Testicular sarcoidosis is a rare but benign entity. It is often mistaken for testicular neoplasm, leading to orchiectomy. It is, therefore, extremely important to identify and correctly diagnose testicular sarcoidosis on sonography to avoid unnecessary orchiectomy. This case study reports a young patient who had a prior history of unilateral orchiectomy for cryporchidism and presented with testicular lesions on the contralateral testis. He was later found to have skin lesions and chest symptoms that led to a diagnosis of sarcoidosis.

Schwannoma is a benign, well-defined, and solitary nerve sheath tumor and accounts for 5% of all soft tissue tumors. It can occur anywhere along the peripheral nervous system. It is a slowly growing tumor and usually presents as a painless, discrete, and firm swelling before being diagnosed, unless it grows in a confined place. Preoperative diagnosis of schwannoma is often difficult. Computed tomography, magnetic resonance imaging, and sonography are useful imaging modalities in the preoperative assessment of nerve sheath tumors. Although imaging may not be reliable in distinguishing nerve sheath tumors from each other, certain imaging characteristics should raise the suspicion of schwannoma.

Antley-Bixler syndrome (ABS)—consisting of ABS type 1 (skeletal only) and ABS type 2, associated with cytochrome 450 mutations and P450 oxidoreductase deficiency (PORD-ABS)—is a heterogeneous syndrome with a constellation of skeletal deformation findings that classically include skull, facial, and appendicular defects. The hallmarks of ABS type 1 include craniosynostosis, midface hypoplasia, radiohumeral/radioulnar synostosis, arachnodactyly, bowing of the femur, congenital fractures, and choanal atresia. ABS has historically been identified at newborn or childhood examination using radiographic, computed tomography, or stillbirth autopsy. However, in recent years, antenatal ultrasonography has identified craniosynostotic conditions in utero. We present a case of PORD with the ABS phenotype diagnosed by sonography in utero at an early gestation (13–16 weeks), which included mutations in the POR gene. Sonographers, sonologists, and perinatologists aware of the diversity of this rare condition will be well prepared to raise the suspicion of Antley-Bixler PORD-type syndrome.

Larsen syndrome is a rare inherited disorder of collagen formation with multiple joint dislocations, cardiac abnormalities, short stature, talipes equinovarus, short and broad fingertips, spatula-like thumbs, supernumerary ossification center in the calcaneus, hearing loss, neurologic impairment, cryptorchidism, and characteristic craniofacial abnormalities. The sonographic prenatal findings in a case of Larsen syndrome at 26 weeks' gestation, which demonstrated joint dislocations, hypertelorism, frontal bossing, micrognathia, and upper and lower limb shortening and confirmed at both 29 and 30 weeks' gestation, are presented and discussed. When evaluating patients with a positive family history of Larsen syndrome, sonographers should carefully scan and meticulously assess the fetal extremities for signs of dislocation and the face for signs of flat features, hypertelorism, micrognathia, and depressed nasal bridge, distinctive features of the syndrome.

This study describes the sonographic features of stent-induced cholangitis, which could be mistaken for biliary dilatation and obstruction. It involves six patients with a mean age of 71 years (range, 29-81 years) who underwent endoscopic biliary stenting because of biliary obstruction. Stenting duration varied from nine days to five months. All patients had prestenting and poststenting sonograms. The sonographic characteristics were analyzed in all of the patients, with the diagnosis being confirmed by retrograde cholangiopancreaticography. All patients showed biliary dilatation without ductal wall thickening on prestenting sonograms. Follow-up sonograms demonstrated diffuse hypoechoic ductal wall thickening in all patients. In four patients, the ductal lumen was obliterated by wall thickening, which initially led to a misdiagnosis of persistent biliary dilatation. The degree of ductal wall thickening did not correlate with stenting duration. Diagnosis of stent-induced cholangitis should be considered when hypoechoic and thickened bile duct walls are found on sonography. Careful scanning technique and meticulous assessment of the sonographic images helped to separate the echo-free ductal lumen from the hypoechoic edematous mucosal lining. When evaluating patients following stenting, sonographers may need to obtain fine detailed views of the common bile duct to be able to differentiate ductal wall edema from biliary dilatation.