Encephalitis as an initial presentation of type 2 amiodarone-induced thyrotoxicosis.

We report a case of a woman in her mid-20s presenting with encephalitis as the initial presentation of type 2 amiodarone-induced thyrotoxicosis (AIT). She was on amiodarone in view of a history of hypertrophic cardiomyopathy. Symptomatology included acute personality change and focal myoclonic jerks.Cerebrospinal fluid analysis showed a non-specific protein count elevation with negative microbiology, virology, autoimmune screen and onconeural antibodies. The electroencephalogram was consistent with a generalised cerebral dysrhythmia. An MRI of the head revealed symmetrical oedema within the motor cortices and a high T2 signal within the cerebellar dentate nuclei, with no restricted diffusion. Blood investigations confirmed thyrotoxicosis with negative antithyroid antibodies. She did not fulfil the criteria for a thyroid storm. Other possible causes of encephalitis were excluded.There was an excellent clinical, laboratory and radiological response to glucocorticoids, suggesting a diagnosis of steroid-responsive encephalitis secondary to type 2-AIT in the absence of a thyroid storm.

Bilateral adrenal and pulmonary haemorrhages as an initial presentation of polycythaemia vera.

We report a case of a man in his early 60s presenting with bilateral adrenal and pulmonary haemorrhages as an initial presentation of polycythaemia vera (PV). Symptomatology included severe compressive chest pain radiating to epigastrium, with unremarkable physical findings, parameters and ECG. Blood investigations showed an elevated haemoglobin (174 g/L, reference range (RR): 141-172g/L) and haematocrit (55.7%, RR: 40.4%-50.4%) levels.Cross-sectional imaging excluded aortic dissection, but imaging repeated 48 hours after his admission for acute dyspnoea and worsening abdominal pain showed bilateral alveolar and adrenal haemorrhages. Cortisol level was 27 nmol/L (RR: 145-619 nmol/L). Investigations confirming PV included the presence of a Janus kinase 2 (JAK2V617F) gene mutation, hypercellularity with erythroid hyperplasia on bone marrow microscopy and a low serum erythropoietin (2.6 mIU/mL, RR: 4.3-29.0 mIU/mL). Aspirin, hydroxyurea, venesection and cortisol replacement were initiated to get good treatment outcome.

Outcomes of endovascular treatment for acute ischaemic stroke in Mater Dei Hospital, Malta.

INTRODUCTION: The aim of this study was to assess the outcomes of endovascular treatment for acute ischaemic stroke in Mater Dei Hospital, Malta and compare them with international data. METHODS: A prospective review of all patients who underwent mechanical thrombectomy from 2015 to the end of 2019 was performed. Eligible patients had large vessel occlusion confirmed on computed tomography angiography. Demographical data, the National Institutes of Health stroke scale at presentation, endovascular procedure details and process times were analysed. The thrombolysis in cerebral infarction score was used to assess the degree of reperfusion. A thrombolysis in cerebral infarction score of 2b-3 was considered as successful recanalisation. Functional outcome (modified Rankin scale score) and mortality at 90 days were measured. Functional independence was defined as a modified Rankin scale score of 2 or less. RESULTS: A total of 132 patients underwent endovascular treatment, one patient was excluded due to incomplete data. The mean age was 71 (range 25-94) years, and the mean National Institutes of Health stroke scale at presentation was 14. Of the 131 patients treated, 69 received intravenous thrombolysis. Successful recanalisation (thrombolysis in cerebral infarction score 2b-3) was achieved in 80% of patients (105/131); 53% of patients (69/131) achieved functional independence at 90 days, with a mortality of 21% at 90 days. Symptomatic intracranial haemorrhage was recorded in 16 patients (12%) There was a statistical difference in the functional independence and mortality rate in favour of the successful recanalisation group. CONCLUSION: Our data are consistent with a favourable clinical outcome after successful recanalisation. Service in Malta is achieving favourable outcomes for patients treated with mechanical thrombectomy for acute ischaemic stroke.

Lithium-associated hyperparathyroidism.

Lithium is a mood stabiliser widely used in the treatment and prophylaxis of mania, bipolar disorders and recurrent depression. Treatment with lithium can give rise to various endocrine and metabolic abnormalities, including thyroid dysfunction, nephrogenic diabetes insipidus and hypercalcaemia. Lithium may induce hypercalcaemia through both acute and chronic effects. The initial acute effects are potentially reversible and occur as a result of lithium's action on the calcium-sensing receptor pathway and glycogen synthase kinase 3, giving rise to a biochemical picture similar to that seen in familial hypocalciuric hypercalcaemia. In the long term, chronic lithium therapy leads to permanent changes within the parathyroid glands by either unmasking hyperparathyroidism in patients with a subclinical parathyroid adenoma or possibly by initiating multiglandular hyperparathyroidism. The latter biochemical picture is identical to that of primary hyperparathyroidism. Lithium-associated hyperparathyroidism, especially in patients on chronic lithium therapy, is associated with increased morbidity. Hence, regular monitoring of calcium levels in patients on lithium therapy is of paramount importance as early recognition of lithium-associated hyperparathyroidism can improve outcomes. This review focuses on the definition, pathophysiology, presentation, investigations and management of lithium-associated hyperparathyroidism.