The development of macrolide resistance that occurred during 3 days of therapy with azithromycin to treat Mycoplasma pneumoniae pneumonia in a paediatric patient is reported. After extended molecular characterization of strains, the parallel occurrence of clones showing the non-mutated wild-type 23S rRNA sequence as well as mutations A2063G and A2064G, which are both responsible for phenotypic resistance, was confirmed for the first time.
Lesch-Nyhan syndrome is a disorder caused by congenital absence of the enzyme hypoxanthineguanine phosphoribosyltransferase and an increase of the enzyme activity of adenine phosphoribosyltransferase. Treatment should be adjusted to patient's age and weight. An adapt treatment with allopurinol and optimal fluid intake reduce the risk of uric acid or xanthine lithiasis. Laboratory monitoring includes testings for serum concentration and urinary excretion of uric acid, xanthine and hypoxanthine. Sole a normal concentration of uric acid is not sufficient for therapy control. Assessment of the urine sediment by microscopy or infrared spectroscopy will enable early detection of uric acid or xanthine lithiasis.
Testicular masses in male individuals with the adrenogenital syndrome (AGS) are a clinical and pathological diagnostic dilemma. The major differential diagnosis of gonadal nodules in this setting includes interstitial Leydig cell tumors and secondary benign tumors possibly of adrenal origin. We report a case of adrenogenital syndrome occurring in a 14-year-old boy. Examinations to clarify the cause of his dwarfism and bilateral testicular masses revealed 21-hydroxylase deficiency. The testes were not tender and were firm and nodular on palpation. The serum levels of adrenocorticotrophic hormone (ACTH), 17 alpha-hydroxyprogesterone (17-alpha-OHP), testosterone, and aldosterone were found to be elevated. Under corticosteroid therapy the serum marker abnormalities were corrected and there was gradual regression of the tumor lesions in both testes. Testicular tumors with adrenogenital syndrome are typically bilateral and develop in untreated or inadequately treated males with AGS.
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