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Stefano Fratoni

Publications and source records attributed to Stefano Fratoni.

6 recordsLinked to original sources
PubMed2006

Extra-osseous osteochondroma-like soft tissue mass of the patello-femoral space.

BACKGROUND: Extraskeletal cartilaginous tumors are uncommon. Osteochondromas usually arise from the metaphyseal region of the growing skeleton. CASE PRESENTATION: A 53 year old man presented with a three years history of anterior knee pain and inability to flex his knee more than 90 degrees . Clinical examination and imaging studies revealed a nodular calcific mass in the anterior portion of the knee, displacing the medial portion of the patellar tendon. Following excision, histopathology confirmed the diagnosis of extra-osseous osteochondroma-like soft tissue mass, with no recurrence 24 months after surgery. CONCLUSION: An integrated clinical-pathologic diagnosis helps to clarify the nature of extraskeletal cartilaginous tumors that can arise at unusual anatomic site. Complete local surgical excision is the management of choice.

Humans↗
PubMed2005

Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction.

OBJECTIVES: This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL). BACKGROUND: Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques. METHODS: We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL. RESULTS: An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively. CONCLUSIONS: This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.

Aged↗
PubMed2005

Chondroma of the subcutaneous bursa of the Achilles tendon.

A 46-year-old female presented a six-month history of posterior heel pain. Clinical and radiographical examination revealed a nodular calcified mass into the subcutaneous tissue of the Achilles tendon bursa. Following excision, histopathology showed an extraskeletal soft-tissue chondroma. Follow up at 24 months showed no recurrence. To our knowledge, this is the first description of a soft tissue chondroma at this site: some soft tissue tumors develop at unusual anatomic location.

Achilles Tendon↗
PubMed2004

Extracranial thrombotically active carotid plaque as a risk factor for ischemic stroke.

CONTEXT: Recent studies suggest that factors other than the degree of carotid stenosis are involved in ischemic stroke pathogenesis, especially modifications of plaque composition and related complications. OBJECTIVE: To examine the role of carotid plaque rupture and thrombosis in ischemic stroke pathogenesis in patients undergoing carotid endarterectomy, excluding those with possible cardiac embolization or with severe stenosis of the circle of Willis. DESIGN, SETTING, AND PATIENTS: A total of 269 carotid plaques selected from an Interinstitutional Carotid Tissue Bank were studied by histology after surgical endarterectomy between January 1995 and December 2002. A total of 96 plaques were from patients with ipsilateral major stroke, 91 plaques from patients with transient ischemic attack (TIA), and 82 plaques from patients without symptoms. MAIN OUTCOME MEASURES: Differences in the frequency of thrombosis, cap rupture, cap erosion, inflammatory infiltrate, and major cardiovascular risk factors between study groups. RESULTS: A thrombotically active carotid plaque associated with high inflammatory infiltrate was observed in 71 (74.0%) of 96 patients with ipsilateral major stroke (and in all 32 plaques from patients operated within 2 months of symptom onset) compared with 32 (35.2%) of 91 patients with TIA (P < .001) or 12 (14.6%) of 82 patients who were without symptoms (P < .001). In addition, a fresh thrombus was observed in 53.8% of patients with stroke operated 13 to 24 months after the cerebrovascular event. An acute thrombus was associated with cap rupture in 64 (90.1%) of 71 thrombosed plaques from patients with stroke and with cap erosion in the remaining 7 cases (9.9%). Ruptured plaques of patients affected by stroke were characterized by the presence of a more severe inflammatory infiltrate, constituted by monocytes, macrophages, and T lymphocyte cells compared with that observed in the TIA and asymptomatic groups (P = .001). There was no significant difference between groups in major cardiovascular risk factors. CONCLUSION: These results demonstrate a major role of carotid thrombosis and inflammation in ischemic stroke in patients affected by carotid atherosclerotic disease.

Aged↗
PubMed2002

[Risk factors of transient cerebral ischemic episodes: hyperfibrinogenemia and carotid histopathology].

Risk factors may play a fundamental role in the evolution from a stable to a vulnerable plaque. In particular, the hyperfibrinogenemia, independently from other risk factors, influences the natural history of cerebrovascular disease modifying the histologic composition of atherosclerotic plaques and precipitates carotid thrombosis resulting from rupture of the plaque. Determination of plasma fibrinogen may help to identify a subset of patients at high risk for a rapid progression of carotid atherosclerosis and related clinical events. We suggest that these patients may benefit of an earlier surgical intervention even if the degree of carotid stenosis is not severe.

Arteriosclerosis↗