to stimuli may mediate cough and NEP may have a role in modulating SP-induced effects.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Efficacy and tolerability of levodropropizine in adult patients with non-productive cough. Comparison with dextromethorphan.

The results of a double-blind, randomized clinical trial involving 209 adult patients of either sex with moderate non-productive cough are reported. The therapeutic efficacy and the tolerability of levodropropizine syrup (60 mg t.i.d. for 5 days) was evaluated in comparison with dextromethorphan syrup (15 mg t.i.d. for 5 days). Efficacy was assessed by the number of coughing spells in a 6h period, the cough frequency classes, the cough intensity and the night awakenings due to cough. Tolerability was evaluated by laboratory results, vital signs and any adverse event occurred during the clinical trial, including presence or absence of somnolence. Independently from the underlying pathology and from the degree of baseline cough severity, the number of coughing spells was significantly (P < 0.05) reduced by both levodropropizine and dextromethorphan already after the 2nd day of treatment, the effect and its time of onset being similar for both drugs. Cough intensity was significantly (P < 0.01) reduced by both drugs throughout the treatment, at an earlier time with levodropropizine than with dextromethorphan. Concurrently with the relief of cough, the number of night awakenings was decreased remarkably and significantly (P < 0.05), with levodropropizine displaying an improvement significantly higher (P < 0.05) than dextromethorphan. No change in laboratory tests values was considered clinically relevant and vital signs were not clinically affected by the study drugs. The number of patients reporting adverse events was significantly higher (P < 0.05) in the dextromethorphan (12.1%) than in the levodropropizine (3.6%) group. Overall, somnolence was reported for a low percentage of patients with both drugs, with the percentage of patients experiencing this side effect being one half in the group treated with levodropropizine (4.6%) as compared with dextromethorphan (10.4%). These results confirm the antitussive effectiveness of levodropropizine and point out a more favourable benefit/risk profile when compared to dextromethorphan.

Adolescent↗
PubMed2002

Therapy for cough: active agents.

Cough is an important defensive reflex of the upper airway and is also a very common symptom of respiratory disease. Cough after an upper respiratory virus infection is transient, and persistent cough is associated with a whole range of conditions such as asthma, rhino-sinusitis, gastro-oesophageal reflux. Treatment directed at these conditions may improve the associated cough. There is often a need, however, to control cough itself, whatever the cause. The most effective drugs in this class are the opioids, such as morphine, codeine or pholcodeine, but at effective doses they have side-effects such as drowsiness, nausea, constipation and physical dependence. Investigations into the cough reflex and into the potential mechanisms of sensitised cough reflex have uncovered several potential targets for novel drugs. New opioids such as k- and d-receptor agonists apart from m-agonists have been developed, in addition to non-opioid, nociceptin. Neurokinin receptor antagonists, bradykinin receptor antagonists, vanilloid receptor VR-1 antagonists may be beneficial by blocking effects of tachykinins, and sensory nerve activation. Local anaesthetics, blockers of sodium-dependent channels, and maxi-K CA2+-dependent channel activators of afferent nerves are inhibitors of the cough reflex. Some of these novel agents may act centrally or peripherally or at both sites as antitussives. Large scale trials of these novel compounds have not been tried in cough in man, but there is a serious need for more effective antitussives devoid of side-effects.

Antitussive Agents↗
PubMed2002

Central pathways for cough in man--unanswered questions.

Central processing of afferent cough impulses occurs in a putative 'cough centre' in the dorsal medulla where the reflex is subject to considerable cortical control. Little is known about the central neurotransmitters and mediators which mediate cough in humans. Previous animal and human studies suggest that the antitussive effect of opiates may be mediated at central 5-HT receptors. In three studies in healthy human volunteers, we have investigated the potential role of central cholinergic and dopaminergic receptors in the mediation of cough, and the potential role of 5-HT receptors in the antitussive action of opiates. Intravenous administration of atropine or physostigmine had no effect on capsaicin-induced cough. Similarly, oral administration of L-dopa, bromocriptine or haloperidol had no effect on capsaicin-induced cough. Compared with saline, intravenous morphine significantly suppressed capsaicin-induced cough and increased drowsiness. Compared with placebo, pretreatment with oral pizotifen significantly attenuated the antitussive effect of morphine, but not the sedative effect. This suggests that in humans, an agonist action at 5-HT2 and/or 5-HT1 receptors may be involved in the antitussive effect of morphine, but not its sedative effect. Further knowledge of central cough pathways in humans must await the availability of more selective receptor agonists and antagonists for human studies. This offers the promise of effective antitussive therapy. The challenge is to find an antitussive agent which can return the abnormal sensitivity of the cough reflex to normal, without adverse effects.

