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.

Thiazide diuretics and primary hyperparathyroidism.

Thiazide diuretics exert a natriuretic and diuretic effect by inhibiting sodium reabsorption in the distal convoluted tubule. Furthermore, thiazide diuretics affect renal calcium handling by increasing calcium reabsorption, leading to hypocalciuria. The effect that thiazide diuretics exert on parathyroid hormone secretion is controversial. Some studies found parathyroid hormone levels were suppressed with the use of thiazide diuretics, while others found that thiazides were associated with initial parathyroid hormone suppression followed by raised parathyroid hormone levels. This makes the relationship between thiazide diuretics and primary hyperparathyroidism interesting. If a patient is taking thiazide diuretics, this may make it harder to establish the aetiology of hypercalcaemia and may unmask normocalcaemic or mild primary hyperparathyroidism. Thiazide diuretics may have a beneficial role in the diagnosis of patients with concomitant hyperparathyroidism and hypercalciuria by distinguishing secondary hyperparathyroidism caused by hypercalciuria from normocalcaemic primary hyperparathyroidism. In addition, thiazide diuretics may have a role in managing patients with primary hyperparathyroidism who have an indication for parathyroidectomy in view of significant hypercalciuria, but are unfit for surgery.

Immobilisation hypercalcaemia.

Hypercalcaemia is a common metabolic abnormality and its differential diagnosis is vast. Immobility is an uncommon cause of hypercalcaemia. Immobilisation hypercalcaemia is independent of parathyroid hormone and is associated with low levels of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D. In addition, it is characterised by elevated levels of markers of bone resorption and low levels of bone-specific alkaline phosphatase, highlighting an imbalance of bone remodelling favouring osteoclastic bone resorption. Although immobilisation hypercalcaemia is a diagnosis of exclusion, physicians need to be aware of this condition to avoid excessive and invasive investigations when all other causes of parathyroid hormone-independent hypercalcaemia have been excluded. Management of immobilisation hypercalcaemia revolves around early mobilisation and rehabilitation together with pharmacotherapeutic agents such as intravenous isotonic saline, calcitonin and bisphosphonates. Denosumab may be a potential alternative yet off-label treatment for immobility hypercalcaemia in patients with renal insufficiency.

Adrenal insufficiency in HIV/AIDS: a review.

INTRODUCTION: Adrenal insufficiency (AI) is one of the most common potentially life-threatening endocrine complications in people living with human immunodeficiency virus (PLHIV) infection and acquired immunodeficiency syndrome (AIDS). AREAS COVERED: In this review, the authors explore the definitions of relative AI, primary AI, secondary AI and peripheral glucocorticoid resistance in PLHIV. It also focuses on the pathophysiology, etiology, diagnosis and management of this endocrinopathy in PLHIV. A literature review was conducted through Medline and Google Scholar search on the subject. EXPERT OPINION: Physicians need to be aware of the endocrinological implications of HIV infection and its treatment, especially CYP3A4 enzyme inhibitors. A high index of clinical suspicion is needed in the detection of AI, especially in PLHIV, as it may present insidiously with nonspecific signs and symptoms and may be potentially life threatening if left untreated. Patients with overt primary and secondary AI require glucocorticoid replacement therapy. Overt primary AI also necessitates mineralocorticoid replacement. On the other hand, the management of relative AI remains controversial. In order to reduce the risk of adrenal crisis during periods of stress, the short-term use of glucocorticoids may be necessary in relative AI.

Amiodarone-induced type 2 thyrotoxicosis.

The authors present a case of a 55-year-old gentleman with a medical history of atrial fibrillation on amiodarone who presented with weight loss, palpitations and exertional dyspnoea. Thyroid function tests revealed thyrotoxicosis with a free thyroxine (T4) of 117 pmol/L and a thyroid-stimulating hormone (TSH) of <0.008 mIU/L. Interleukin-6 level was low. The negative TSH-receptor antibody status, the presence of a small thyroid gland with heterogeneous echotexture and decreased internal vascularity on ultrasound together with the relatively quick drop in free T4 and free tri-iodothyronine (T3) levels once prednisolone therapy was added to carbimazole suggested that this was typical of amiodarone-induced thyrotoxicosis (AIT) type 2. Subsequently, carbimazole was discontinued and treatment with prednisolone was continued. This case highlights that AIT management may be challenging and it is of paramount importance to establish the type of AIT present as this will guide management and is key to improving prognosis.

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.

Paradoxical deterioration in seizure control due to anticonvulsant-induced hypocalcaemia.

Hepatic cytochrome P450 enzyme induction is associated with certain antiepileptic drugs (AEDs) and may result in hypocalcaemia secondary to vitamin D deficiency. We report a case of a 44-year-old man with a history of epilepsy, who presented with breakthrough seizures after having previously been seizure-free for 11 years. Investigations revealed severe hypocalcaemia with a corrected calcium of 1.7 mmol/L. His phenytoin dose was increased, and he was started on calcium supplementation. He was discharged with a corrected calcium level of 2.05 mmol/L but was readmitted 1 week later with further seizures and a corrected calcium of 1.89 mmol/L. 25-hydroxyvitamin D was low. AED-induced hypocalcaemia was suspected, which had been made paradoxically worse by the increase in phenytoin dose. Alfacalcidol was prescribed and he was switched from phenytoin to levetiracetam with resolution of hypocalcaemia and no further seizures. The authors recommend screening for calcium and vitamin D deficiency in patients on enzyme-inducing AEDs.

