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1.
BMJ Case Rep ; 20142014 Mar 28.
Artículo en Inglés | MEDLINE | ID: mdl-24682140

RESUMEN

Central pontine myelinolysis (CPM), which is a component of the osmotic demyelination syndrome (ODS), is a frequent neurological complication that follows rapid correction of hyponatraemia. However, there are other predisposing risk factors (chronic alcoholism, hypokalaemia) that perpetuate the development of ODS. We report a case of a 39-year-old woman with a history of chronic alcoholism who presented to us with progressive neurological deficits (paraparesis, paresthesias). She was initially detected to have coexisting hypokalaemia which was eventually rectified with potassium supplementation. However, she continued to experience progressive worsening of her neurological symptoms despite adequate potassium supplementation. Therefore, a neurological opinion was sought for and she was diagnosed with CPM based on a background of chronic alcoholism and malnutrition; an MRI of the brain showed a hyperintense signal in the central pontine region. Following the diagnosis of CPM, she was rehabilitated with occupational and physiotherapy.


Asunto(s)
Alcoholismo/complicaciones , Mielinólisis Pontino Central/diagnóstico , Adulto , Femenino , Humanos , Hipopotasemia/complicaciones , Imagen por Resonancia Magnética , Desnutrición/complicaciones , Mielinólisis Pontino Central/etiología
2.
Indian J Endocrinol Metab ; 16(5): 840-2, 2012 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-23087879

RESUMEN

A 6 years male child was referred to our Endocrinology clinic with complaints of failure to thrive and he displayed the characteristic features of Russell Silver Syndrome which included short stature, relative macrocephaly, triangular facies and bilateral clinodactyly. He had a birth weight of 2.14 kg and an expected target height of 170 cm. He was subjected to a hormonal analysis which revealed a normal thyroid profile, but low serum markers of growth namely IGF-1=68 ng/ml (52-297 ng/ml) and basal growth hormone (GH) (1.5 µg/l). No defects were detected on MRI of the sella. Therefore a growth hormone stimulation test with Clonidine was performed which confirmed complete GH deficiency (at 0 min=0.16 µg/l, 60 min=0.27 µg/l, 120 min=4.73 µg/l). He was commenced on rhGH therapy at 8 years of age (height=102 cm, SDS=-4.53), due to financial restraints. Following initiation of GH therapy (1.5 IU/day) for 19 months, a height gain of 15 cm was obtained (Height=117 cm, SDS=-3.05). Bone age at 9 yr. was between 7-8 years.

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