The American review of respiratory disease
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Am. Rev. Respir. Dis. · Oct 1976
Comparative StudyOf guinea pigs and men. The 1976 J. Burns Amberson Lecture.
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Am. Rev. Respir. Dis. · Aug 1976
Use of fibrinogen/fibrin degradation products and soluble fibrin complexes for differentiating pulmonary embolism from nonthromboembolic lung disease.
To help differentiate pulmonary embolism from other lung diseases, we measured the degradation products of fibrinogen and fibrin and soluble fibrin complexes in normal control subjects and patients with pulmonary embolism, lung cancer, pneumonia, chronic obstructive pulmonary disease, tuberculosis, asthma, and several miscellaneous disorders. A separate group of patients, who were suspected of having pulmonary embolism but had negative pulmonary angiography, were also tested. ⋯ Both tests were negative in only 3 per cent of patients with pulmonary embolism but in 35 per cent of nonthromboembolic diseases (P less than 0.005), 54 per cent of those with negative pulmonary angiography (P less than 0.001), and 79 per cent of normal control subjects (P less than 0.001). The combination of fibrinogen/fibrin degradation products and soluble fibrin complexes is more valuable than either test alone in the diagnostic separation of thromboembolic from nonthromboembolic pulmonary diseases.
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Am. Rev. Respir. Dis. · Jul 1976
Case ReportsProbable familial congenital bronchiectasis due to cartilage deficiency (Williams-Campbell syndrome).
Two siblings in whom respiratory symptoms developed immediately after birth subsequently were found to have bronchiectasis with strikingly similar distribution of lesions (mainly lower lobes). Inspiratory and expiratory bronchograms performed on one of the siblings demonstrated marked ballooning and collapse of proximal bronchi during tidal breathing. ⋯ This would be the first reported familial occurrence of this syndrome. The familial pattern and the neonatal onset of symptoms support the theory of a congenital basis for this variety of bronchiectasis.
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Am. Rev. Respir. Dis. · May 1976
Protease inhibitors in patients with chronic obstructive pulmonary disease: the alpha-antitrypsin heterozygote controversy.
A group of 163 patients with chronic obstructive pulmonary disease, from the pulmonary service of a large urban hospital, were evaluated for their protease inhibitor (Pi) type by starch gel and crossed immunoelectrophoresis, for serum concentrations of alpha1-antitrypsin and alpha1-antichymotrypsin, and for pulmonary function. Of the patients with emphysema, 17.8% were of Pi type Z; 50% of these were less than 45 years of age, compared to 13% of those of Pi type M. ⋯ Concentrations of both alpha1-antitrypsin and alpha1-antichymotrypsin were increased and were correlated. No patient had a deficiency of alpha1-antichymotrypsin.
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Evidence suggests the following pathogenesis for neurogenic pulmonary edema. The initial phase results from a centrally mediated, massive, sympathetic discharge. ⋯ In addition, pulmonary hypertension and hypervolemia injure pulmonary blood vessels, altering pulmonary capillary permeability and producing lung hemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary edema persists in the face of normal hemodynamics and normal cardia function.