Cough↗
PubMed1998

Cough receptor sensitivity to capsaicin and tartaric acid in patients with Mycoplasma pneumonia.

There has been no detailed study of cough sensitivity during acute lower respiratory infection. The aim of this study was to clarify cough sensitivity in Mycoplasma pneumonia, which is a well known acute lower respiratory infection with persistent nonproductive cough. We examined cough sensitivity to inhaled capsaicin and tartaric acid in both the acute and the convalescent phases of Mycoplasma pneumonia, cell differentials in bronchoalveolar lavage fluid, and pathologic findings of transbronchoscopic bronchial biopsy specimens. Although dry cough was observed in all patients during Mycoplasma pneumonia, cough sensitivity in the acute phase [capsaicin: 19.8 (GSEM, 0.214) microM, tartaric acid: 0.26 (GSEM, 0.356) M] were not enhanced compared with those in both control subjects [capsaicin: 27.9 (GSEM, 1.24) microM, tartaric acid: 0.316 (GSEM, 0.079) M] and patients in the convalescent phase [capsaicin: 15.7 (GSEM, 0.219) microM, tartaric acid: 0.50 (GSEM, 0.326) M] when all symptoms including cough had disappeared. The percentage of lymphocytes and neutrophils in bronchoalveolar lavage fluid BALF was significantly greater than in the control subjects, and lymphocyte-dominant bronchitis was observed in biopsied specimens. We conclude that cough threshold to inhaled capsaicin or tartaric acid was not enhanced during acute Mycoplasma pneumonia with lymphocyte-predominant bronchitis. This is the first report examining cough sensitivity in patients with acute lower respiratory infection with pneumonia.

Adult↗
PubMed2002

Effect of suplatast tosilate, a Th2 cytokine inhibitor, on cough variant asthma.

STUDY OBJECTIVE: Th2 cytokines play an important role in the pathogenesis of asthma. Our study objective was to determine the effect of suplatast tosilate, a Th2 cytokine inhibitor, on patients with cough-variant asthma. METHODS: Twenty patients with cough-variant asthma (CVA) were assigned to a suplatast tosilate (100 mg three times daily) group or a placebo group for 6 weeks in a double-blind randomized study. The cough scores, medication scores, pulmonary function, bronchial hyperresponsiveness to methacholine, cough threshold for capsaicin, percentage of eosinophils and concentrations of eosinophilic cationic protein (ECP) in hypertonic saline-induced (induced) sputum were evaluated. The main outcome measures were capsaicin cough threshold and concentrations of ECP in induced sputum. RESULTS: In the suplatast group, the cough scores and the medication scores decreased significantly over time. The percentage of eosinophils in induced sputum significantly decreased from 53.5+/-5.6% to 13.6+/-2.6%. The cough threshold for capsaicin improved significantly from 2.72+/-3.41 microM to 39.7+/-22.7 microM in the suplatast group. The concentrations of ECP in induced sputum decreased significantly from 435+/-123 microg/l to 56+/-34 microg/l in the suplatast group. The bronchial responsiveness to methacholine changed from 8.45+/-3.43 units to 11.4+/-3.76 units in the suplatast group. CONCLUSIONS: Suplatast improved the cough scores and the cough threshold for capsaicin in patients with CVA without significant side effects, suggesting the effectiveness of suplatast in the treatment of CVA. Suplatast also decreased the percentage of eosinophils and concentrations of ECP in induced sputum, suggesting improvement in eosinophilic inflammation in patients with CVA. Further pharmacodynamic research is needed to explain the precise mechanism.

Adult↗
PubMed2004

A preliminary study of PEFR monitoring in patients with chronic cough.

