The behaviour of bronchial reactivity to PGF2α was studied in asthmatic patients under various experimental conditions. Premedication with aminophylline, i.v., and, to a lesser extent, with DSCG afforded a partial protection, while beclomethasone dipropionate was inactive under this point of view. Diftalone, a new non-steroid anti-inflammatory agent, was well tolerated in 9 aspirin-intolerant asthmatic patients, and did not modify the bronchial response to PGF2α which was found to be generally lower than that of other aspirin-tolerant asthmatic patients. PGE1-2 and DSCG prevented the bronchospasm induced by inhalation or ingestion of acetylsalicylic acid in a small group of patients. Good protection was also reached with PGE1-2 in the exercise-induced bronchospasm.
Eight asthmatics with respiratory intolerance to NSAIDs and two subjects (one asthmatic, one healthy) only sensitive (asthma) to pyrazolone drugs were challenged under single-blind conditions with a new NSAID, carprofen. No adverse effects were observed in patients sensitive to pyrazolones. Among the other patients, only three developed considerable bronchial obstruction which was rapidly reversed by inhalation of a beta 2-stimulant (fenoterol: 2 puffs). Two subjects developed nasal obstruction with rhinorrhoea: in conjunction with bronchoconstriction in one patient and alone in the other. In conclusion, acute administration of carprofen in patients with respiratory intolerance to NSAIDs, in contrast to most other NSAIDs, never creates a situation of real danger even though in some patients it may considerably increase nasal and bronchial resistance.
The pharmacological therapy of asthmatic syndromes is based essentially on the programmed use of disodium cromoglycate, beta-2-stimulants, antimuscarinics, theophyllines and corticosteroids. However, the continual progress being made in pathogenesis and pharmacology suggests, to an ever-increasing extent, the application of new therapeutic approaches for these diseases, some of which are fairly interesting from a speculative point of view although they are as yet of limited practical value. Calcium antagonists and alpha-blockers have a mild anti-reactive effect but this is not sufficiently potent to justify use of these products in the treatment of asthma unless there are also cardiovascular disorders for which these drugs are particularly indicated. Despite the initial promising prospects, all attempts to obtain PGE analogues of therapeutic value as antiasthmatics have proved fruitless. Research into orally active chromone derivatives has proved equally unproductive. On the other hand, certain new inhalatory chromones are decidedly more promising. Specific antagonization of mediators (histamine, prostaglandin, leukotrienes) did not produce the effect hoped for in asthma, but this was foreseeable insofar as the major pathogenic mediators are too vast in number (and no doubt there are still many more to be discovered) to allow one to conceive it possible to achieve a satisfactory therapeutic effect by merely blocking some of them. Inflammation of the bronchial wall is currently considered to be one of the basic pathogenic factors provoking the recurrence of asthma: this is proved indirectly by the potent antiasthmatic effect of corticosteroids which are the most effective anti-inflammatory agents. As regards nonsteroidal anti-inflammatory drugs (NSAID), however, matters are more complicated. Some patients (approximately 10% of all adult asthmatics) suffer from violent asthmatic attacks after taking NSAIDs. For this reason the possibility of desensitization treatment was suggested whereby gradually increasing doses of aspirin (ASA) or another NSAID are given. However, the results proved negative insofar as only the rhinitic component showed any real improvement while the asthma remained more or less unchanged. In a low percentage of asthmatic patients (less than 1 %) NSAIDs lead to sudden and extensive bronchodilatation. However, if they are administered repeatedly, this effect tends to wear off quickly: thus, the possibility of using these for long-term treatment on a regular basis can be excluded.
Starting from a paper published in 1964 by Wilson et al., we explored the possibility of classifying the clinical and functional deficit of patients with chronic obstructive lung disease into six classes, class 0 representing normality and class 5 greatest severity. Each symptom or sign was classified into six degrees of increasing severity. Next, we looked for a possible dependence of the collegially assigned score on anthropometric, clinical, or instrumental data in each case. More particularly, we tried (1) to identify such combinations of variables as would permit classification of the patient with the smallest possible error, and (2) to determine which of the variables reflected the severity of the case more faithfully. The results emerging from this study suggest the possibility of evaluating and classifying respiratory impairment in three different ways, as follows (1). On the basis of clinical data only. This method is the easiest to use and affords a fairly good determination coeficient(R2=0.812) (2). Using only some combinations of laboratory data (static and dynamic pulmonary volumes, blood gases, etc.), with or without the addition of vital statistics and anthro-pometric data. These subensembles would allow a posteriori estimates in cases where the subject is no longer available for questioning and examination. In that case the best multiple regression affords a determination coefficient R2 = 0.82. (3). Using all clinical and laboratory data available. In that case, the best multiple regression (R2 = 0.899) for predictive purposes is that which includes the sum of clinical data, the pulmonary volumes before and after pharmacological bronchodilation, and the PaCO2 value. For practical purposes, however, the most convenient function is the one that includes the sum of clinical data plus FEV1 and RV (R2 = 0.863). Even with the best of the three functions proposed in this paper, however, the standard error of estimate entails tolerance limits sometimes amounting to one whole class of severity. Still, the probability of making an error exceeding one class of severity occurs in only 3.7% of the cases, an average which seems quite acceptable from the clinical point of view.
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