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Dimitra Stathi Department of Endocrinology and Diabetes, Guy’s and St Thomas’ NHS Trust, London, UK
School of Cardiovascular Medicine & Sciences, King's College London, London, UK

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Sufyan Hussain Department of Endocrinology and Diabetes, Guy’s and St Thomas’ NHS Trust, London, UK

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Danielle Crawley Department of Oncology, Guy’s and St Thomas’ NHS Trust, London, UK

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Janaka Karalliedde Department of Endocrinology and Diabetes, Guy’s and St Thomas’ NHS Trust, London, UK
School of Cardiovascular Medicine & Sciences, King's College London, London, UK

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Summary

A Caucasian man in his 60s with recent diagnosis of metastatic renal cell carcinoma presented to the emergency department with a 5-day history of severe polyuria, polydipsia and fatigue and 1-day history of confusion, abdominal pain, nausea and vomiting. Investigations revealed an overlap of diabetic ketoacidosis (DKA) and hyperosmolar hyperglycaemic state (HHS). He had received the first dose of immunotherapy with nivolumab and ipilimumab 3 weeks prior to this attendance. New-onset type 1 diabetes (T1DM) was confirmed based on the clinical features at presentation, seropositivity for glutamic acid decarboxylase antibodies and significant insulin deficiency. He is currently on a multiple daily injections of insulin and uses intermittent-scanned glucose monitoring. Given the irreversible impact on beta-cell function and clinical response with insulin resulting in improved diabetes control, immunotherapy was resumed for his metastatic cancer with good radiological response. Although rare, new-onset T1DM can present with DKA and HSS overlap after a single dose of nivolumab/ipilimumab in individuals without pre-existing history of diabetes.

Learning points

  • Although rare, new onset of T1DM after immunotherapy can present with DKA and HSS overlap after a single dose of nivolumab/ipilimumab in individuals without pre-existing history of diabetes and normal glycaemic parameters.

  • Due to the irreversible destruction of beta-cells, treatment with steroids is not indicated in contrast to other settings such as immunotherapy-induced hypophysitis.

  • Presence of low c-peptide levels post-acute presentation is indicative of an irreversible impact on beta-cell function and supports resuming immunotherapy given the significant benefits on cancer prognosis.

  • Clinicians must maintain a high index of suspicion in regards to diagnosis and management of new-onset type 1 diabetes and advice patients on reporting symptoms suggestive of diabetes and/or diabetes-related hyperglycaemic emergencies.

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Sophie Bondje Lister Hospital, Stevenage, UK

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Camilla Barnes Lister Hospital, Stevenage, UK

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Felicity Kaplan Lister Hospital, Stevenage, UK

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Summary

Milk–alkali syndrome (MAS) is a triad of hypercalcaemia, metabolic alkalosis and renal insufficiency. In this study, we present a case of milk–alkali syndrome secondary to concurrent use of over-the-counter (OTC) calcium carbonate-containing antacid tablets (Rennie®) for dyspepsia and calcium carbonate with vitamin D3 (Adcal D3) for osteoporosis. A 72-year-old woman presented with a 2-day history of nausea, vomiting, epigastric pain, constipation, lethargy and mild delirium. Past medical history included osteoporosis treated with daily Adcal D3. Initial blood tests showed elevated serum-adjusted calcium of 3.77 mmol/L (normal range, 2.2–2.6) and creatinine of 292 µmol/L (45–84) from a baseline of 84. This was corrected with i.v. pamidronate and i.v. fluids. She developed asymptomatic hypocalcaemia and rebound hyperparathyroidism. Myeloma screen, vasculitis screen and serum angiotensin-converting enzyme (ACE) were normal, while the CT of the chest, abdomen and pelvis showed renal stones but no malignancy. A bone marrow biopsy showed no evidence of malignancy. Once the delirium resolved, we established that prior to admission, she had been excessively self-medicating with over-the-counter antacids (Rennie®) as required for epigastric pain. The increasing use of calcium preparations for the management of osteoporosis in addition to easily available OTC dyspepsia preparations has made MAS the third most common cause of hypercalcaemia hospitalisations. Educating patients and healthcare professionals on the risks associated with these seemingly safe medications is required. Appropriate warning labels on both calcium preparations used in the management of osteoporosis and OTC calcium-containing preparations would prevent further similar cases and unnecessary morbidity and hospital admission.

Learning points

What is known?

