Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The findings in a patient who developed low-pressure pulmonary edema on two separate occasions immediately following the ingestion of a single triamterene-hydrochlorothiazide tablet (Dyazide) are presented. It is postulated that this was related to the hydrocholorothiazide component of the drug. Although 12 cases have been reported, the pathophysiology remains obscure. Mitogenic stimulation of the patient's lymphocytes to concanavalin A, phytohemagglutinin, and pokeweed mitogen was assessed. Blastogenic responses to Staphylococcus aureus antigen, triamterene, and hydrochlorothiazide were also assessed. No hypersensitivity response could be demonstrated to either triamterene or hydrochlorothiazide. The initially low white blood cell count, associated with hemoconcentration, increased in the first 24 h in the hospital. This observation is consistent with intrapulmonary sequestration of granulocytes causing pulmonary edema.
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PMID:Hydrochlorothiazide-associated pulmonary edema. 276 37

Hydrochlorothiazide is one of most commonly prescribed antihypertensive diuretics. In this case, an allergic reaction to hydrochlorothiazide resulted in severe pulmonary edema. Hydrochlorothiazide, one of the most commonly prescribed drugs, is a diuretic which is usually well tolerated. Common side effects include dizziness, weakness, fatigue, and cramps. These side effects are usually caused by fluid and electrolyte imbalances. Acute pulmonary edema, first reported by Steinberg in 1968, is a rare but potentially life-threatening allergic reaction to hydrochlorothiazide. This case illustrates many of the typical presenting features of the reaction.
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PMID:Acute pulmonary edema caused by ingestion of hydrochlorothiazide. 908 57

Hydrochlorothiazide-induced pulmonary edema is an unusual but life-threatening adverse reaction. It causes hypoxemia, hypotension, tachycardia, fever, and occasionally electrocardiographic and echocardiographic abnormalities. The mechanism of production is, probably, idiosyncratic.
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PMID:Recurrent hydrochlorothiazide-induced pulmonary edema. 960 16

Hydrochlorothiazide (HCTZ)-induced pulmonary disease has been described as either an allergic interstitial pneumonitis or a cause of noncardiogenic pulmonary edema. The mechanism of this rare life-threatening side effect is largely unknown. Many patients show peripheral leukopenia and extensive immunologic studies reveal decreased levels of serum immunoglobulins. However, evaluation of the peripheral blood may not reflect local lung changes. Literature reports of bronchoalveolar differentials on such patients are scarce. Bronchoscopy was performed on our patient, and the lavage revealed a significant percentage of neutrophils (70%) and no eosinophils.
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PMID:Hydrochlorothiazide-induced noncardiogenic pulmonary edema: BAL fluid analysis. 2120 80

Hydrochlorothiazide has been shown to cause rare, but serious non-cardiogenic pulmonary edema. We present a case report of a patient with apparent septic shock and acute respiratory distress syndrome (ARDS) requiring life-sustaining veno-venous extracorporeal membrane oxygenation (VV-ECMO). Upon further review of the literature and the chronology of the patient's presentation, her condition was most likely due to an immune-mediated reaction to hydrochlorothiazide. This represents the first case, to our knowledge, of such a severe reaction to hydrochlorothiazide supported with ECMO therapy.
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PMID:Life-threatening idiopathic reaction to hydrochlorothiazide treated with veno-venous extracorporeal membrane oxygenation. 2917 3