Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Varying degrees of respiratory distress developed in 3 dogs in which hyperadrenocorticism was diagnosed. The respiratory distress was attributed to pulmonary artery thrombosis. Radiography revealed pleural effusion, increased diameter and blunting of the pulmonary arteries, lack of perfusion of the obstructed pulmonary vasculature, and overperfusion of the unobstructed pulmonary vasculature. Thrombosis was confirmed by nonselective angiocardiography in each case. In 1 case, selective angiocardiography showed marked reduction of the transit time of contrast medium from the right atrium to the aorta. Hypertension proximal to the site of thrombosis was confirmed in 2 cases by showing increases in the right ventricular systolic pressures (80 mm of Hg in one case and 54 mm of Hg in the other case). In 3 cases, there was moderate hypoxemia with hypocapnia, suggesting a ventilation-perfusion mismatch. Clinical findings other than respiratory distress included hepatomegaly, ventral edema, orthopnea, and a jugular pulse. Pulmonary artery thrombosis, as it occurred in these 3 cases, was compared with the disease in man. It was concluded that pulmonary artery thrombosis should be suspected in cases of intractable dyspnea, right-sided heart failure of unexplained origin, and acute unexplainable death.
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PMID:Pulmonary artery thrombosis in three dogs with hyperadrenocorticism. 723 99

This report presents the case of a 67-year-old woman affected by glioblastoma. After a few days of adjuvant therapy with temozolomide and prophylaxis with trimetrophin-sulfamethoxazolo to prevent Pneumocystis Jiroveci, she had progressive and rapid worsening of symptoms with weakness, dyspnea and orthopnea. She had peripheral edema and proximal hyposthenia of the lower limbs. Chest CT showed bilateral ground-glass opacities and laboratory exams revealed hypoxemia and hypocapnia, an initial reduction in platelet and white blood cells, and an elevation of LDH, AST, ALT, and active urinary sediment. Blood cultures, bronchoalveolar lavage (BAL) data and transbronchial biopsy showed no infections, and in particular no evidence of Pneumocystis Jiroveci pneumonia. Histological examination revealed a typical pattern of AIP. She was treated with broad-spectrum antibiotics and high-dose steroids. The symptoms worsened and respiratory failure required mechanical ventilation. The pneumonia was not responsive to medical or invasive care. She died after ten days of hospitalization. At present very little can be found in the literature about lung toxicity caused by temozolomide. This case can be added as a new report describing this risk. The combination therapy with temozolamide and trimetophin-sulfamethoxazolo could have a synergistic action inducing various forms of pulmonary toxicity. ESTABLISHED FACTS: Acute interstitial pneumonia is a common manifestation of lung toxicity caused by drugs. The clinical course is favorable with a good response to corticosteroids. NOVEL INSIGHT: This is the first fatal case of lung toxicity caused by Temozolomide. Clinicians must be aware that a combination therapy including trimetophin-sulfamethoxazolo could have a synergistic action in inducing pulmonary toxicity.
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PMID:A fatal case of acute interstitial pneumonia (AIP) in a woman affected by glioblastoma. 2441 Mar 8