Search

Amerigo Filia was born on July 18, 1873, in Sassari, Sardinia, Italy. After attaining his Medicine degree at the University of Turin in 1900, he went to Rome to study Pediatrics at the School of Pediatrics directed by Professor Luigi Concetti. His academic career began in Sassari when he was appointed as teacher of Pediatrics in 1911, becoming Full Professor in 1917, Dean of the School of Medicine and Surgery in 1918 and, finally, Rector of the University in 1919. He distinguished himself as the founder of the Pediatric Clinic and the School of Pediatrics in Sassari, both being the first ones in Sardinia, and as the promoter of the restoration of the front of the main building of the University of Sassari (“Palazzo dell’Università”), as well as of new buildings to host Scientific Institutes and Clinics. Moreover, in 1923, he succeeded in preventing the suppression of Sassari University as a consequence of the “Gentile” reform. As documented by his scientific publications, Filia’s research activity included both experimental and clinical studies focusing on the renal excretion of high dose of arsenic, the effects of Lactobacilli in infantile enteritis, as well as on renal tuberculosis and pulmonary echinococcosis in children. Amerigo Filia died suddenly on December 21, 1925, in Rome, where he was participating in a university competition as a committee member.

Ceftriaxone treatment of bacterial infections can be associated with biliary complications, more commonly in children than adults, in a dose-dependent manner. This study describes a clinical case series of children with ceftriaxone-related cholelithiasis. We performed a retrospective analysis of cases of ceftriaxone-related biliary complications admitted to the Pediatric Clinic, Department of Clinical and Experimental Medicine, University of Sassari, Italy, during the period 2005-2015. Four children with cholelithiasis occurring during, or soon after, the treatment with ceftriaxone are reported. Case 1 (6-month-old), case 2 (9-year-old) and case 4 (10-year-old) were symptomatic, while case 3 (3-year-old) was asymptomatic. After the ultrasonographic diagnosis of gallstones (cases 1 and 2) or biliary sludge (cases 3 and 4), ceftriaxone treatment was withdrawn, and ursodeoxycholic acid (UDCA) was started in cases 1 and 2. A complete recovery was observed in all but case 1, in whom cholelithiasis was still detectable at one-year follow-up by ultrasonography. This case underwent a triple antibiotic protocol for bacterial meningitis. The protocol included rifampicin, which is known to have an effect in decreasing hepatic concentration of bile salts. Therefore, in this case, both rifampicin and UDCA were of no benefit in preventing or treating ceftriaxone biliary complications. The current pharmacological approach for the treatment of ceftriaxone-related cholelithiasis seems to be ineffective, likely due to the high calcium content of gallstones. Therefore, the best strategy of intervention for ceftriaxone biliary complications in children remains the prevention of the risk factors.