Pulmonary capillary haemangiomatosis - An unusual cause of hypoxia.

We describe the case of a 58-year-old man who presented with progressive dyspnoea on exertion and severe exertional hypoxia. There was a paucity of radiological findings, mild pulmonary hypertension, and no demonstrable anatomical shunt. Post mortem examination of lung tissue suggested a diagnosis of pulmonary capillary haemangiomatosis. The case is unusual in displaying few radiological findings. We postulate that the severe hypoxia was due to shunting through the abnormal capillary proliferations.

An early phase of slow myocardial activation may be necessary in order to benefit from cardiac resynchronization therapy.

BACKGROUND: Not all patients with a QRS duration longer than 140 milliseconds respond to cardiac resynchronization therapy (CRT). The same QRS duration may correspond to different spatiotemporal patterns of myocardial activation that influence response to CRT. METHODS: Electrocardiographic imaging based on 80 chest wall electrodes was used to construct the spatiotemporal myocardial activation map in 46 consecutive patients before CRT. The cumulative percentage of myocardium activated was plotted against time expressed in terms of quintiles of the overall QRS duration. Changes in the left ventricular ejection fraction and end-diastolic diameter, maximum oxygen consumption per minute, brain natriuretic peptide level, and 6-minute walk distance after 6 months of CRT were compared across different patterns with 1-way analysis of variance. RESULTS: Data from 34 patients were available for analysis. Four spatiotemporal patterns of myocardial activation could be identified: triphasic (fast-slow-fast) (13), uniform (8), fast-slow (7), and slow-fast (6). The overall QRS duration was similar in the 4 groups (166 +/- 19 vs 138 +/- 21 vs 157 +/- 26 vs 152 +/- 37 milliseconds, P = not significant [NS]). The ejection fraction showed a trend of greater increases for the triphasic (6.5% +/- 7.0%) and slow-fast (15.5% +/- 6.4%) patterns than for the uniform (4.0% +/- 13.3%) and fast-slow (8.0% +/- 6.1%) patterns (P = NS). The end-diastolic diameter showed a trend of greater decreases for the triphasic (-3.7% +/- 5.3%) and slow-fast (-7.0% +/- 6.7%) patterns than for the uniform (0.8% +/- 6.7%) and fast-slow (0.0% +/- 4.6%) patterns (P = NS). The maximum oxygen consumption per minute showed a trend of greater increases for the triphasic (1.2 +/- 4.2 mL/kg/min) and slow-fast (4.1 +/- 2.7 mL/kg/min) patterns than for the uniform (0.1 +/- 4.1 mL/kg/min) and fast-slow (1.0 +/- 2.1 mL/kg/min) patterns (P = NS). The brain natriuretic peptide level decreased significantly more for the triphasic (-450 +/- 1269) and slow-fast (-3121 +/- 1512) patterns than for the uniform (762 +/- 1036) and fast-slow (718 +/- 2530) patterns (P = .0003). The 6-minute walk distance increased significantly more for the triphasic (29 +/- 89) and slow-fast (40 +/- 23) patterns than for the uniform (6 +/- 87) and fast-slow (37 +/- 45) patterns (P = .0003). CONCLUSIONS: Different spatiotemporal patterns of myocardial activation exist among patients with broad QRS complex and may affect response to CRT. An early phase of slow myocardial activation (the triphasic fast-slow-fast and the slow-fast patterns) may be necessary for a patient to benefit from CRT.

Staphylococcus aureus enterotoxins induce IL-8 secretion by human nasal epithelial cells.

BACKGROUND: Staphylococcus aureus produces a set of proteins which act both as superantigens and toxins. Although their mode of action as superantigens is well understood, little is known about their effects on airway epithelial cells. METHODS: To investigate this problem, primary nasal epithelial cells derived from normal and asthmatic subjects were stimulated with staphylococcal enterotoxin A and B (SEA and SEB) and secreted (supernatants) and cell-associated (cell lysates) IL-8, TNF-alpha, RANTES and eotaxin were determined by specific ELISAs. RESULTS: Non-toxic concentrations of SEA and SEB (0.01 microg/ml and 1.0 microg/ml) induced IL-8 secretion after 24 h of culture. Pre-treatment of the cells with IFN-gamma (50 IU/ml) resulted in a further increase of IL-8 secretion. In cells from healthy donors pretreated with IFN-gamma, SEA at 1.0 mug/ml induced release of 1009 pg/ml IL-8 (733.0-1216 pg/ml, median (range)) while in cells from asthmatic donors the same treatment induced significantly higher IL-8 secretion - 1550 pg/ml (1168.0-2000.0 pg/ml p = 0.04). Normal cells pre-treated with IFN-gamma and then cultured with SEB at 1.0 mug/ml released 904.6 pg/ml IL-8 (666.5-1169.0 pg/ml). Cells from asthmatics treated in the same way produced significantly higher amounts of IL-8--1665.0 pg/ml (1168.0-2000.0 pg/ml, p = 0.01). Blocking antibodies to MHC class II molecules added to cultures stimulated with SEA and SEB, reduced IL-8 secretion by about 40% in IFN-gamma unstimulated cultures and 75% in IFN-gamma stimulated cultures. No secretion of TNF-alpha, RANTES and eotaxin was noted. CONCLUSION: Staphylococcal enterotoxins may have a role in the pathogenesis of asthma.