Maurizio Rocco

Eosinophil-rich squamous carcinoma of the oral cavity: a study of 13 cases and delineation of a possible new microscopic entity

We report 13 cases of squamous cell carcinoma (SCC) of the oral cavity characterized by a prominent eosinophilic infiltration of the stroma. All patients were adults, 10 men and 3 women (aged 54 to 92 years; median, 71 years). They presented with tumors of the gingiva (5 cases), tongue (3 cases), palatine tonsil (2 cases), palate (2 cases), and mucosal aspect of lip (1 case). Metastatic involvement of regional lymph nodes was seen in 5 cases. The metastatic foci were associated with heavy eosinophilia as well. No patient had an abnormal eosinophil count in blood. Microscopically, the clusters of eosinophils were characteristically noticed in intimate admixture with the advancing edge of squamous carcinoma, either as nests or small tumor cords. The pattern of eosinophilic infiltration was comparable, regardless of tumor site or grade. Data from our series indicate that SCC with a reactive inflammatory infiltrate rich in eosinophils is consistently associated with stromal invasion. This observation may be useful in dealing with small tissue fragments where subepithelial stromal invasion cannot be easily assessed by conventional criteria. In addition, our data seem to confirm that eosinophil-rich SCC, although associated with metastatic involvement of cervical lymph node, seems to pursue a less aggressive course if compared with ordinary SCC.

Plasma cell myeloma presenting with diffuse pleural involvement: a hitherto unreported pattern of a new mesothelioma mimicker.

We described 2 cases of plasmacytoma presenting with a preponderant involvement of the pleural membranes simulating clinically, radiologically, and on gross pathologic inspection a primary mesothelioma. The patients were an 80-year-old man and a 45-year-old woman. In both cases, the clinical presentation was that of a serosal tumor, including effusions and pleural thickening. In the former, the serosal infiltration raised the suspicion of mesothelioma reinforced by history of occupational exposure to asbestos. Patient general condition deteriorated rapidly. Postmortem examination revealed unilateral encasing of the lung within a thick, irregular neoplastic rind. In addition, tumoral involvement was seen in the homolateral third rib and the clavicle. Histologic examination of pleural masses demonstrated diffuse infiltration by highly atypical, pleomorphic plasma cells with kappa chain restriction. In the second case, clinical presentation was also suspicious of mesothelioma. Nonetheless, a pleural biopsy specimen showed irregular sheets of plasma cells showing kappa light chain restriction. A bone marrow aspirate was also positive for abnormal plasma cell infiltrates. Despite chemotherapy, the patient died 4 months after presentation. Although rarely, it seems that plasmacytoma may present with an exclusive or preponderant pleural involvement; and it may therefore be added to the list of pseudomesotheliomatous tumors.

Adopting integrated care pathways in non-small-cell lung cancer: from theory to practice.

Introduction: Integrated care pathways (ICPs) have been proposed as effective strategies for quality improvement. To date, limited data are available that detail the methodology to design an optimal care pathway for patients with non–small-cell lung cancer (NSCLC). The main aim of this study was to assess the quality of health care delivered to lung cancer patients referred to a hub university hospital. Methods: All professionals involved with the management of NSCLC patients, in cooperation with health care researchers, identified 11 quality indicators and associated benchmarks. These were used to estimate the quality and efficiency of health care delivered to a cohort of 175 NSCLC patients. Results: The gap between “desired” and “actual” performance has been measured by benchmarking current practice against key quality indicators. Diagnostic workup, multidisciplinary team care and medical treatment of advanced disease have emerged as areas of good performance. Conversely, the management of early-stage disease offers room for improvement, in terms of both accuracy of nodal staging and surgical timeliness. Conclusions: Analyzing the process of caring for NSCLC patients is feasible and offers room for improvement. Acquired knowledge may be shared with hospital administrators, guide the revision of ICPs, and enable the delivery of consistent, high-quality clinical standards.

Immediate causes of death in short-term surviving heart transplant recipients

From 1985 to 1992, 1068 cardiac transplants have been performed in the Italian units. The immediate causes of death of 142 of the 148 orthotopic cardiac transplantation recipients who died within the first 6 postoperative months were surveyed. Deaths were grouped into three periods: perioperative (⩽1 month, 68.3%), early (>1 ⩽3 months, 23.2%), and advanced (>3 ⩽6 months, 8.5%). Acute graft failure (arising from the ischemic damage to the donor heart, from surgical problems, from severe pulmonary hypertension, or from multiorgan failure) accounted for 49% of perioperative deaths and, along with noncardiac emergencies (23% of perioperative deaths), was significantly more frequent in this period than in the subsequent ones. The dissection of thoracic arteries was responsible for 4% of postoperative deaths, occurring exclusively among patients transplanted for ischemic or valvular heart disease. In the early and advanced periods, untreatable acute rejection (13%) and fatal infections (38%), mostly saprophytic, were significantly more frequent. Ischemic heart damage secondary to graft vasculopathy already caused 26% of deaths between the fourth and sixth months after transplantation. Some diseases, such as acute rejection, had the same frequency as both underlying disease and immediate cause of death. On the contrary, graft failure is more common as primary disease, leading to death also through noncardiac complications and saprophytic infections. Bacterial infections have the same frequency as both prime and immediate cause of death, viral infections are more common as primary disease, and the opposite is true for saprophytic infections.

