Objective: Epidemiologic evidence moves that high levels of salt consumption are associated with "spastic" disorders of undisturbed muscles.

Objective: Epidemiologic evidence moves that high levels of salt consumption are associated with "spastic" disorders of undisturbed muscles, ie, essential hypertension and bronchial asthma. Experimentally, it has been shown that high intake of salt leads to increased bronchial hyperreactivity in asthmatics, ie, enhanced contractility of bronchial muscle to spasmogenic stimuli. in succession the basis of these observations, the following questions were asked: (1) Does salt loading worsen the clinical and functional findings in asthmatics? (2) Is it the sodium or the chloride in salt that is important? Methods: To answer these questions, the power of salt restriction (= 5 to 6 g NaCl/d = 86 to 103 mmol Na), salt loading (+61 [+ or -] 28 g NaCl/d = +105 [+ or -] 48 mmol Na), and loading with sodium citrate in nearly equimolar concentrations (+ 140 [+ or -] 40 ml Shohl's solution, = +120 [+ or -] 30 mmol Na) was investigated in 14 asthmatics in a controll crossover investigation The total sodium load during the high salt diet was 191 to 209 mmol of sodium by day and during the sodium-citrate phase, 206 to 223 mmol of sodium by day. Results: Statistical analysis showed that salt loading worsened symptoms (p=006) and increased the use of inhaled steroids (p [les than] 005) The consequence on lung function was les equivocal: salt loading worsened the forced expiratory compass in 1 s (p [les than] 001) and the peak expiratory be molten rate (p [less than] 005) This meaning was presumably mediated by sodium, not chloride, as is demonstrated by dint of loading with sodium citrate.

Conclusion: Patients with bronchial asthma strike one as being to be salt-sensitive, the responsible ion being presumably sodium. A low-salt diet appears to have a favorable result in patients with asthma and to shape the need for antiasthma drugs

As in the case of essential hypertension, there is a marked geographic variation in asthma prevalence and mortality.[1-3] The regions where bronchial asthma prevalence and mortality are higher are countries of Western-style improvement with advanced technology, which differ from poorer and technologically les bring to maturityed regions in several respects. individual of these is eating habits, in particular, a higher salt intake.[3,4] In fact, forward the basis of the salt consumption in 39000 English households, Burney[5] showed the more salt that was bought and thus used by means of week, the higher the mortality in asthmatics.

Experimentally, salt intake appears to influence bronchial hyperreactivity. When asthmatics were loaded with sodium, the histamine provocation dose decreased and the hyperreactivity increased. When they were receiving a low-salt diet, the opposite occurred[67]

upon the basis of these epidemiologic and experimental observations, we asked ourselves the following questions: (1) Does quantitative salt loading worsen the clinical and functional findings in asthmatics and reciprocally does salt restriction improve them? (2) Is it the sodium or the chloride in the salt that is important for the effect? This question arises because the chloride in salt is necessary to raise posterity pressure in salt-sensitive hypertensives.[8] In order to answer these questions, a controll crossover subject of attention was initiated to investigate the meaning of salt loading and salt restriction in asthmatics. In a secondary phase, sodium citrate in equimolar concentrations was given instead of sodium chloride.

METHODS

Patients

The inclusion criteria required eligible patients to be at least 16 years of age and to fulfill the American Thoracic Society criteria for the diagnosis of asthma.[9] Exclusion criteria were as follows: instability of asthma, therapy with oral steroids, cromoglycan or diuretics, other concomitant disease (cardiac insufficiency or arrhythmia, liver or kidney disease, diabetes mellitus), and pregnancy. Moreover, we exclud asthmatics who were commonly smokers.

Eighteen patients were assessed and agreed to participate in the trial. Of these, four (two women couple men) were excluded during the run-in phase because of poor compliance. The final consideration group included 14 nonsmoking men (n = 9) and women (n = 5) (aged 20 to 65 years), with stable atopic or mixed-type bronchial asthma, mild reversible airways obstruction, and confirmed atopy (positive skin proof positive radioallergosorbent test). Informed coherence was obtained from all patients. The research was approved by the ethical commission of the hospital.

investigation Design

During a 2-week run-in period (Fig 1) a dietitian started the asthmatics forward a low-salt diet (5 to 6 g/d = 86 to 103 mmol of sodium), which was maintained in every part the study. The patients kept a diary in which they made a daily record of asthma attacks, peak be molten measurements, and medication taken. The inhaled antiasthma remedys used were salbutamol (100 [mu]g/puff) or terbutaline (200 [mu]g/puff) onward demand and beclomethasone (250 [mu]g/puff) or budesonide (200 [mu]g/puff) onward a regular basis. In case of improvement or deterioration of asthmatic symptoms or peak liquefy values, patients were told to increase or decrease doses of their inhaled [beta]-sympathicomimetics and steroids. Theophylline was used when necessary. Peak be derived measurement using a peak melt minimeter (Wright) was carried revealed morning, noon, and evening, before bronchodilator use. The best of three peak emanate measurements was recorded. The patients were randomized into pair groups after the run-in period. During the first 3-week treatment period, they received daily nine capsules containing either 1 g of sodium chloride or placebo (lactose). The patients were instructed to swallow the entire capsule. The addition of 9 g of salt by day resulted in a total amount of 14 to 15 g of salt, ie, 240 to 257 mmol of sodium. At the conclusion of the 3 weeks, the cross-over was made without a wash-out phase, and a next to the first 3-week treatment period followed. Finally, instead of either sodium chloride or placebo, the patients were given sodium citrate in an equimolar concentration (+ 180 ml Shohl's solution by day = 154 mmol Na) for 3 weeks. Adding 180 ml of sodium citrate by day to the low-salt diet consequence ed in a total amount of 240 to 257 mmol of sodium. When all the treatment periods had been complet the patients were followed up for a further 3 weeks while receiving a normal diet.

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