  • An association between high-dose calcium supplementation and hypercalcaemia crisis has been seen in case studies.

  • After as little as 1 week of excessive calcium carbonate ingestion, patients can present with symptomatic hypercalcemia, acute renal failure and metabolic alkalosis (1).

  • Women aged 50 and younger need 1 g of calcium per day, while aged 51 and older need 1.2 g (1).

  • Although the amount of calcium required for MAS is generally thought to be more than 4 g per day, there have been reports at intakes as low as 1.0–1.5 g per day in pre-existing risk factors including renal impairment (2).

What this study adds?

  • The danger of excessive ingestion of antacid is not adequately highlighted to prescribers and patients.

  • Appropriate warning labels on OTC calcium-containing preparations could prevent unnecessary morbidity and hospital admission.

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Ziad Hussein Department of Endocrinology, University College London Hospital, London, UK
Department of Medicine, University College London, London, UK

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Marta Korbonits William Harvey Research Institute, Barts and the London School of Medicine, Queen Mary University of London, London, UK

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Stephanie E Baldeweg Department of Endocrinology, University College London Hospital, London, UK
Department of Medicine, University College London, London, UK

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Teng-Teng Chung Department of Endocrinology, University College London Hospital, London, UK

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Summary

We observed a novel therapeutic response with cabergoline in a male patient with a dopamine-secreting head and neck paraganglioma (HNPGL), macroprolactinoma and germline succinate dehydrogenase C mutation (SDHC). The macroprolactinoma was treated with cabergoline which gave an excellent response. He was found to have raised plasma 3-methoxytyramine of 1014 pmol/L (NR: 0–180 pmol/L); but it was unclear if this was a drug-induced phenomenon from dopamine agonist (DA) therapy. Cabergoline was stopped for 4 weeks and the 3-methoxytyramine level increased significantly to 2185 pmol/L, suggesting a biochemical response of his HNPGL. Subsequently, Gallium-68 Dotatate PET and MRI (Gallium-68 Dotatate PET/MRI) demonstrated a second lesion in the sacrum. Both the HNPGL and metastatic sacral deposit received external beam radiotherapy with a good biochemical and radiological response.

Conclusion

Our case report highlights the rare potential of germline SDHC mutations causing metastatic paraganglioma and concurrent pituitary tumours. Cabergoline treatment may lower elevated 3-methoxytyramine levels and, therefore, mask the biochemical evidence of metastatic disease but also may have therapeutic relevance in dopamine-secreting pheochromocytomas/paragangliomas (PPGLs).

Learning points

  • Several neuroendocrine tumours (NETs) express dopamine D2 and D4 receptors. In this case report, cabergoline significantly reduced plasma 3-methoxytyramine level in a patient with functional HNPGL. Cabergoline might have therapeutic relevance in dopamine-secreting PPGLs.

  • Paragangliomas associated with SDHC mutation classically present with asymptomatic non-functional HNPGL and have rare metastatic potential.

  • The association of pheochromocytoma or paraganglioma and pituitary adenoma is now a well-described rare association (<1%), designated as the three P association. While the three P association is most commonly seen with succinate dehydrogenase B and D mutations, it has also been described in patients with SDHA and SDHC mutations.

  • Cabergoline treatment may lower elevated 3-methoxytyramine levels and mask the biochemical evidence of metastatic disease. Regular functional imaging with Gallium-68 Dotatate PET/MRI provides better evidence of metastatic disease.

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Eseoghene Ifie Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, Oxford, UK

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Samson O Oyibo Department of Endocrinology, Peterborough City Hospital, Peterborough, UK

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Hareesh Joshi Department of Endocrinology, Peterborough City Hospital, Peterborough, UK

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Olugbenro O Akintade Department of Elderly Care Medicine, Peterborough City Hospital, Peterborough, UK

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Summary

Iron (ferric carboxymaltose) infusion therapy is used to treat severe iron deficiency which is not responding to the first-line oral iron therapy. However, it can also cause severe renal wasting of phosphate resulting in severe hypophosphataemia in some patients. Despite the growing number of case reports, this side effect is not well known to healthcare professionals. The product labelling information sheet does mention that hypophosphataemia can be a side effect, but also says that this side effect is usually transient and asymptomatic. We report a challenging case of a patient who developed severe, symptomatic and prolonged hypophosphataemia after an intravenous iron infusion for severe iron deficiency.