Parietal centripetal and centrifugal thickening neovascularization in the descending anterior coronary artery. Possible relations with the problem of collateral circulation.

Left coronary arteries of 30 human hearts, obtained at autopsy, were injected with contrast medium. A control group was formed from anterior descending coronary arteries free of atherosclerosis and a study group from anterior descending coronary arteries with areas of atherosclerotic injury. The following differences in the two groups were noted. The control group did not show successfully injected vessels in intima and media, while cases with atherosclerotic injury have them; the number of injected vessels in presence of atherosclerotic injury was three times greater than in healthy coronary arteries; there was a decreasing gradient from outside to in, in the number of injected vessels in both groups; and finally in atherosclerotic vessels we noted a lack of balance between parietal thickening and the residual lumen (conspicuous thickening was accompanied by a small reduction in the lumen). We interpret centrifugal thickening as a possible compensatory mechanism in the major branches for an inadequate canalization of vessel, and suggest possible formation of coronary collateral circulation from vasa vasorum by a process of neovascularization.

Atypical presentation of idiopathic granulomatous myocarditis mimicking idiopathic giant cell myocarditis: diagnostic, therapeutic and prognostic insights

Myocarditis is the cause of up to 8% of heart transplants [1]. Specific types of myocarditis as idiopathic giant cell myocarditis (IGCM) and cardiac sarcoidosis (or granulomatous myocarditis, GM) require different management because of the risk of recurrence after transplantation. IGCM and GM are sometimes grouped together, but recently there has been a distinction made between the two on clinical and pathological bases [2]. We describe a case with a clinical course mimicking IGCM, but with histopathological findings of GM in the explanted heart. A 39-year-old man was referred for cardiac transplantation in September 2004 for severely dilated cardiomyopathy with refractory heart failure. In 1987 he was treated successfully with mesalazine for ulcerative proctocolitis. Cardiac examination, in 2002, showed no pathological findings. In May 2004, the patient began complaining of asthenia, fatigue and ankle edema with paresthesia of the arms; in June, congestive heart failure was diagnosed because of severely dilated cardiomyopathy with depressed ejection fraction (EF, 20%) and a small amount of pericardial fluid. The coronary arteries were normal. Electrocardiogram (ECG) showed sinus rhythm with low voltage in all leads and incomplete right bundle branch block. He was treated with angiotensin converting enzyme (ACE) inhibitors, diuretics, betablockers and spironolactone. Episodes of sustained ventricular tachycardia were treated with an implantable cardioverter defibrillator, resynchronization therapy, and amiodarone. Laboratory exams showed elevated creatinine phosphokinase (CPK), elevated hepatic markers and lymphocytopenia T. A muscle biopsy excluded peripheral myopathy. The clinical situation deteriorated rapidly and he was transplanted in October 2004. The explanted heart weighted 350 g; the ventricles were dilated; the ventricular walls were 12 mm thick on the left and 7 mm on the right. The myocardium appeared diffusely marbled and multiple irregular greyish-white areas were noted on both the ventricular walls and interventricular septum. The papillary muscles, chordae tendinae, orifices, ostia, valves and coronary vessels were unremarkable. Sections taken from the ventricular walls, septum and atria showed myocyte necrosis, inflammatory cell infiltration comprising lymphocytes, histiocytes, some eosinophils and some giant cells. The inflammatory infiltrates formed noncaseating granulomas with rare giant cells surrounded by B and T (CD8 lymphocytes). The same histopathological pattern was observed in the right ventricle and atria. The histopathology was consistent with GM with features of lymphocytic and histiocytic myocarditis (Fig. 1). The immediate post-operative course was uneventful and the patient was started on standard immunosuppressive therapy with cyclosporin, mycofenolate and corticosteroids. Echocardiograms performed on day one and five after transplant were within normal limits, although the patient was beginning to develop hypotension and oliguria. Endomyocardial biopsy on the sixth day was grade 0. The symptoms worsened and the patient was treated with infusions of furosemide, dopamine and dobutamine, and pulsed, supplemental high-dose intravenous prednisolone along with the standard immunosuppressive maintenance regimen. The next day the patient had to be intubated, ventilated and started on noradrenaline because of