Purpose
The negative correlation between BPH-size and incidence of prostate cancer (PCa) is well-documented in the literature, however the exact mechanism is not well-understood. The present study uses histo-anatomical imaging to study prostate volume in correlation to prostate capsule thickness, and glandular epithelial cell density within the peripheral zone (PZ).
Materials and Methods
Specimens were selected from radical prostatectomies ranging from 20 to 160 mL based on ease of anatomical reconstruction by the slides. A total of 60 patients were selected and underwent quantitative measurements of prostate capsule thickness and glandular epithelial density within the PZ using computer-based imaging software. Pearson's correlation and a stepwise multiple linear regression analysis was conducted to determine the relationship between these measured parameters and the clinical characteristic of these patients.
Results
Pearson's correlation analysis revealed a strongly significant, negative correlation between prostate volume and glandular epithelial cell density (r(58)=−0.554, p<0.001), and a strongly significant, positive correlation between prostate volume and average capsule thickness (r(58)=0.462, p<0.001). Results of multiple regression analysis showed that average glandular epithelial cell density added statistically to this prediction (p<0.05).
Conclusions
The results suggest that growth of the transition zone in BPH causes increased fibrosis of the PZ, leading to atrophy and fibrosis of glandular cells. As 80% of PCa originates from the glandular epithelium within the PZ, this observed phenomenon may explain the inverse correlation between BPH and PCa that is well-documented in the literature.
Systemic lupus erythematosus (SLE) is an autoimmune disease with varying dermatological findings. We review a unique presentation of SLE with a literature review. A previously healthy early adolescent female presented with painful, oral mucosal bullae filled with sanguineous fluid. She endorsed a tender right knee, but examination revealed no additional abnormalities. CBC demonstrated severe pancytopaenia. Further workup, including Coombs positive RBCs and positive ANA, anti-Smith, and anti-dsDNA antibodies, confirmed Lupus as the aetiology of this patient’s presentation. A form of blistering SLE and resultant thrombocytopaenia was likely responsible for the patient’s oral manifestations. After receiving 60 g intravenous immunoglobulin and 3 days high-dose pulse corticosteroids, her dermatological symptoms resolved. Although cases of blistering SLE with mucosal bullae have been described in the literature, this is the first documented case of haemorrhagic mucosal bullae as the presenting symptom of thrombocytopaenia in SLE in a paediatric patient.
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