Gearoid Kingston

Attenuation of Pancreatitis-Induced Pulmonary Injury by Aerosolized Hypertonic Saline

BACKGROUND The immunomodulatory effects of hypertonic saline (HTS) provide potential strategies to attenuate inappropriate inflammatory reactions. This study tested the hypothesis that administration of intratracheal aerosolized HTS modulates the development of lung injury in pancreatitis. METHODS Pancreatitis was induced in 24 male Sprague-Dawley rats by intraperitoneal injection of 20% L-arginine (500 mg/100 g body weight). At 24 and 48 h, intratracheal aerosolized HTS (7.5% NaCl, 0.5 mL) was administered to 8 rats, while a further 8 received 0.5 mL of aerosolized normal saline (NS). At 72 hours, pulmonary neutrophil infiltration (myeloperoxidase activity) and endothelial permeability (bronchoalveolar lavage and wet:dry weight ratios) were assessed. In addition, histological assessment of representative lung tissue was performed by a blinded assessor. In a separate experiment, polymorphonucleocytes (PMN) were isolated from human donors, and exposed to increments of HTS. Neutrophil transmigration across an endothelial cell layer, VEGF release, and apoptosis at 1, 6, 12, 18, and 24 h were assessed. RESULTS Histopathological lung injury scores were significantly reduced in the HTS group (4.78 +/- 1.43 vs. 8.64 +/- 0.86); p < 0.001). Pulmonary neutrophil sequestration (1.40 +/- 0.2) and increased endothelial permeability (6.77 +/- 1.14) were evident in the animals resuscitated with normal saline when compared with HTS (0.70 +/- 0.1 and 3.57 +/- 1.32), respectively; p < 0.04). HTS significantly reduced PMN transmigration (by 97.1, p = 0.002, and induced PMN apoptosis (p < 0.03). HTS did not impact significantly upon neutrophil VEGF release (p > 0.05). CONCLUSIONS Intratracheal aerosolized HTS attenuates the neutrophil-mediated pulmonary insult subsequent to pancreatitis. This may represent a novel therapeutic strategy.

Intravascular papillary endothelial hyperplasia (Masson's tumour) of the oral mucosa

Intravascular papillary endothelial hyperplasia (IPEH) is an unusual benign vascular lesion that is caused by an excessive proliferation of endothelial cells in blood vessels. These lesions are benign and therefore have an excellent prognosis and are usually cured by simple excision. Recurrences are extremely rare. IPEH has been rarely described in the oral region and in this case report we will outline an uncommon presentation and discuss pathogenesis, differential diagnosis and histopathological aspects. The purpose of this report is to alert clinicians to consider this unusual lesion when formulating a differential diagnosis of an enlarging blue oral mucosal lesion.

Malignant peripheral nerve sheath tumour presenting as a pneumothorax

Malignant peripheral nerve sheath tumours are rare and aggressive soft-tissue sarcomas of ectomesenchymal origin. These tumours commonly occur in patients with neurofibromatosis Type 1 with a cumulative lifetime risk of 10%. The vast majority of cases present with clinical evidence of a soft-tissue mass with or without features of nerve irritation and loss of function arising from the lesion of origin. The primary presentation of a malignant peripheral nerve sheath tumour with a pneumothorax in the absence of widespread metastatic disease in a patient with no medical or family history of neurofibromatosis has never been reported in the literature. We present a unique case of a systemically well 34-year-old male who presented with clinical evidence of a right-sided pneumothorax. The chest radiograph identified the right-sided pneumothorax and revealed an apical pleural mass that was confirmed by intravenous contrast-enhanced CT of the thorax. The patient was referred for video-assisted thorascopic surgical pleurodesis and biopsy of the lesion. Histopathology analyses confirmed the diagnosis of malignant peripheral nerve sheath tumour. To the best of our knowledge, no such case reports have been published in the literature. A diagnosis of malignant peripheral nerve sheath tumour should be considered as one of the rarer possibilities in patients presenting with pneumothoraces in association with apical pleural lesions.

A primary cardiac sarcoma presenting with superior vena cava obstruction

Superior vena cava (SVC) obstruction leads to a constellation of symptoms and signs that encompass the SVC syndrome. Today, malignancy accounts for 65% of all cases. The most common neoplastic causes are non–small cell lung cancer (50%), small cell lung cancer (25%), lymphoma, and metastasis. Primary cardiac tumors are an extremely rare cause of SVC obstruction. We describe the case of a 48-year-old man who presented with dyspnea, confusion, and facial swelling with cyanosis. The patient developed life-threatening airway obstruction after administration of anxiolytic. The diagnosis of SVC obstruction secondary to a primary cardiac sarcoma was established based on clinical, radiologic, and post-mortem findings. This is one of very few reported cases of a primary cardiac sarcoma causing SVC obstruction.

The pathology of depopulated bovine ureter xenografts utilized for vascular access in haemodialysis patients.

Aims:  Vascular access for long‐term haemodialysis is obtained through the surgical fashioning of arteriovenous fistulae, utilizing the patients’ native blood vessels, or by insertion of synthetic grafts or non‐synthetic gluteraldehyde cross‐linked biological xenografts. These non‐native grafts have high complication rates and a depopulated bovine ureter xenograft has recently been developed as an alternative. The aim was to undertake the first systematic review of the histopathology of bovine ureter xenografts (n = 25) utilized for haemodialysis vascular access in humans.

Endometrial glands and stroma within uterine smooth muscle proliferations: an introduction of the concept of an adenomyotic leiomyoma.

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CD56 immunoreactivity in ovarian sex cord‐stromal tumours

Perhaps in time our proposed form of association between leiomyomata and adenomyosis will be found to complement the above-mentioned theory that the pathogenesis of adenomyosis may involve an initial phase of subendothelial smooth muscle hyperplasia. Other differential diagnoses such as adenomatoid tumour or leiomyomata containing adenocarcinoma should be relatively easily excluded by the presence of accompanying endometrial stroma in cases of adenomyosis. It should be clarified that there exists an entirely separate entity to that under discussion, the atypical polypoid adenomyoma, in which there is frank cytological atypia and prominent squamous metaplasia. In conclusion, it is difficult to determine the precise histogenesis of individual cases featuring benign endometrial glands and stroma within uterine smooth muscle proliferations, but we believe that the range of possibilities includes the presence of adenomyosis within leiomyomata–an explanation which has received little consideration in the medical literature.