Adrenal infarction in pregnancy is an extremely rare event. We report a case of a 29-year-old pregnant woman at the twenty-fourth week of gestation that presented with an acute episode of severe localized right upper quadrant pain. Her preliminary blood investigations and abdominal ultrasonography were essentially unremarkable. A diagnosis of right adrenal infarction was subsequently established on the basis of a non-enhanced swollen right adrenal gland on CT scanning of the abdomen with contrast, consistent with the clinical presentation. She was treated with subcutaneous low molecular weight heparin (LMWH) until 2 weeks postpartum. A thrombophilia screen post-partum revealed a significantly elevated factor VIII level and a hypercoagulable state that justified prolonged anticoagulation. This case highlights the importance of a high index of suspicion for adrenal infarction in pregnancy on the clinical grounds of otherwise unexplained acute abdominal pain accompanied by suggestive radiological findings, especially in the presence of thrombophilia.

Acute myocardial infarction (AMI) is usually seen in the setting of atherosclerosis and its associated risk factors. Myocardial infarction in the young poses a particular challenge, as the disease is less likely, due to atherosclerosis. We report the case of a 37-year-old female patient who presented with ST segment elevation anterolateral AMI. The only abnormality on routine blood investigation was raised hemoglobin and hematocrit. After further testing, she was diagnosed according to the World Health Organization (WHO) criteria with polycythemia vera. This case illustrates the importance of recognizing polycythemia vera as an important cause of thrombosis, which can present initially as AMI, and to emphasize the early recognition of the disease in order to initiate appropriate management strategies.

Summary Measurement of glycated haemoglobin (HbA1c) has been utilised in assessing long-term control of blood glucose in patients with diabetes, as well as diagnosing diabetes and identifying patients at increased risk of developing diabetes in the future. HbA1c reflects the level of blood glucose to which the erythrocyte has been exposed during its lifespan, and there are a number of clinical situations affecting the erythrocyte life span in which HbA1c values may be spuriously high or low and therefore not reflective of the true level of glucose control. In the present case series, we describe the particulars of three patients with diabetes who had spuriously low HbA1c levels as a result of dapsone usage. Furthermore, we discuss the limitations of HbA1c testing and the mechanisms by which it may be affected by dapsone in particular. Learning points: Various conditions and medications can result in falsely low HbA1c. Dapsone can lead to falsely low HbA1c by inducing haemolysis and by forming methaemoglobin. Capillary glucose measurement, urine glucose measurements and fructosamine levels should be used as alternatives to HbA1c for monitoring glycaemic control if it was falsely low or high.

A 25-year-old woman brought to the hospital with symptoms of acute confusion, disorientation, diplopia, hearing loss and unsteady gait which started 4 days prior to her presentation with rapid worsening in its course until the day of admission. She had a surgical history of laparoscopic sleeve gastrectomy 2 months earlier which was complicated by persistent vomiting around one to three times per day. She lost 30 kg of her weight over 2 months and was not compliant to vitamin supplementation. CT of the brain was unremarkable. Brain MRI was done which showed high signal intensity lesions involving the bilateral thalamic regions symmetrically with restricted diffusion on fluid-attenuated inversion recovery imaging. Other radiological investigations, such as magnetic resonance venography and magnetic resonance angiography of the brain were unremarkable. An official audiogram confirmed the sensorineural hearing loss. A diagnosis of Wernicke’s encephalopathy due to thiamin deficiency post-sleeve gastrectomy was made based on the constellation of her medical background, clinical presentation and further supported by the distinct MRI findings. Consequently, serum thiamin level was requested and intravenous thiamin 500 mg three times per day for six doses was started empirically, then thiamin 250 mg intravenously once daily given for 5 more days. Marked improvement in cognition, eye movements, strength and ambulation were noticed soon after therapy. She was maintained on a high caloric diet with calcium, magnesium oxide, vitamin D supplements and oral thiamin with successful recovery of the majority of her neurological function with normal cognition, strength, reflexes, ocular movements, but had minimal resolution of her hearing deficit. Serum thiamin level later was 36 nmol/L (67–200).

Background: Radioiodine (RAI) is widely used for the treatment of hyperthyroidism. Most patients respond to RAI therapy with a normalization of TFTs and improvement in clinical symptoms within 4-8 weeks. Hypothyroidism may occur from 4 weeks on, with 40% of patients being hypothyroid by 8 weeks and >80% by 16 weeks. American thyroid association guidelines recommend testing for free T4, total T3, and TSH within the first 1-2 months after RAI. Biochemical monitoring should be continued at 4- to 6-week intervals for 6 months, or until the patient becomes hypothyroid and stable on thyroid replacement therapy. Our local protocol is to monitor thyroid function more frequently and earlier, week 1,3,6,9,12,24 post RAI therapy to avoid any delay in starting treatment if required. Methods: 79 patients with hyperthyroidism underwent definiive treatment with RAI between January 2012 and June 2017. Monitoring of thyroid function tests were examined retrospectively to determine timing of initiation of treatment for either hypothyroidism or persistent hyperthyroidism post RAI. Results: Treatment started for both hypothyroidism and persistent hyperthyroidism in 47/79 patients, 41 developed hypothyroidism while 6 became hyperthyroid. 19/41 developed hypothyroidism within 9 weeks post RAI, while 9/41 developed hypothyroid within 3 weeks post RAI. Median time to commence treatment was 13.6 weeks. Conclusion: Frequent early monitoring of thyroid function tests post RAI may avoid delay in starting treatment for patients developing either hypo- or hyperthyroidism.

