Objectives: The clinical features of scurvy may resemble metabolic disorders and hamper early diagnosis. Case report: A three-year old male child was admitted to hospital with complaints of growth retardation, irritability, joint deformities, limited mobility, wheezing and frequent illness. Severe malnutrition, coarse facial appearance, gingival hypertrophy, organomegaly, significant osteoporosis, and anemia that did not respond to iron treatment were detected and differential diagnosis for metabolic disorders were considered. Screening for inborn errors revealed generalized aminoaciduria and elevated blood free carnitine. Enzyme analyses excluded lysosomal storage disorders. Dietary history of the patient revealed very poor consumption of vitamin C which was about 13% of RDA and had continued for a long period. Vitamin C level was 0.05 mg/L (n: 4-21) in plasma, 2.85 mg/24 hour (n:10-30) in urine, and 1.03 mg/6 hours in urine after intravenous loading. The patient was given 200 mg/day vitamin C orally. Irritability and bone sensitivity decreased after the first two days and clinical improvement ensued. Conclusion: Clinical features in scurvy resemble symptoms observed in some metabolic disorders. Careful clinical evaluation, dietary history and vitamin C assay may exclude uneccessary metabolic work-up. Background: Menkes disease (MD) is an X-linked disorder of copper transport caused by ATP7A gene mutations. Treatment with parenteral copper-histidine can change prognosis when initiated in early stages of neurological disease. Case Reports: Patient 1 was diagnosed of MD (15 bp del.exon1) at the age of 2 months, showing hypotonia, joint hyperlaxity and femoral fracture. No seizures were reported. Parenteral copper-histidine was started at the age of 5 months and continued for 9 years. At 10 years of age attends normal school and has no seizures. Current MRI shows marked tortuosity of intracranial vessels without brain atrophy. Connective tissue abnormalities include joint hyperlaxity, bone deformities and asymptomatic urinary bladder diverticula. Mild renal tubulointerstitial damage is due to chronic copper supplementation. Patient 2 was diagnosed of MD (c1971t>A mutation) at the age of 3 months after admission for refractory epilepsy. Treatment started immediately but neurological status did not improve. He developed severe mental retardation and intractable epilepsy. He was under treatment until the age of 5 years when he died. Discussion: Early treatment in Menkes disease is critical for the prevention of neurological damage although diagnosis is difficult in presymptomatic stage. Long term effects of treatment include bone deformities and tubulointerstitial damage. Background: Wilson disease is an autosomal recessive disorder in which copper accumulates in tissues due to deficit of hepatic ATPase. Clinical picture is extremely variable. Hepatic manifestation is the most common feature in childhood. Neuropsychiatric disorder appears in adulthood. Case Report: We present a case of a family with variable clinical picture in 2 siblings. 14 years old boy was sent with 3 years history of unexplained hepatopathy first revealed during acute gastritis. Detailed examinations were performed including ceruloplasmin, which was normal during first year. Accidently 17 years old brother was present at a first visit. He presented with hypertonic-hypokinetic syndrome which developed during 3 months and was explained by psychiatric treatment for anxiety and depression with progressive cognitive deterioration and rigidity. Suspected Wilson disease in both was confirmed by patognomic laboratory findings (low ceruloplasmin, high urine copper excretion), MRI findings in older one and definitely by DNA analysis. Because of persistent hyperbilirubinemia and otherwise negative findings in their sister all the siblings were examined and Gilbert syndrome was confirmed.