Learning points:

  • Clinicians prescribing ferric carboxymaltose (Ferinject®) should be aware of the common side effect of hypophosphataemia, which could be mild, moderate or severe.

  • Patients receiving iron infusion should be educated concerning this potential side effect.

  • Pre-existing vitamin D deficiency, low calcium levels, low phosphate levels or raised parathyroid hormone levels may be risk factors, and these should be evaluated and corrected before administering intravenous iron.

  • Patients may require phosphate and vitamin D replacement along with monitoring for a long period after iron infusion-induced hypophosphataemia.

  • Every incident should be reported to the designated body so that the true prevalence and management thereof can be ascertained.

Open access
S F Wan Muhammad Hatta New Cross Hospital, Wolverhampton, UK
Faculty of Medicine, Universiti Teknologi MARA, Sungai Buloh Campus, 47000 Sungai Buloh, Selangor, Malaysia

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L Kandaswamy New Cross Hospital, Wolverhampton, UK

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C Gherman-Ciolac New Cross Hospital, Wolverhampton, UK

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J Mann New Cross Hospital, Wolverhampton, UK

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H N Buch New Cross Hospital, Wolverhampton, UK

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Summary

Myopathy is a well-known complication of hypercortisolism and commonly involves proximal lower-limb girdle. We report a rare case of Cushing’s syndrome in a 60-year-old female presenting with significant respiratory muscle weakness and respiratory failure. She had history of rheumatoid arthritis, primary biliary cirrhosis and primary hypothyroidism and presented with weight gain and increasing shortness of breath. Investigations confirmed a restrictive defect with impaired gas transfer but with no significant parenchymatous pulmonary disease. Respiratory muscle test confirmed weakness of respiratory muscles and diaphragm. Biochemical and radiological investigations confirmed hypercortisolaemia secondary to a left adrenal tumour. Following adrenalectomy her respiratory symptoms improved along with an objective improvement in the respiratory muscle strength, diaphragmatic movement and pulmonary function test.

Learning points:

  • Cushing’s syndrome can present in many ways, a high index of suspicion is required for its diagnosis, as often patients present with only few of the pathognomonic symptoms and signs of the syndrome.

  • Proximal lower-limb girdle myopathy is common in Cushing’s syndrome. Less often long-term exposure of excess glucocorticoid production can also affect other muscles including respiratory muscle and the diaphragm leading to progressive shortness of breath and even acute respiratory failure.

  • Treatment of Cushing’s myopathy involves treating the underlying cause that is hypercortisolism. Various medications have been suggested to hinder the development of GC-induced myopathy, but their effects are poorly analysed.

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Ploutarchos Tzoulis Department of Diabetes, The Whittington Hospital, Whittington Health NHS Trust, London, UK

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Richard W Corbett Department of Medicine, Imperial College London, London, UK

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Swarupini Ponnampalam Department of Diabetes, The Whittington Hospital, Whittington Health NHS Trust, London, UK

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Elly Baker Department of Diabetes, The Whittington Hospital, Whittington Health NHS Trust, London, UK

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Daniel Heaton Department of Diabetes, The Whittington Hospital, Whittington Health NHS Trust, London, UK

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Triada Doulgeraki Medical School, University of Athens, Athens, Greece

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Justin Stebbing Department of Surgery and Cancer, Imperial College London, London, UK

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Summary

Five days following the 3rd cycle of nivolumab, a monoclonal antibody, which acts as immune checkpoint inhibitor against the programmed cell death protein-1, for metastatic lung adenocarcinoma, a 56-year-old woman presented at the hospital critically ill. On admission, she had severe diabetic ketoacidosis (DKA), as evidenced by venous glucose of 47 mmol/L, blood ketones of 7.5 mmol/L, pH of 6.95 and bicarbonate of 6.6 mmol/L. She has had no personal or family history of diabetes mellitus (DM), while random venous glucose, measured 1 week prior to hospitalisation, was 6.1 mmol/L. On admission, her HbA1c was 8.2% and anti-GAD antibodies were 12 kIU/L (0–5 kU/L), while islet cell antibodies and serum C-peptide were undetectable. Nivolumab was recommenced without the development of other immune-mediated phenomena until 6 months later, when she developed hypothyroidism with TSH 18 U/L and low free T4. She remains insulin dependent and has required levothyroxine replacement, while she has maintained good radiological and clinical response to immunotherapy. This case is notable for the rapidity of onset and profound nature of DKA at presentation, which occurred two months following commencement of immunotherapy. Despite the association of nivolumab with immune-mediated endocrinopathies, only a very small number of patients developing type 1 DM has been reported to date. Patients should be closely monitored for hyperglycaemia and thyroid dysfunction prior to and periodically during immunotherapy.