It is important to make a differential diagnosis of cough variant asthma in patients with chronic cough. To examine whether or not peak expiratory flow rate (PEFR) is useful for the differential diagnosis of cough variant asthma in such patients, diurnal variation rates of PEFR were calculated in 23 patients who presented with dry cough lasting four or more weeks and who showed no abnormalities on chest radiographs. None of the patients had wheezes, and pulmonary function testing at the time of visit to the hospital revealed no abnormalities. During the control period, the mean diurnal variation rate of PEFR in 23 patients was 16.3 +/- 7.9%. Six, nine and eight patients had PEFR diurnal variations rates of <10% (Group 1), 10-19% (Group 2), and > or = 20% (Group 3), respectively. At week 3 of treatment with bronchodilators, only Group 3 showed a significant decrease in PEFR diurnal variation rate from 25.7% to 10.1%. The cough score decreased significantly in Group 3 only. These patients had enhanced bronchial hyperresponsiveness and showed eosinophils in induced sputum, leading to the diagnosis of cough variant asthma (CVA). After making the diagnosis of CVA, an inhaled corticosteroid or a Th2 cytokine production inhibitor suplatast tosilate was administered to patients; consequently, they showed no recurrence of cough. PEFR monitoring allowed the detection of morning dip and was suggested to be potentially useful for the differential diagnosis of cough variant asthma in patients with chronic cough.

Adult↗
PubMed2005

The role of substance P and bradykinin in the cough reflex and bronchoconstriction in guinea-pigs.

In this study we investigated the ability of aerosolized substance P to induce either cough or bronchoconstriction in guinea-pigs. We have also examined whether pre-treatment, by the inhaled route, of animals with a combination of the neutral endopeptidase inhibitor, phosphoramidon (10(-3) M), and the diaminopeptidase IV inhibitor, diprotin A (10(-3) M), enhances the airway response to substance P. Moreover, we also assessed whether aerosol pre-treatment of guinea-pigs with either substance P or bradykinin, at 10(-4) M, affects the citric acid-induced cough and/or bronchoconstriction. Challenge of guinea-pigs with substance P only at 10(-3) M resulted in significant bronchconstriction but only a weak and variable cough response (1.1+/-0.6; P>0.05). Pre-treatment of guinea-pigs with both phosphoramidon and diprotin A resulted in a small non-significant increase in the cough response (2.8+/-0.9 vs. 1.1+/-0.6; P>0.05) but significantly enhanced substance P-induced bronchoconstriction (P<0.05). Moreover, exposure of guinea-pigs to substance P (10(-4) M) prior to citric acid challenge (0.6 M) resulted in a significant (P<0.05) enhancement of the citric acid-induced bronchoconstriction but not the citric acid-induced cough (11.7+/-1.8 vs. 12.8+/-1.5; P>0.05). In contrast, exposure of guinea-pigs to bradykinin (10(-4) M) prior to the citric acid challenge resulted in a significant enhancement of the cough response (9.2+/-1.9 vs. 25.8+/-2.5; P<0.05) but not the bronchoconstriction (P>0.05). These data do not support a major peripheral role for substance P in the cough reflex, although bradykinin is able to sensitize the cough reflex. Furthermore, these data suggest that bronchoconstriction, induced by citric acid, is not responsible for the cough associated with this irritant.

Animals↗
PubMed2005

Pulmonary chemokines and their receptors differentiate children with asthma and chronic cough.

