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A 9-year-old boy presented with progressive fingernail dystrophy evolving over 9 months, with initial brittleness and yellow discolouration progressing to complete distal onycholysis, which had not responded to empirical interventions for nutritional or trauma issues (including biotin supplements, topical vitamin E oil and nail hardening preparations). The patient was asymptomatic and maintained normal growth velocity. His height (135 cm), weight (39 kg) and body mass index 20.4 remain at the 75th, 95th and 95th percentiles, respectively; similar in all parameter centiles compared with his only other available measurement 3 months previously. The patient’s developmental history had been unremarkable. Physical assessment revealed symmetric nail plate thinning and distal separation across all fingernails, featuring roughened surfaces without periungual inflammation or subungual debris (figures 1 and 2). Toenails showed milder discolouration and fragility. Laboratory evaluation ruled out haematological (normal complete blood count, notably haemoglobin 132 g/L, normal for age: 115–155 g/L), nutritional (normal iron/zinc/vitamin D) and fungal aetiologies. Metabolic workup uncovered isolated hypertriglyceridaemia (333 mg/dL; normal for age <75 mg/dL), with normal total cholesterol (165 mg/dL; normal <170 mg/dL), high-density lipoprotein (42 mg/dL; normal >40 mg/dL), low-density lipoprotein (89 mg/dL; normal <110 mg/dL) and normal liver function tests, prompting consideration of systemic contributors to the persistent onychodystrophy. Table 1 summarises the laboratory investigations.