A case of severe relapsing sulphonylurea-induced hypoglycaemia.

The authors report a case of a 64-year-old woman who was diagnosed with severe relapsing sulphonylurea-induced hypoglycaemia. Sulphonylureas are frequently used in patients with type 2 diabetes mellitus. They promote insulin secretion independent of the prevailing glucose level and thus are associated with an increased risk of hypoglycaemia. In patients with adequate renal function, gliclazide's effect lasts 10-24 hours and it is usually completely eliminated within 144 hours postdose. Since our patient suffered from chronic kidney disease, gliclazide's effect was prolonged and she was experiencing spontaneous hypoglycaemic episodes up to 21 days postomission of gliclazide. This case highlights two important aspects. Primarily, the prolonged effect of sulphonylureas in patients with impaired renal function, hence highlighting the need to be cautious prior to prescribing sulphonylureas in such patients. Secondly, the importance of prolonged observation of patients on sulphonylureas even after the initial hypoglycaemic event is corrected, due to the extended effects of such drugs.

An unusual presentation of multiple myeloma.

The authors report a case of a 58-year-old woman, ex-smoker, who was referred to the respiratory clinic with a presumed unresolving airspace shadowing in the right lung. Further evaluation of the shadowing with a CT thorax revealed rib lesions, a pancreatic lesion and multiple liver lesions, making the diagnosis of metastatic pancreatic carcinoma most likely. However, further blood investigations and imaging eventually revealed the cause for the shadowing to be multiple myeloma, since the unresolving shadowing was actually a rib lesion.

Stress-induced hyperglycaemia.

Stress-induced hyperglycaemia is an important clinical entity. It is an adaptive immune-neurohormonal response to physiological stress in an attempt to increase metabolic substrates to struggling organs during a time of crisis. However, this acute hyperglycaemia is also responsible for a number of detrimental effects implying that treatment is necessary. Hence, admission hyperglycaemia is not necessarily equivalent to a diagnosis of diabetes mellitus but the blood glucose level needs to be interpreted in context of the patient's presenting complaint and previous glycaemic status. Stress-induced hyperglycaemia is associated with increased morbidity and short-term mortality. Thus prompt recognition of stress-induced hyperglycaemia and high risk hyperglycaemic patients with the stress hyperglycaemia ratio can help improve inpatient management. Patients with stress-induced hyperglycaemia who have recovered from their acute illness should be followed up as they remain at risk for incident diabetes. This review focuses on the definition, pathophysiology, targets, management and significance of stress-induced hyperglycaemia.

Influenza A: another cause of SIADH?

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a frequent cause of hyponatraemia. It is a dilutional hyponatraemia secondary to impaired urinary dilution in the absence of renal disease or any identifiable non-osmotic stimulus known to induce antidiuretic hormone secretion. SIADH can arise secondary to various respiratory tract infections; however, the association between SIADH and influenza A infection is described in only a few cases in the literature. The authors present a case report of influenza A that may have caused a profound SIADH-related hyponatraemia.

Beer, hyponatraemia and cardiac conduction defects.

The authors report a case of a 68-year-old man who was diagnosed with an irreversible second-degree atrioventricular (AV) Mobitz II 2:1 block temporally associated with profound hyponatraemia. The cause of the hyponatraemia was beer potomania. The co-occurrence of reversible first, second and third-degree heart blocks and hyponatraemia has been described in a few published case reports. However, this case is noteworthy as the AV block persisted, despite correction of serum sodium concentration as opposed to other published cases, which meant that the patient required a permanent pacemaker.

The non-resolving lung cavity: a case of pulmonary cystic echinococcosis.

The authors report a case of a 20-year-old woman who was diagnosed with pulmonary cystic echinococcosis. She was admitted to hospital with a 1-week history of unresolving cough, coloured sputum with occasional haemoptysis and fever despite oral antibiotics. Radiology revealed a cavitating right lower lobe lung abscess. After 4 weeks of treatment, follow-up radiology showed incomplete resolution. Bronchoscopy revealed a white, avascular cystic lesion in the right lower lobe and serology testing for Echinococcus granulosus was positive. Repeat imaging eventually confirmed the cystic lesion with the 'air bubble'sign. A thorough travel history, a high index of clinical suspicion and close follow-up are essential in making a diagnosis of pulmonary cystic echinococcosis.

Multifocal necrotising fasciitis and septic shock complicating varicella infection in an adult.

A 35-year-old woman with a 3-day history of chickenpox, presented to the hospital in septic shock and with multifocal, non-adjacent lesions of necrotising fasciitis. Necrotising fasciitis is a rare yet life-threatening complication of chickenpox. Blood cultures and wound swabs confirmed the presence of Streptococcus pyogenes. The initial emergency management included oxygen, aggressive fluid resuscitation and antimicrobial therapy. Once the patient was stabilised, surgical management ensued. This included debridement and eventual grafting of the necrotic skin lesions. Intensive management and follow-up for 8 weeks were required before the patient was deemed fit for discharge.