Pelvic Inflammatory Disease: Multimodality Imaging Approach with Clinical-Pathologic Correlation.

Pelvic inflammatory disease (PID) is a common medical problem, with almost 1 million cases diagnosed annually. Historically, PID has been a clinical diagnosis supplemented with the findings from ultrasonography (US) or magnetic resonance (MR) imaging. However, the diagnosis of PID can be challenging because the clinical manifestations may mimic those of other pelvic and abdominal processes. Given the nonspecific clinical manifestations, computed tomography (CT) is commonly the first imaging examination performed. General CT findings of early- and late-stage PID include thickening of the uterosacral ligaments, pelvic fat stranding with obscuration of fascial planes, reactive lymphadenopathy, and pelvic free fluid. Recognition of these findings, as well as those seen with cervicitis, endometritis, acute salpingitis, oophoritis, pyosalpinx, hydrosalpinx, tubo-ovarian abscess, and pyometra, is crucial in allowing prompt and accurate diagnosis. Late complications of PID include tubal damage resulting in infertility and ectopic pregnancy, peritonitis caused by uterine and/or tubo-ovarian abscess rupture, development of peritoneal adhesions resulting in bowel obstruction and/or hydroureteronephrosis, right upper abdominal inflammation (Fitz-Hugh-Curtis syndrome), and septic thrombophlebitis. Recognition of these late manifestations at CT can also aid in proper patient management. At CT, careful assessment of common PID mimics, such as endometriosis, adnexal torsion, ruptured hemorrhagic ovarian cyst, adnexal neoplasms, appendicitis, and diverticulitis, is important to avoid misinterpretation, delay in management, and unnecessary surgery. Correlation with the findings from complementary imaging examinations, such as US and MR imaging, is useful for establishing a definitive diagnosis. (©)RSNA, 2016.

SeSAME/EAST syndrome--phenotypic variability and delayed activity of the distal convoluted tubule.

BACKGROUND: Mutations in the K(+) channel KCNJ10 (Kir4.1) cause an autosomal recessive syndrome featuring seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME). Kir4.1 localizes to the basolateral membrane of the renal distal convoluted tubule, and its loss of function mimics renal features of Gitelman syndrome, with hypokalemic alkalosis, hypomagnesemia, and hypocalciuria. Presentation early in life due to seizures provides an opportunity to investigate the development of the electrolyte defect with age. METHODS: We used DNA sequencing, electrophysiology, confocal imaging, and biochemistry to identify a new KCNJ10 mutation in a previously unreported family and determine its impact on channel function. We examined medical records to follow the development of electrolyte disorders with age. RESULTS: The four affected members were all homozygous for a novel T57I mutation that confers biochemical loss-of-function. Electrolytes in affected children were normal in the first years of life but showed significant worsening with age, resulting in clinically significant defects at age 5-8 years. Similar findings were seen in other SeSAME patients. CONCLUSIONS: These findings provide evidence for a delayed activity of salt reabsorption by the distal convoluted tubule and suggest an explanation for the delayed clinical presentation of subjects with Gitelman syndrome.