BACKGROUND: Cough is a frequent symptom in children, but the differentiation of asthmatic cough from cough of other origins can be difficult. Chemokines recruit T lymphocytes to inflamed tissues, and the corresponding chemokine receptors are differentially expressed on T H 1 and T H 2 cells. OBJECTIVE: We sought to determine whether levels of T H 1/T H 2-related chemokines and their receptors differ in bronchoalveolar lavage fluid (BALF) from 12 children with allergic asthma, 15 nonatopic children with chronic cough, and 10 children without airway disease. METHODS: The T H 1-related (IFN-gamma-inducible protein of 10 kd [IP-10], IFN-gamma-inducible T cell alpha chemoattractant [ITAC], monokine induced by IFN-gamma [Mig], and IFN-gamma) and T H 2-related (thymus- and activation-regulated chemokine [TARC], macrophage-derived chemokine [MDC], IL-5, and IL-4) chemokines and cytokines were quantified in BALF by ELISA and a particle-based multiplex array. Percentages of pulmonary lymphocytes expressing CXCR3 + and CCR5 + (T H 1) and CCR4 + and CCR3 + (T H 2) chemokine receptors were determined in BALF by flow cytometry. RESULTS: Pulmonary CCR4 + CD4 + cells and levels of TARC and MDC were significantly increased in asthmatic children versus children with chronic cough or without airway disease. In asthmatic children CCR4 + CD4 + cells correlated positively with levels of TARC, MDC, and serum IgE levels and negatively with FEV 1 . In contrast, CXCR3 + CD8 + cells and levels of ITAC were significantly increased in children with non-atopic chronic cough compared with the other groups. In children with chronic cough, CXCR3 + CD8 + cells correlated with levels of ITAC and IFN-gamma. CONCLUSION: Pulmonary CCR4 + CD4 + and CXCR3 + CD8 + cells and their ligands TARC, MDC, and ITAC clearly differentiate asthmatic children from nonatopic children with chronic cough. The analysis of these markers could facilitate the diagnostic discrimination of asthma versus other reasons for chronic cough in children.

Adolescent↗
PubMed2004

Acute and chronic cough.

Individuals are generally content to self-medicate for acute cough. It is only when the cough becomes persistent that they seek medical assistance. It is not known why patients cough in association with an acute upper respiratory tract infection (URTI), although interest has focused on how viruses may influence airway sensory nerve function and contribute to heightened cough reflex sensitivity. Why some patients develop a persistent cough following a viral URTI is also unclear. Much more is known about the causes and aggravants of chronic cough although there is no broad agreement as to the best way to manage such patients. Asthma, upper gastrointestinal dysfunction and rhinitis are frequently associated with chronic cough, although the impact of cough in suppurative lung disease and interstitial lung fibrosis is rarely considered. The development of effective treatments for cough remains a challenge and will require co-operation between clinicians, scientists and the pharmaceutical industry.

Acute Disease↗
PubMed2004

Sensory regulation of the cough reflex.

Coughing is a highly coordinated reflex that serves to protect the airways from a variety of potentially harmful stimuli. However, in airways disease the cough reflex threshold is lowered and coughing can become exaggerated and inappropriate. Excessive coughing not only affects an individual's quality of life, but may contribute to the pathology of the disease. Understanding the neural components of the cough reflex is essential for establishing new treatments for cough disorders. This review will summarize the current understanding of the afferent neural pathways mediating cough, including how interactions between airway afferent nerve fibre subtypes may modulate the cough reflex pathway and underlie the manifestation of cough disorders.

Animals↗
PubMed2005

Reproducibility and validity of a Yan-style portable citric acid cough challenge.

Although many different methods of measuring cough reflex sensitivity have been published, few are simple enough to use outside of a hospital or laboratory environment. The aim of this study was to develop a simple, quick, and portable cough challenge, assess its reproducibility, and compare its results with those measured by an existing established hospital protocol. Twenty-five volunteers performed cough challenges based on an established hospital dosimeter protocol, and, on a separate occasion, by a protocol inhaling citric acid from DeVilbiss 40 hand-held nebulisers (citric acid concentrations of 10-3000 mM). Reproducibility of the hand-held cough challenge was assessed in 11 volunteers. Cough thresholds were consistently higher by the hand-held method than by the hospital dosimeter method. The geometric mean citric acid concentrations causing two coughs (threshold D2) were 3.14 and 2.77 log mM, respectively (p<0.001). The geometric mean (95% CI) difference between the tests was 0.51 log mM (0.18-0.83) of the average of the two values. Cough D2 thresholds attained by the two techniques did, however, show significant correlation (r=0.95, p<0.0001). The coefficient of repeatability for the hand-held method was 0.40 log mM. Administering citric acid from DeVilbiss 40 hand-held nebulisers offers a rapid, portable, and reproducible cough challenge in healthy volunteers. The results correlate well with an existing Mefar dosimeter challenge, but give two to three times greater cough thresholds.

Anticoagulants↗
PubMed2006

Modulation of citric acid-induced cough following lipopolysaccharide-mediated neutrophilia in the guinea pig.

