We aimed to examine the major causes of isolated chronic hypertransaminasemia in asymptomatic children and develop a comprehensive diagnostic flow diagram. A MEDLINE search inclusive of publications throughout August 2012 was performed. We found only a small number of publications that had comprehensively investigated this topic. Consequently, it was difficult to construct a diagnostic flowchart similar to those already available for adults. In children, a "retesting panel" prescription, including gamma-glutamyl transpeptidase and creatine kinase in addition to aminotransferases, is considered a reasonable approach for proficiently confirming the persistence of the abnormality, ruling out cholestatic hepatopathies and myopathies, and guiding the subsequent diagnostic steps. If re-evaluation of physical and historical findings suggests specific etiologies, then these should be evaluated in the initial enzyme retesting panel. A simple multi-step diagnostic algorithm incorporating a large number of possible pediatric scenarios, in addition to the few common to adults, is available. Accurately classifying a child with asymptomatic persistent hypertransaminasemia may be a difficult task, but the results are critical for preventing the progression of an underlying, possibly occult, condition later in childhood or during transition. Given the high benefit/cost ratio of preventing hepatic deterioration, no effort should be spared in diagnosing and properly treating each case of persistent hypertransaminasemia in pediatric patients.
The aim of this study was to call the attention to the often disregarded message that hypertransaminasemia may be a marker of both liver and muscle diseases by presenting personal case reports and a systematic literature review. Three male children (mean age 5.7 years) were inappropriately addressed, during the last 12 months, to our paediatric liver unit for diagnostic work-up of a chronic hypertransaminasemia of unknown origin. In one of them, a liver biopsy had already been performed. On admission, physical examination, evaluation of serum levels of creatine kinase, and dystrophin genetic testing finally led to a diagnosis of muscular dystrophy. One hundred fourteen similar cases, 21 with unnecessary liver biopsy, were found by Medline search. Expensive and invasive tests planned to investigate liver diseases should be postponed until alternative sources of increased serum aminotransferases, primarily myopathic injury, have been excluded.
The results of reported studies confirmed that at least some of the new drugs, with greater efficacy and/or minor side-effects, will be used clinically.
We present the case of an extremely low birth weight infant with diffuse gingival noma, initially misdiagnosed as thrush. Multidrug-resistant Pseudomonas aeruginosa strain was cultured and treated with systemic and local colistin with complete healing. Noma neonatorum from multidrug-resistant pathogens may appear in neonatal intensive care units. Old antibiotics may help.Noma (cancrum oris) is a devastating gangrenous disease that leads to destruction of facial tissue with significant morbidity and mortality in children and young adults. Noma has virtually disappeared from Europe and North America, but it is still common among children and young adults in India, Africa, and South America. Noma is a polymicrobial opportunistic infection related to malnutrition and immune dysfunction. In the neonate, a similar but distinct condition, known as "noma neonatorum" was described in 1977, in which gangrenous lesions involve the mucocutaneous junctions of oral, nasal, and anal area, and, occasionally, the eyelids and the scrotum. The neonatal disease has been linked to Pseudomonas aeruginosa, prematurity, and low birth weight. There is no established treatment, and mortality is almost inevitable in the few reported cases. In this study, we present the first European case of noma neonatorum from a multidrug-resistant strain of P aeruginosa.
I read with interest the recent paper regarding validation of a monoclonal stool antigen test for Helicobacter pylori detection in young children (1). The authors report on the accuracy of a monoclonal stool antigen test for young children. The test had 100% sensitivity but only 76% specificity using the established cutoffs. Using the data from their trial they suggested new cutoff values that increased the specificity to 98% and suggested that the new cutoff values should be used in their population. The table only provided the data using the adjusted cutoff values. Although the test appeared reasonably accurate with the established cutoff, the conclusion that the adjusted cutoff would improve the results in their population was not a valid conclusion, but was rather a data-derived hypothesis that must be tested in another study. One good analogy that describes data-derived cutoff values is the shooting of an arrow and then drawing the target around where it landed. Thus, the authors' suggestion regarding the need for validation was correct but was misplaced in that validation of their proposed cutoffs must be done before their reported improvement in test results can be accepted as valid. A table with the results using the established results would also be of interest to readers.
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