ABSTRACT
Aim: To present a case of acromegaly with coexisting thyrotoxicosis and to emphasize the relevance of screening the screening the thyroid before initiating treatment for thyrotoxicosis. Presentation of the Case: A 55-year-old lady presented with palpitations, and weight loss of two months’ duration. She also noted her fingers and toes had swollen up, inability to incise properly since two years. Upon examination, she had morphological features clinically diagnostic of acromegaly. Her thyroid was enlarged was on investigation found to have biochemical evidence of thyrotoxicosis. Fine needle aspiration cytology of the thyroid yielded colloid goiter. Insulin like growth factor-1 was elevated. Serum growth hormone after an oral glucose tolerance test was elevated. Magnetic resonant imaging (MRI) of the brain revealed a hypo enhancing focal lesion of size 11X10X12 mm at the pituitary region with delayed contrast enhancement suggestive of pituitary adenoma. Patient was started on anti-thyroid medications and referred to higher centre, and is awaiting surgery for pituitary adenoma. Discussion: Among patients with acromegaly the incidence of thyroid diseases is around 78% and it has the most common presentation being nodular thyroid disease as the initial presentation. It is uncommon to see patients presenting with symptoms of thyrotoxicosis initially, who had florid morphological features of acromegaly. The prevalence of toxic nodular goiter to the tune of 14.3% in acromegaly. Goiters seen in acromegaly were euthyroid or autonomous, are due to the elevated growth hormone levels independent of TSH action. In about 13 to 17%, thyroidectomies were performed before acromegaly was diagnosed. When patients with acromegaly presents with a weight loss should arouse the possibilities of thyroid cancer or hyperthyroidism. Conclusion: Screening the thyroid is important, as inadvertent thyroidectomies were performed before acromegaly was diagnosed. When acromegaly co-exists with thyroid dysfunction, the burden of cardiovascular abnormality should be addressed especially, to reduce the morbidity and mortality rate.
ABSTRACT
Aim: Our aim is to present a case of hypernatremia which has led on to a flaccid quadriparesis due to brain stem demyelination. Rapid correction of hypernatremia as a cause for pyramidal tract demyelination is not documented in the literature. Presentation of Case: A 53 year old male was brought to the emergency services with suspected stroke. He was treated with intravenous mannitol and oral glycerine from the primary health centre. We detected hypoglycemia (blood sugarwas 50mg/dl-Ref range: ≤70mg%) and dextrose was given intravenously. Subsequently the patient went into a hypernatremic state with serum sodium 170milli equivalents /liter which was corrected rapidly. This was corrected over 48 hours to 140milli equalents/litre. The rate of correction exceeded 0.62millimols/liter/hour (Ideal: 0.5 mmol/L/h). On the 6th day the patient developed acute quadriparesis. Magnetic resonance imaging (MRI) of brain revealed bilateral symmetric demyelination of the corticospinal tracts. Over six months the neurological deficit improved with complete resolution of the changes in previous Discussion: Osmotic Demyelination Syndrome (ODS) has been a recognized complication of rapid correction of hyponatremia. Experiments in animals and clinical experience suggest that correction of chronic hyponatremia should be kept at a slow rate to combat this complication. The characteristic sites include pons and basal ganglia. Such a complication has not been described due to rapid correction of hypernatremia.This is probably the first case report in the literature where acute onset of quadriparesis resulted from demyelination of the pyramidal tract consequent to a rapid correction of hypernatremia. We had to wait about 6 months for the patient to obtain a complete functional recovery and the neuro imaging was repeated after 6 months to confirm the disappearance of the initial findings thus implicating rapid correction of hypernatremia as the cause of his morbidity. Conclusion: This is the first time extrapontine reversible myelinolysis due to rapid correction of hypernatremia has been documented. To prevent this potentially fatal complication it will be prudent if hypernatremia is corrected slowly.