RESUMO
BACKGROUND: Multiparametric (mp) magnetic resonance imaging (MRI)-ultrasound fusion-targeted biopsy (TB) has improved the detection of clinically significant prostate cancer (csCaP) using the Prostate Imaging Reporting and Data System (PI-RADS) reporting system, leading some authors to conclude that TB can replace the 12-core systematic biopsy (SB). We compared the diagnostic performance of TB with SB at our institution. METHODS: Eighty-three men with elevated prostate-specific antigen levels (6.6 ng/mL, interquartile range [IQR] 4.5-9.2) and abnormal mp-MRI (127 lesions, PI-RADS ≥3, median size: 1.1 cm, IQR 0.8-1.6) underwent simultaneous TB and SB. Diagnosis of any CaP (Gleason score, [GS] ≥6) and csCaP (GS ≥7) was compared using the McNemar's exact test. RESULTS: SB showed higher, but not statistically significant, detection rates of any CaP and csCaP (51.8% and 34.9%) versus TB (44.6% and 28.9%) (P = 0.286 and P = 0.359, respectively). TB outperformed SB in the quantification of 56.6% CaP and detecting cancer in anterior sectors (7.2%). Compared to SB, TB missed twice the amount of any CaP and csCaP. SB alone detected 22.2% of all csCaPs and upgraded 20.6% of TB-detected CaP. SB identified cancer invisible on mp-MRI (13.7% of all CaP) or missed by TB due to a small size (<1 cm) and sampling error (7% of lesions). CONCLUSION: A combination of SB with TB remained necessary for achieving the highest cancer detection rates. Limiting prostate biopsy to TB alone can miss csCaP due to the presence of synchronous high-grade cancer invisible on MRI or failure to hit the target. TB is the best approach for anterior lesions and tumor quantification.
RESUMO
Vascular Ehlers-Danlos Syndrome (VEDS) is a rare autosomal dominant disorder caused by mutations in the COL3A1 or COL1A1 genes. Its mortality is secondary to sudden and spontaneous rupture of arteries or hollow organs. The genotype influences the distribution of arterial pathology with aneurysms of intra-abdominal visceral arteries being relatively uncommon. We describe the case of a young man with probable VEDS who died of a spontaneous rupture and dissection of the cystic artery. The patient initially presented with abdominal pain due to an unrecognized spontaneous perforation of the small intestine complicated by sepsis. We postulate that inflammatory mediators may have triggered the arterial rupture due to remodeling and weakening of vessel walls. The phenotype of the patient's vascular damage included bilateral spontaneous carotid-cavernous sinus fistulae and dissection with pseudoaneurysm formation of large- and medium-sized arteries, predominantly the abdominal aorta and its branches. The autopsy uncovered a long history of vascular events that may have been asymptomatic. These findings along with a positive family history supported the VEDS diagnosis. Loeys-Dietz, Marfan, and familial thoracic aortic aneurysm and dissection syndromes were ruled out based on the absence of arterial tortuosity, eye abnormalities, bone overgrowth, and the distribution of vascular damage among other features. Interestingly, microscopic examination of the hippocampus revealed a focus of neuronal heterotopia, commonly associated with epilepsy; however, the patient had no history of seizures. The natural course of VEDS involves the rupture and dissection of arteries that, if unrecognized, can lead to a rapid death after bleeding into free spaces.
RESUMO
INTRODUCTION: Inadequate perfusion and abnormal cellular metabolism are among the mechanisms of organ dysfunction in sepsis. Concomitant hepatorenal failure during the late phase of sepsis is poorly understood. CASE REPORT: The autopsy of a child who developed sepsis-induced hepatorenal failure revealed bile cast nephropathy, hepatic centrilobular necrosis and cholangitis lenta, a type of sepsis-induced cholestasis, with no biliary obstruction, fibrosis or cirrhosis. The liver and renal function declined at the same rate as procalcitonin increased. DISCUSSION: Failure of resolution and persistent inflammation in sepsis can result in ductular injury and stagnation of bile with subsequent cholemia. The kidney failure was associated with the formation of intratubular bile casts. CONCLUSION: This case illustrates how severe cholestasis in combination with bile cast nephropathy may be potential and unrecognized contributors to hepatorenal failure in sepsis. Whether bile toxicity causes renal failure in the context of cholangitis lenta should be further studied.