Learning points:

  • Nivolumab can induce fulminant type 1 diabetes, resulting in DKA.

  • Nivolumab is frequently associated with thyroid dysfunction, mostly hypothyroidism.

  • Nivolumab-treated patients should be monitored regularly for hyperglycaemia and thyroid dysfunction.

  • Clinicians should be aware and warn patients of potential signs and symptoms of severe hyperglycaemia.

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Charlotte Boughton Endocrinology Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

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David Taylor Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

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Lea Ghataore Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

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Norman Taylor Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

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Benjamin C Whitelaw Endocrinology Department of Clinical Biochemistry (Viapath), King’s College Hospital NHS Foundation Trust, London, UK

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Summary

We describe severe hypokalaemia and hypertension due to a mineralocorticoid effect in a patient with myelodysplastic syndrome taking posaconazole as antifungal prophylaxis. Two distinct mechanisms due to posaconazole are identified: inhibition of 11β hydroxylase leading to the accumulation of the mineralocorticoid hormone 11-deoxycorticosterone (DOC) and secondly, inhibition of 11β hydroxysteroid dehydrogenase type 2 (11βHSD2), as demonstrated by an elevated serum cortisol-to-cortisone ratio. The effects were ameliorated by spironolactone. We also suggest that posaconazole may cause cortisol insufficiency. Patients taking posaconazole should therefore be monitored for hypokalaemia, hypertension and symptoms of hypocortisolaemia, at the onset of treatment and on a monthly basis. Treatment with mineralocorticoid antagonists (spironolactone or eplerenone), supplementation of glucocorticoids (e.g. hydrocortisone) or dose reduction or cessation of posaconazole should all be considered as management strategies.

Learning points:

  • Combined hypertension and hypokalaemia are suggestive of mineralocorticoid excess; further investigation is appropriate.

  • If serum aldosterone is suppressed, then further investigation to assess for an alternative mineralocorticoid is appropriate, potentially using urine steroid profiling and/or serum steroid panelling.

  • Posaconazole can cause both hypokalaemia and hypertension, and we propose that this is due to two mechanisms – both 11β hydroxylase inhibition and 11β HSD2 inhibition.

  • Posaconazole treatment may lead to cortisol insufficiency, which may require treatment; however, in this clinical case, the effect was mild.

  • First-line treatment of this presentation would likely be use of a mineralocorticoid antagonist.

  • Patients taking posaconazole should be monitored for hypertension and hypokalaemia on initiation and monthly thereafter.

Open access
Emilia Sbardella Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Oxford, UK
Department of Experimental Medicine, Sapienza University of Rome, Rome, Italy

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George Farah Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Oxford, UK

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Ahmed Fathelrahman Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Oxford, UK

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Simon Cudlip Department of Neurological Surgery

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Olaf Ansorge Department of Neuropathology, John Radcliffe Hospital, University of Oxford, Oxford, UK

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Niki Karavitaki Institute of Metabolism and Systems Research, University of Birmingham and Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partner, Birmingham, UK

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Ashley B Grossman Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Oxford, UK

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Summary

Pituitary adenomas are a common intracranial neoplasm, usually demonstrating a benign phenotype. They can be classified according to pathological, radiological or clinical behaviour as typical, atypical or carcinomas, invasive or noninvasive, and aggressive or nonaggressive. Prolactinomas account for 40–60% of all pituitary adenomas, with dopamine agonists representing the first-line treatment and surgery/radiotherapy reserved for drug intolerance/resistance or in neuro-ophthalmological emergencies. We present the case of a 62-year-old man with an apparently indolent prolactin-secreting macroadenoma managed with partial resection and initially showing a biochemical response to cabergoline. Five years later, the tumour became resistant to cabergoline, despite a substantial increase in dosage, showing rapid growth and causing worsening of vision. The patient then underwent two further transsphenoidal operations and continued on high-dose cabergoline; despite these interventions, the tumour continued enlarging and prolactin increased to 107 269 U/L. Histology of the third surgical specimen demonstrated features of aggressive behaviour (atypical adenoma with a high cell proliferation index) not present in the tumour removed at the first operation. Subsequently, he was referred for radiotherapy aiming to control tumour growth.

