[The therapy of bronchial asthma]. / Terapia dell'asma bronchiale.

Asthma (Greek word that means "breathlessness" or "open-mouth breath") is a chronic inflammatory disorder of the airways, with extensive infiltration of the airway lumen and wall with eosinophils, mast cells, activated T-lymphocytes. Airway inflammation is associated with airway hyperresponsiveness, recurrent episodes of reversible airflow limitation and respiratory symptoms such as wheezing, chest tightness, breathlessness and cough with mucus production. Curiously, asthma worsens particularly at night and in the early hours of the morning. The current consensus on asthma therapy suggests that pharmacological control of asthma can be achieved with antiinflammatory "controller" medications such as inhaled glucocorticoids and cromones. Short-acting bronchodilators act as "reliever" medications and rapidly reverse acute manifestations of asthma. Asthmatic exacerbations require the repetitive administration of inhaled short-acting beta-2-agonist and the early introduction of oral glucocorticoids. Rarely the severity of exacerbation requires the administration of oxygen (that, if available, is not contraindicated), intravenous bronchodilators, glucocorticoids and epinephryne and mechanical ventilation.

Pidotimod activity against chronic bronchitis exacerbations.

The efficacy of pidotimod ((R)-3-[(S)-(5-oxo-2-pyrrolidinyl) carbonyl]-thiazolidine-4-carboxylic acid, PGT/1A, CAS 121808-62-6) in the management of infectious exacerbations of chronic bronchitis was evaluated in a double-blind, placebo-controlled study in parallel groups over 5 months (60 days of treatment and 90 days of follow-up). The study enrolled 580 patients, of whom 514 could be evaluated. The pidotimod group had fewer and shorter infectious episodes, fewer days of antibiotic therapy and fewer days unable to undertake normal activities. The difference vs. placebo was significant during the follow-up period and, in those subjects with a less severe history, during the treatment period also. Pidotimod was well tolerated.

Neonatal metabolic acidosis: effect of chloride from normal saline flushes.

Metabolic Acidosis is a reported complication of total parenteral nutrition (TPN). A large number of infants receiving TPN in an NICU were noted to have metabolic acidosis. We evaluated the effect of lowering the chloride intake on the incidence of metabolic acidosis in low birth weight (LBW) infants on TPN. Standard TPN solutions were adjusted to provide about 2-3 mEq/kg/day chloride instead of 5-7 mEq/kg/day provided previously. Most infants on TPN received approximately another 1-3 mEq/kg/day from intravenous and arterial line flushes with normal saline. Ten infants who had been on the original TPN solutions were compared to 10 infants who were on the revised TPN solutions. Serum pH, bicarbonate, and base deficit were used to measure acidosis. Medical records were reviewed for the number of days the infants had abnormal values. Serum chloride levels were also recorded. While similar in gestational age, birth weight, age during study period, days on TPN, and days on orally supplemented parenteral nutrition, the group with higher chloride intake had significantly more days of metabolic acidosis. They also had significantly higher serum chlorides. It is concluded that a total chloride load in excess of 6 mEq/kg/day in LBW infants receiving TPN is associated with more metabolic acidosis. Also, if saline is used for clearing of intravenous and arterial lines, standard TPN solutions should be formulated with consideration of the total chloride load.