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Infantile hemangioma is the most common benign tumor of infancy, affecting 1–2% of infants. Hemangiomas of the airway constitute an even smaller percentage, but their management can be challenging due to the potential for life threatening airway compromise. A Subglottic hemangioma (SGH) makes up 1.5% of all congenital laryngeal anomalies, it is twice more common in females than males and have been linked to low birth weight and prematurity. It is during the early proliferative phase (1–3 months of life) that patients became symptomatic, developing characteristic stridor which may progress to respiratory distress. In this early stage, a SGH is often mistaken for a more common condition such as croup. The aim of this case is to underline what a recurrent dyspnea or laryngeal stridor in the first 6 months might hide Case report A 4 months-old-girl who was born at term of natural childbirth (birth weight 2.500 kg-SGA), presented with several weeks of unremitting stridor, substernal retractions. She was diagnosed to have bronchiolitis and she had been hospitalized twice in an another hospital and treated with oral steroids and nebulized racemic epinephrine without significant improvement in her symptoms; Than she had been sent to our hospital. She had intercostal and subcostal retractions. Both lungs had equal contribution to respiration, respiratory sounds were coarse and she had both inspiratory and expiratory stridors which were more obvious on bilateral sibilant rales, and inspiratory phase. She also had wheezing. Laboratory tests, echocardiogram and electrocardiogram were normal. Her follow-up showed that she was not responding to treatment and her respiratory distress was increasing, thus she had a laryngofibroscopy that did not reveal any clear structural abnormalities, and performed a CT scan of the neck, that revealed a laryngeal mass, confirmed by an MRI of the neck, which showed a solid tissues of low intensity on T1-weighted spin-echo images and of hyperintensity on T2-weighted spin-echo images (6x8 mm), compatible with SGH. After her workup was complete, she received an initial dose of propranolol at 0.5 mg/kg, which was increased to 2 mg/kg, and no adverse effects were noted. SGH is a rare but potentially life-threatening disease. A high index of suspicion is vital for the early, accurate diagnosis of this disease. Propranolol treatment has many advantages, it is non-invasive and it has a low complication rate; thus, the use of propranolol as a first-line treatment for SGH is proposed.

Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating illness, characterize-ed by a monophasic course frequently associated with infections or previous immunization. Regarding pathogenesis, encephalomyelitis is associated with some immunological mechanisms. Post-infection or post-vaccination inflammatory reactions in the perivenular region in the central nervous system (CNS) may be explained by a molecular mimicry mechanism. An antecedent infection was identified in 72–77% of paediatric patients. We present a case of a 5 year-old girl in follow up for autoimmune thrombocytopenia (AT) and autoimmune haemolytic anaemia (AHA) in steroid treatment, with history of left hemiparesis, language delay, from as a consequence of perinatal suffering, who has developed ADEM. This patient presented with progressive weakness of limbs, neck pain associated with fever from one day. It was acute in onset and gradually progressive. She became quickly hypotonic and hyporesponsive and had reduced level of consciousness. Within 12 hours of admission, the patient developed sphincter incontinence and dysphagia. After exclusion of papilloedema, lumbar puncture has been performed. An urgent MRI was performed, which showed multiple subcortical lesions of varying size showing hyperintensities in TR at the bridge and in T2 at the medulla . Cerebrospinal fluid (CSF) study showed cell count of 40 cells/mm3 , protein 58 mg/dL, glucose 54 mg/dL. No oligoclonal bands were present in CSF. Blood and CSF cultures were negative like other infectiological analyzes. Also CSF-PCR for the presence of bacteria and virus was negative. Her autoimmune profile with antinuclear antibody was also negative. The clinical features and the MRI findings were suggestive of ADEM. Partial quadriplegia, and reduction of reflexes, as seen in the myelitic form of ADEM, were present. She had developed ADEM while on the maintenance dose of prednisolone. After diagnosis, intravenous methylprednisolone was given at 30 mg/kg daily for 5 days. After 48 hours there was a significant improvement in the patient‘s clinical condition. A regimen of oral steroid was advised after intravenous therapy . The patient responded well to steroid therapy. No residual lesion was found on follow-up. AT and AHA are relatively uncommone. There are studies postulating the possibility of a combination of several autoimmune diseases. Very few cases have been found with this rare association in the literature. Follow-up of these patients is essential for detecting the development of other autoimmune disease in such cases.

BACKGROUND Cystinuria is an inherited autosomal recessive disorder, characterised by the impaired reabsorbtion of cystine, lysine, ornithine and arginine in the proximal tubule with an increased urinary excretion, resulting in a risk of renal stone formation because of the low solubility of cystine in urine. The estimated rate is 1:15000–20000 live births. This disease is caused by mutations of the genes SLC3A1 (2 P21) and/or SLC7A9 (19q13.11), encoding heavy subunit of a transepithelial dibasic aminoacid transport protein, responsible of type A and B, respectively. The main goal of the treatment is to prevent the recurrent urinary stone formation, and it’s based on hydration therapy, urine alkalinization and cystine chelating drugs. When medical treatment is ineffective, surgery should be considered. CASE REPORT An 8 years old girl was referred to our hospital for recent UTI and low back pain on both sides. Renal ultrasound showed kidney stones on both sides and a grade II of hydronephrosis on the right. A metabolic alkalosis and a low urinary excretion of citrate were discovered. Investigations revealed urinary levels of cystine (418 mmol/molcreat U), lisine, arginine and ornithine upper normal range. The patient has been treated with potassium citrate, antibiotic and hiperhydration. By a molecular analysis a compound heterozygosity for a mutation of the gene SLC3A1 was discovered. Both parents were asymptomatic heterozygous carriers of the same mutation. In a long-term follow up a clinical improvement was assessed, in fact the low back pain disappeared. In addition in different occasions, an urine alkalinization was documented, while the levels of urinary cystine were still high. For this reasons, the patient started the treatment with tiopronin. Conclution Frequent clinical, laboratory tests and ultrasound follow-up is needed to encourage patient compliance and assess efficacy and tolerance of treatment. If there is not an improvement, a cysteine chelation treatment should be evaluated, despite its side effects, or surgery if medical treatment is ineffective.