Giant parathyroid lipoadenoma case report: A parathyroid phenomenon.

INTRODUCTION: Parathyroid lipoadenomas are a rare parathyroid phenomenon and an unusual cause of primary hyperparathyroidism. A difficult diagnosis to make, there are less than 100 cases in the literature since they were first described in 1958, and to our knowledge this is the largest parathyroid lipoadenoma to be reported. PRESENTATION OF CASE: A minimally-invasive parathyroidectomy with intraoperative parathyroid hormone monitoring was performed in the case of a male with a large neck mass and symptomatic primary hyperparathyroidism. A giant parathyroid lipoadenoma was excised, with an appropriate decrease in intraoperative parathyroid hormone level observed. DISCUSSION: This lesion poses a challenge to the surgeon, radiologist and pathologist alike and is an important addition to the scant literature available. Clinically it presents similarly to a simple adenoma. The high adipose content of this lesion leads to difficulty localising it on imaging, and the histology study can lead pathologists astray. CONCLUSION: We highlight the importance of having the parathyroid lipoadenoma as a differential diagnosis for patients who develop primary hyperparathyroidism.

Prospective assessment of C4d deposits on circulating cells and renal tissues in lupus nephritis: a pilot study.

Complement activation plays a key role in the pathogenesis of lupus nephritis (LN), a severe complication of systemic lupus erythematosus (SLE). We prospectively evaluated 15 LN subjects and two control groups: 13 non-SLE renal subjects (control A) and 239 SLE subjects without LN (control B). All had C4d levels on circulating erythrocytes (E-C4d), reticulocytes (R-C4d) and platelets (P-C4d) measured by flow cytometry, while C4d deposition in renal tissue was semiquantitatively assessed in LN subjects and control A using immunoperoxidase staining. Compared with control A, LN biopsies had higher glomerular-C4d scores (p = 0.003), which were associated with more frequent granular glomerular immunofluorescence staining and electron dense deposits (p < 0.001). Compared with control A and B groups, LN subjects had higher E-C4d (p = 0.002 and p = 0.005) and R-C4d levels (p = 0.002 and p = 0.008), respectively. LN subjects were more likely to have P-C4d compared with control A (p = 0.016). In LN, only E-C4d correlated with National Institutes of Health (NIH) activity index (r = 0.55, p = 0.04). In conclusion, LN biopsies showed frequent glomerular-C4d staining associated with immune complex deposits. LN subjects had higher E-C4d and R-C4d levels compared with both control groups. E-C4d levels also correlated with NIH activity index. These findings suggest a potential role of C4d on circulating cells as a biomarker for lupus nephritis.

Inhibition of major integrin αV ß3 reduces Staphylococcus aureus attachment to sheared human endothelial cells.

Essentials Staphylococcus aureus (S. aureus) binds and impairs function of vascular endothelial cells (EC). We investigated the molecular signals triggered by S. aureus adhesion to EC. Inhibition of the EC integrin αVß3 reduces S. aureus binding and rescues EC function. αVß3 blockade represents an attractive target to treat S. aureus bloodborne infections. SUMMARY: Background Vascular endothelial dysfunction with associated edema and organ failure is one of the hallmarks of sepsis. Although a large number of microorganisms can cause sepsis, Staphylococcus aureus (S. aureus) is one of the primary etiologic agents. Currently, there are no approved specific treatments for sepsis, and the initial management bundle is therefore focused on cardiorespiratory resuscitation and mitigation of the immediate threat of uncontrolled infection. The continuous emergence of antibiotic-resistant strains of bacteria necessitates the development of new therapeutic approaches for this disease. Objective To identify the molecular mechanisms leading to endothelial dysfunction as a result of S. aureus binding. METHODS: Binding of wild type and Clumping factor A (ClfA) deficient S. aureus Newman to the endothelium was measured in vitro and in the mesenteric circulation of C57Bl/6 mice. The effects of the αV ß3 blocker-cilengitide-on bacterial binding, endothelial VE-cadherin expression, apoptosis, proliferation and permeability were assessed. Results The major S. aureus cell wall protein ClfA bound to endothelial cell αV ß3 in the presence of fibrinogen. This interaction resulted in disturbances in barrier function mediated by VE-cadherin in endothelial cell monolayers, and ultimately cell death by apoptosis. With a low concentration of cilengitide, ClfA binding to αV ß3 was significantly inhibited both in vitro and in vivo. Moreover, preventing S. aureus from attaching to αV ß3 resulted in a significant reduction in endothelial dysfunction following infection. Conclusion Inhibition of S. aureus ClfA binding to endothelial cell αV ß3 by cilengitide prevents endothelial dysfunction.

The prognostic significance of CD44s and CD44v6 expression in stage two breast carcinoma: an immunohistochemical study.

AIMS: Expression of the v6 variant isoform of CD44 has been causally associated with the development of metastases. This study, using immunohistochemical techniques, examined the prognostic significance of CD44s and CD44v6 expression. METHODS: A cohort of 109 women presenting with stage 2 breast cancer, with a minimum follow-up of 5 years, were assessed. RESULTS: Eighty percent of patients demonstrated CD44v6 expression on immunohistochemical studies. CD44v6 expression in tissue sections was found to be independent of age, tumour size, grade, and lymph-node status. No significant association was demonstrated between CD44v6 expression and either disease-free or overall survival. Similar findings were observed for CD44s. CONCLUSIONS: CD44s and CD44v6 do not appear to be useful as prognostic indicators in early breast cancer. The increased expression of variant CD44 isoforms seen in breast neoplasia may merely be a marker for loss of control of alternative splicing within tumour tissue.

Prognostic implications of p53 and bcl-2 expression in 108 women with stage two breast cancer.

BACKGROUND: The mortality and morbidity of patients with breast cancer can vary even between individuals with similar histological stage at diagnosis. Identification of those individuals with prognostically poorer tumours is an essential prerequisite in planning adjuvant therapies. Some prognostic indices of tumour size, grade, oestrogen receptor status and nodal status are well established. AIM: The aim of this study was to examine the prognostic role of information relating to proto-oncogene and tumour suppressor gene expression. METHODS: 108 women with stage II breast cancer were studied. Tumour expression of p53 and bcl-2 were scored and then correlated with recurrence and mortality. RESULTS: We have shown that individuals poorly expressing bcl-2 in their tumours have a poorer disease-free and overall survival than those who express bcl-2. When p53 was strongly expressed, it was associated with poorer disease-free and overall survival. CONCLUSION: The profiling of individual tumour genetic expression of proto-oncogenes may allow for more specific identification of patients at higher risk of recurrence in breast cancer.