Background: RAI is used as definitive treatment for hyperthyroidism, but administered activities vary between institutions. We used a fixed activity of RAI therapy for Grave’s disease (GD) and toxic multinodular goitre (TMNG), and calculated activity for toxic adenoma (TA). We reviewed treatment outcomes at one year. Methods: Thyroid function tests 1 year post RAI were reviewed retrospectively to asess outcome for 79 hyperthyroid patients divided into 3 etiological groups: those with GD treated with 200MBq, TMNG treated with 400 MBq and TA treated with calculated activity (50-434 MBq), between January 2012 and June 2017. 24 hour isotope uptake results were examined retrospectively to assess relationship to clinical outcome. Results: 48/79 patients had GD (60.8%%), 16/79 TMNG (20.2%) and 15/79 TA (19%). Patients with GD were younger (median 46 years) compared to those with TMNG and TA (median 62 and 59 years respectively). There were more females in both groups (85.5% female in GD, 93.7% in TMNG and 83.3% in TA). At one year post-RAI, more patients with GD were rendered hypothyroid 28/48 compared to TMNG and TA (62.5% vs. 18.75% vs. 53.33%) and fewer patients with GD were rendered euthyroid (25% vs. 46.6% vs. 53.3%) or had persistent hyperthyroidism compared to those with TMNG/TA (12.5% vs. 0% vs. 0%). 12/28 patients with GD who developed hypothyroidism had 24 hour uptake >60% and all patients with 24 hour uptake >60% became hypothyroid in GD and TMNG groups. Conclusion: We used low activity RAI (200 MBq) as treatment for GD, an activity below international recommendations, with comparable outcomes and cure rate 87.5%. All patients with 24 hour uptake >60% in GD and TMNG group developed hypothyroidism post RAI indicating that lower activity RAI should be considered to reduce risk of hypothyroidism.

Neonatal diabetes (NDM) is defined as diabetes that occurs in the first 6 months of life, the majority of cases are due to sporadic mutations. ATP-sensitive potassium channels located in the beta cells of the pancreas play a major role in insulin secretion and blood glucose homeostasis. Mutations that alter the function of these channels may lead to NDM. We report a case of a 26-year-old Irish woman who was diagnosed with NDM at the age of 4 weeks and treated as type 1 diabetes mellitus, with multiple daily injections of insulin with suboptimal glycaemic control and frequent episodes of hypoglycaemic. She underwent genetic testing for NDM and was diagnosed with a KCNJ11 gene mutation. She was transitioned to high dose glibenclamide at the age of 16 years, but the trial failed due to poor glycaemic control and patient preference, and she was restarted on insulin. At 24 years of age, she was successfully transitioned from insulin (total daily dose 50 units) to high dose sulfonylurea (SU) (glibenclamide 15 mg twice daily). This resulted in optimal control of blood glucose (HbA1C fell from 63 to 44 mmol/mol), lower rates of hypoglycaemic and better quality of life. This case demonstrates that a second trial of SU in later life may be successful.

Hypothyroidism is a recognized side effect of thalidomide drugs. We herein report a case of 83-year-old Irish female with a diagnosis of multiple myeloma and a background history of type 2 diabetes mellitus and hypertension. Our patient received pomalidomide and multiple courses of chemotherapy and achieved very good initial response for her multiple myeloma but subsequently she relapsed. She did not have any past history of thyroid disease or family history of thyroid disorders. Prior to treatment with pomalidomide, her thyroid function test was completely normal. She was commenced on pomalidomide in February 2017. Four weeks post treatment, she presented with worsening fatigue, and as a part of her workup, a thyroid function test was performed. Her free T4 was low at 7.2 pmol/L (reference range: 9.0–20.0) while her TSH was elevated at 44.7 mIU/L (reference range: 0.35–4.94). Pomalidomide treatment was terminated, and she was commenced on thyroid hormonal therapy replacement therapy with thyroxine with good clinical and biochemical response. Practitioners prescribing pomalidomide should be aware of this potential complication and patients who are receiving immunomodulatory drugs like pomalidomide should undergo regular thyroid hormone levels screen.Learning points:Overt hypothyroidism is a side effect of pomalidomide.Thyroid function test should be included as a screening test with regular review in patients receiving pomalidomide.Unexplained worsening fatigue in patients receiving pomalidomide should raise the possibility of overt hypothyroidism.