This investigation examined a possible correlation between lipopolysaccharide (LPS)-induced pulmonary neutrophilia and cough. Conscious male guinea pigs were acutely exposed to aerosolized LPS and thereafter at various times challenged with citric acid aerosol (CA; 250mM) to induce cough followed by bronchoalveolar lavage (BAL) to quantitate inflammatory cell accumulation. LPS caused a hyporesponsive cough at 24h post-LPS with neutrophilia apparent from 2h post-LPS. By 96h post-LPS both cough and neutrophilia had returned towards normal. Dexamethasone (DEX, 2mgkg(-1)/day for 3 days prior) did not affect the cough hyporesponsiveness at 24h; however it attenuated LPS-induced BAL fluid neutrophilia. Since LPS can stimulate inducible nitric oxide synthase (iNOS) we hypothesized that the cough hyporesponsiveness may involve nitric oxide. To investigate this we treated animals with an aerosolized iNOS inhibitor 1400W (1mM) immediately prior to LPS. 1400W had no significant effect on either cough hyporesponsiveness or BAL fluid neutrophilia at 24h post-LPS. Despite differing effects on neutrophilia, these findings clearly indicate that neither DEX nor iNOS inhibition had any direct effect on LPS-induced cough hyporesponsiveness. The mechanism underlying the LPS-induced cough hyporesponsiveness does not appear to be directly linked to LPS-induced neutrophilic inflammation.

Administration, Inhalation↗
PubMed2006

Experimentally induced cough.

The experimental induction of cough has become an important component of clinical cough research. Measurement of cough reflex sensitivity allows the evaluation of the effect of pharmacological and other interventions on the cough reflex, as well as the performance of epidemiological studies relevant to cough. The most commonly used tussive agents include capsaicin, citric acid and ultrasonically nebulized distilled water (fog). Methodological considerations are vital to the performance of high quality, reproducible cough challenge, which is especially important when measuring the effect of an experimental intervention on cough reflex sensitivity. For the optimal execution of clinical trials employing inhalation cough challenge, the subject population must be carefully selected, and the usefulness and potential limitations of data obtained from cough challenge studies need to be appreciated.

Antitussive Agents↗
PubMed2006

Geography and cough aetiology.

Cough is the most common complaint that leads patients to seek medical attention. Especially chronic persistent cough is annoying, and requires appropriate diagnosis and treatment. Recent cough guidelines and original papers on cough epidemiology from various countries show remarkable differences in the aetiology of chronic cough among countries, especially between US, UK and Japan. Entities associated with rhinosinus disease (post-nasal drip/upper airway cough syndrome reported from the US, rhinitis or rhinosinusitis from the UK, and sinobronchial syndrome from Japan), and eosinophilic lower airway disorders (cough variant asthma, non-asthmatic eosinophilic bronchitis and atopic cough) are most confusing and might involve significant overlap. In this article, issues related to chronic cough aetiology are discussed, including geographic issues, e.g. 'simple' geography or difference in race, and difference in patient characteristics possibly arising from difference in the medical system.

Chronic Disease↗
PubMed2006

Altitude-related cough.

Cough is a troublesome condition which affects many visitors to high altitude. Traditionally it has been attributed to the inspiration of the cold, dry air which characterizes the high altitude environment. This aetiology was brought into question by observations and experiments in long duration hypobaric chamber studies in which cough still occurred despite controlled temperature and humidity. Anecdotally however, exercise, possibly via the associated increase in ventilation, does appear to precipitate cough at altitude. It is likely that the term, altitude-related cough, covers a number of conditions and aetiologies. These aetiologies are discussed and include water loss from the respiratory tract; high altitude pulmonary oedema; acute mountain sickness; bronchoconstriction; respiratory tract infections; vasomotor rhinitis and post-nasal drip; and alterations in the central control of respiration. We hypothesize that there are two forms of altitude-related cough: a cough which may occur at relatively low altitudes and which is related to exercise and persists despite descent and a cough which does not occur at altitudes below 5000-6000 m and which improves rapidly with descent to lower altitude. The treatment of altitude-related cough is symptomatic and frequently ineffective. Further work is required to understand the nature and aetiology of the cough which occurs at high altitude before effective therapies can be developed.

Acute Disease↗