Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A patient with probable hydrochlorothiazide-induced pulmonary edema is described. A 70-year-old woman experienced nausea, diaphoresis, and severe respiratory distress approximately 1/2 hour after taking an Aldactazide tablet. She had experienced a flu-like syndrome after taking a single tablet two weeks previously. The patient was mildly tachycardic with a blood pressure of 74/0 mm Hg. A chest X-ray revealed cardiomegaly and bilateral pulmonary edema suggestive of congestive heart failure. The pulmonary capillary wedge pressure was normal. It was felt that the patient had developed a noncardiac pulmonary edema possibly secondary to hydrochlorothiazide ingestion. Nine other cases reported in the literature also are described. Pharmacists should be aware of this potential life-threatening reaction and avoid patient reexposure to the drug.
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PMID:Hydrochlorothiazide-induced pulmonary edema. 669 86

Careful management of fluid and electrolytes may require the rational use of diuretic agents in some neonatal pathological conditions. High efficacy diuretics include "loop" diuretics--furosemide, bumetanide and ethacrynic acid. The elimination half-life and renal effects of furosemide are prolonged in newborn infants as compared with adults. In congestive heart failure, the mean net losses associated with a 1 mg i.v. dose of furosemide, are 28 ml/kg, 3.6 mmol/kg and 0.3 mmol/kg respectively for water, sodium and potassium. The furosemide--dopamine (2 micrograms/kg/min) combination may improve renal insufficiency in the course of respiratory distress syndrome (RDS). Furosemide also decreases the deleterious renal effects of indomethacin. Beneficial effect of furosemide has not been clearly demonstrated in RDS and bronchopulmonary dysplasia (BPD). Metabolic alkalosis, hypokalemia, renal calcifications, cholelithiasis and worsening in BPD outcome have been related to long-term administrations of furosemide. The risk of furosemide induced-ototoxicity has not been clearly assessed in newborn infants. Medium efficacy diuretics (thiazides) act primarily in the early distal tubule. Chlorothiazide may reduce calcium urinary excretion in neonates receiving long-term furosemide therapy. Weak diuretics (potassium-sparing diuretics and carbonic anhydrase inhibitors) cause excretion of less than 5% of the filtered sodium. Potassium-sparing diuretics are usually reserved for neonates with congestive heart failure and are always used in combination.
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PMID:[Diuretics in the neonatal period]. 756 38