Propylthiouracil-related diffuse alveolar hemorrhage with negative serologies and without capillaritis.

Propylthiouracil (PTU) has been held responsible for diffuse alveolar hemorrhage (DAH) with positive antineutrophil cytoplasmic antibody (ANCA) and capillaritis. We describe a case of a 23-year-old pregnant female with Grave's disease treated with PTU who presented with flu-like symptoms and progressive dyspnea. Open lung biopsy showed DAH without evidence of capillaritis. All serologies were negative. Five days after PTU withdrawal and intravenous steroid therapy, the patient improved dramatically. She remained symptom free without relapse 9 months after the episode. To the best of our knowledge, this is the first reported case of PTU-related alveolar hemorrhage with negative serologic markers and without capillaritis.

Membrane diffusion in diseases of the pulmonary vasculature.

INTRODUCTION: We examined pulmonary diffusing capacity (D(LCO)) and its partition in pulmonary vascular diseases without evident parenchymal disease to assess the pattern and proportionality of change in membrane diffusion (D(m)) and capillary blood volume (V(c)). Disproportionate reduction in D(m) relative to V(c) (low D(m)/V(c)) in these diseases has been attributed to associated alveolar membrane/parenchymal disease, thus providing a potentially important diagnostic tool. METHODS: Diseases included: idiopathic pulmonary arterial hypertension (n=6), chronic thromboembolic disease (n=5), and intravenous drug use (n=14), providing a spectrum of pulmonary vascular diseases. V(c) and D(m) were determined as described by Roughton and Forster. RESULTS: All diseases showed a reduced V(c) (59+/-10, 69+/-14, 71+/-21 % predicted, respectively) and D(m) (76+/-22, 53+/-19, 63+/-16 % predicted, respectively) with no differences between groups (p>0.05). Disproportionate reduction of D(m) (D(m)/V(c) % predicted <1) was seen in all diseases (range 0.36-1.89). A mathematical analysis is presented to illustrate that changes in vascular geometry may additionally influence the proportionality of changes in D(m) and V(c). The mathematical analysis suggests that when reduction in patency of some vessels co-exits with compensatory dilatation of the remaining vasculature, a disproportionate reduction in D(m) relative to V(c) may result. CONCLUSIONS: The balance between vascular curtailment and compensatory dilatation may contribute to the variability of the D(m)/V(c) relationship seen in pulmonary vascular disease. Disproportionate reduction in D(m) relative to V(c) may result from this imbalance and need not imply subclinical alveolar membrane and/or parenchymal disease.