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1.
Neuro Endocrinol Lett ; 37(1): 9-11, 2016.
Artículo en Inglés | MEDLINE | ID: mdl-26994379

RESUMEN

Pituitary apoplexy is a life-threatening illness due to acute infarction of the pituitary gland. The most common symptoms associated with pituitary apoplexy are headache, nausea, vomiting, visual impairment, hypopituitarism, and altered mental status. Diabetic ketoacidosis is a common acute complication of diabetes mellitus and is itself associated with similar symptoms. We present the case of a 38 year old woman, who presented with altered mental status and biochemical alterations suggestive of diabetic ketoacidosis who was found to have a pituitary apoplexy. The low frequency of this condition coupled with an acute and usually dramatic presentation that includes non-specific symptoms makes it a diagnostic challenge. Pituitary apoplexy can simulate a wide range of neurological conditions.


Asunto(s)
Cetoacidosis Diabética/diagnóstico , Apoplejia Hipofisaria/diagnóstico , Adulto , Diagnóstico Diferencial , Femenino , Humanos , Imagen por Resonancia Magnética , Obesidad/complicaciones
2.
Am J Med Sci ; 354(2): 165-171, 2017 08.
Artículo en Inglés | MEDLINE | ID: mdl-28864375

RESUMEN

BACKGROUND: Current evidence linking vitamin B12 deficiency with metformin use is inconsistent. Hence, there is uncertainty regarding the diagnostic approach in this scenario. Furthermore, this possible association has not been studied in the complete spectrum of patients with diabetes. MATERIALS AND METHODS: We conducted a cross-sectional, controlled study with the objective of assessing differences in serum vitamin B12 levels among patients with and without diabetes with different metformin-treatment regimens. A total of 150 participants were recruited: patients with diabetes (group 1: metformin alone ≥850mg/day, group 2: patients with type 2 diabetes naive to treatment and group 3: metformin ≥850mg/day, in addition to any other oral glucose lowering agent or insulin, or both) and without diabetes (group 4: polycystic ovary syndrome or group 5: healthy individuals). Serum vitamin B12, folate levels and complete blood counts were obtained for the entire population. Methylmalonic acid and homocysteine were obtained for patients when vitamin B12 levels were found to be borderline or low. RESULTS: When patients with or without diabetes were compared, no significant difference was found in relation to their vitamin B12 levels (517.62 versus 433.83; P = 0.072). No difference in vitamin B12 levels was found among participants with metformin use and metformin naive participants (503.4 versus 462.3; P = 0.380). CONCLUSIONS: Irrespective of metformin use, no significant difference in the serum levels of vitamin B12 was observed, both in patients with and without diabetes. In the light of the body of evidence and the results of this study, a universal recommendation for vitamin B12 deficiency screening cannot be made.


Asunto(s)
Hipoglucemiantes/efectos adversos , Metformina/efectos adversos , Deficiencia de Vitamina B 12/inducido químicamente , Adolescente , Adulto , Anciano , Estudios Transversales , Diabetes Mellitus Tipo 2/tratamiento farmacológico , Femenino , Humanos , Masculino , Metformina/uso terapéutico , Persona de Mediana Edad , Vitamina B 12/sangre , Deficiencia de Vitamina B 12/sangre , Adulto Joven
3.
Eur Endocrinol ; 12(2): 104-106, 2016 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-29632597

RESUMEN

Tumour-induced osteomalacia (TIO), is a rare paraneoplasatic syndrome found in >95% of benign tumours that secrete fibroblast growth factor 23 - a phosphaturic circulating hormone. A rare case of a TIO secondary to a sarcoma, in a 21-year old man with history of bone fractures and distinctive physical and biochemical characteristics is presented and discussed.

4.
Eur Endocrinol ; 11(2): 102-104, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-29632580

RESUMEN

The association of chronic tophaceous gout with severe hypercalcaemia is exceptional. In this case, a 42-year old man with a long-standing history of gout arrived at the emergency room with altered mental status. Laboratory work up revealed a uric acid of 14.0 mg/dl, corrected calcium of 14.5 mg/dl, phosphorous of 6.3 mg/dl, parathyroid hormone (PTH) was suppressed (<3.0 pg/ml), 25-dihydroxyvitamin D 25.2 ng/ml, parathyroid hormone related-protein (PTHrP) was 45.0 pg/ml and calcitriol 19.6 pg/ml. Biopsy histopathology result showed deposits of monosodium urate crystals surrounded by granulomatous inflammation. The association of chronic tophaceous gout with severe hypercalcaemia is extremely rare and has been usually described to be secondary to 1-25 dihydroxyvitamin D (calcitriol) secretion. In this case, calcitriol levels were normal and this possibility was excluded. On the other hand, PTHrP had never been, until now, described as the responsible cause of hypercalcaemia in gout. In our case, baseline PTHrP and calcium values were elevated and after medical treatment both returned to normal values. PTHrP usually causes hypophosphataemia and in this case the abnormal renal function could have diminished this last effect.

5.
Case Rep Neurol Med ; 2014: 652523, 2014.
Artículo en Inglés | MEDLINE | ID: mdl-25431711

RESUMEN

Osmotic demyelination syndrome (ODS) is a life-threatening demyelinating syndrome. The association of ODS with hyperosmolar hyperglycemic state (HHS) has been seldom reported. The aim of this study was to present and discuss previous cases and the pathophysiological mechanisms involved in ODS secondary to HHS. A 47-year-old man arrived to the emergency room due to generalized tonic-clonic seizures and altered mental status. The patient was lethargic and had a Glasgow coma scale of 11/15, muscle strength was 4/5 in both lower extremities, and deep tendon reflexes were diminished. Glucose was 838 mg/dL; serum sodium and venous blood gas analyses were normal. Urinary and plasma ketones were negative. Brain magnetic resonance revealed increased signal intensity on T2-weighted FLAIR images with restricted diffusion on the medulla and central pons. Supportive therapy was started and during the next 3 weeks the patient progressively regained consciousness and muscle strength and was able to feed himself. At 6-month follow-up, the patient was asymptomatic and MRI showed no residual damage. In conclusion, the association of ODS with HHS is extremely rare. The exact mechanism by which HHS produces ODS still needs to be elucidated, but we favor a rapid hypertonic insult as the most plausible mechanism.

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