Pulmonary carcinoid tumorlet is a rare pathology and appears to be always associated with other lesions such as bronchiectasis and fibrosis. While the caus e-effect relationship between tumorlet and the accompanying pathological changes in the surrounding mesenchymal tissue remains to be defined, it has been postulated that pulmonary fibrosis may be the primary pathology underlying the development of tumorlet. In this paper, we present a case where a tumor (<0.5 cm) was detected in the right upper lobe of a 71-year old woman. Cells of the tumor displayed markers characterizing for their neuroendocrine origin. No histological evidence for inflammation, interstitial fibrosis and remodeling of vascular structure was observed. However, immunohistochemistry assay demonstrated a strong production of the profibrotic factors VEGF and TGF-β1 by tumor cells. These findings suggest that carcinoid tumorlet can be an isolated lesion and pulmonary fibrosis that “often co-exists” with tumorlet may be secondary to the paracrine effects of fibrotic growth factors produced by tumorlet.

Background

An increasing number of authors employing intravascular ultrasound (IVUS) and virtual histology (VH-IVUS) have investigated the effect of statin use on plaque volume (PV) and plaque composition. However, inconsistent results have been reported. Therefore, we conducted a meta-analysis to determine the appropriate regimen of statins to effectively stabilize vulnerable coronary plaques.

Methods

Online electronic databases were carefully searched for all relevant studies. We compared mean values of PV and plaque composition between baseline and follow-up in patients receiving statin therapy. We pooled treatment effects and calculated mean differences (MD) with the 95% confidence interval (CI) using a random-effects model. By stratified analyses, we explored the influence of clinical presentation, dose and duration of statin treatment, and low-density lipoprotein-cholesterol (LDL-C) levels on the effects of statins.

Results

Seventeen studies involving 2,171 patients were analyzed. Statin therapy significantly decreased PV (−5.3 mm3; 95% CI: –3.3 mm3 to −7.2 mm3; P < 0.001), without heterogeneity. When considering the dose and duration of statins used, only subgroups employing a high dose and long duration demonstrated a significant reduction in PV (p < 0.001). A significant decrease in PV was noted if achieved LDL-C levels were <100 mg/dL (p < 0.001). Statin treatment could induce a twofold decrease in PV in patients with acute coronary syndrome (ACS) compared with that observed in patients with stable angina pectoris (SAP). A regressive trend was seen for necrotic core volume (MD: –2.1 mm3; 95% CI: –4.7 mm3 to 0.5 mm3, P = 0.11). However, statin use did not induce a significant change for fibrotic, fibro-fatty, or dense calcium compositions.

Conclusions

Our meta-analysis demonstrated that statin therapy (especially that involving a high dose and long duration and achieving <100 mg/dL LDL-C levels) can significantly decrease PV in patients with SAP or ACS. These data suggested that statins can be used to reduce the atheroma burden for secondary prevention by appropriately selecting the statin regimen. No significant change in plaque composition was seen after statin therapy.