Why the study?
Is increased serum ACE activity in sarcoidosis related to altered alveolar-capillary permeability?
Is increased serum ACE activity in sarcoidosis related to altered alveolar-capillary permeability?
Excess serum ACE in sarcoidosis may originate in the alveolar space due to increased alveolar-capillary membrane permeability.
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Associates serum ACE with alveolar permeability markers in sarcoidosis; hypothesis-generating and should not yet change practice.
The effect of altered alveolar-capillary permeability on angiotensin converting enzyme (ACE) activity in serum (SACE) was studied in 45 patients with sarcoidosis and 21 healthy controls. In sarcoidosis increased albumin concentrations in the bronchoalveolar lavage fluid (L albumin) and increased ratios of L albumin to albumin in serum (S albumin) indicated an increased permeability of the alveolar-capillary membrane. ACE activity in the lavage fluid (LACE) was correlated with the number of alveolar macrophages in controls, indicating that it may come from these cells. LACE was high in active sarcoidosis while in inactive disease it was similar to that in controls. SACE in sarcoidosis was significantly increased. Ninety per cent of patients with increased L albumin had increased SACE. SACE activity was significantly correlated with concentrations of L albumin and with LACE activity. The relationships between signs of increased membrane permeability and SACE and between LACE and SACE suggest that excess SACE in sarcoidosis may, at least partly, originate in the alveolar space.
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Eklund et al. (1986) studied this question.
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