Learning points:

  • The development of secondary resistance to dopamine agonists (DAs) is a serious sign as it may be associated with de-differentiation of the prolactinoma and thus of aggressive or malignant transformation.

  • Significant de-differentiation of the adenoma documented on consecutive histologies suggests a possible transition to malignancy.

  • A combination of histological ‘alarm’ features associated with persistent growth and escape from DAs treatment in recurrent adenomas should alert clinicians and demands close follow-up.

  • A multidisciplinary approach by pathologists, endocrinologists and neurosurgeons is essential.

Open access
Nicola Tufton Bartshealth NHS Trust, St Bartholomew's Hospital, West Smithfield, London, EC1A 7BE, UK

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Nazhri Hashim Bartshealth NHS Trust, St Bartholomew's Hospital, West Smithfield, London, EC1A 7BE, UK

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Candy Sze Bartshealth NHS Trust, St Bartholomew's Hospital, West Smithfield, London, EC1A 7BE, UK

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Mona Waterhouse Bartshealth NHS Trust, St Bartholomew's Hospital, West Smithfield, London, EC1A 7BE, UK

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Summary

A 57-year-old female presented 17 days after treatment with radioactive iodine (RAI) for difficult-to-control hyperthyroidism. She was febrile, had a sinus tachycardia, and was clinically thyrotoxic. Her thyroid function tests showed a suppressed TSH <0.02 mU/l, with free thyroxine (FT4) >75 pmol/l and total triiodothyronine (TT3) 6.0 nmol/l. She was diagnosed with thyroid storm and was managed with i.v. fluids, propylthiouracil (PTU) 200 mg four times a day, prednisolone 30 mg once daily and propanolol 10 mg three times a day. She gradually improved over 2 weeks and was discharged home on PTU with β blockade. On clinic review 10 days later, it was noted that, although she was starting to feel better, she had grossly abnormal liver function (alanine transaminase (ALT) 852 U/l, bilirubin 46 μmol/l, alkaline phosphatase (ALP) 303 U/l, international normalized ratio (INR) 0.9, platelets 195×109/l). She was still mildly thyrotoxic (TSH <0.02 mU/l, FT4 31 pmol/l, TT3 1.3 nmol/l). She was diagnosed with acute hepatitis secondary to treatment with PTU. Ultrasound showed mild hepatic steatosis. PTU was stopped and she was managed with fluids and prednisolone 60 mg once daily and continued β blockade. Her liver function gradually improved over 10 days (bilirubin 9 μmol/l, ALT 164 U/l, ALP 195 U/l, INR 0.9, platelets 323×109/l) with conservative management and had normalised by clinic review 3 weeks later. This case highlights the potentially fatal, but rare, complications associated with both RAI and PTU, namely, thyroid storm and acute hepatitis respectively.

Learning points

  • Thyroid storm is an important, albeit rare, endocrinological emergency.

  • Thyroid storm following RAI treatment is extremely rare.

  • Management is with i.v. fluids, β blockade, anti-thyroid drugs and steroids.

  • High dose glucocorticoid steroids can block the peripheral conversion of T4 to active T3.

  • Liver dysfunction, acute hepatitis and potential hepatic failure are significant adverse drug reactions known to occur with PTU treatment. Supervising clinicians should be vigilant for evidence of this developing and intervene accordingly.

  • Clinicians need to be aware of possible interactions between regular paracetamol use and PTU in predisposing to liver impairment.

Open access
Anastasia Dimakopoulou
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Karunakaran Vithian Colchester Hospital University NHS Foundation Trust, Colchester, UK

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David Gannon Colchester Hospital University NHS Foundation Trust, Colchester, UK

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Allan Harkness Colchester Hospital University NHS Foundation Trust, Colchester, UK

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Summary

A 55-year-old female patient presented to the endocrine clinic with Grave's disease. She was initially treated with carbimazole. After an early relapse, a decision was made to proceed with radioactive iodine therapy. Four days after radioiodine administration, she presented to the emergency department with chest tightness and dyspnea due to heart failure. Biochemistry revealed thyrotoxicosis and significantly elevated Troponin-T. There was ST segment elevation on electrocardiography. However, coronary angiography was normal. Ventricular function was fully restored after 6 weeks of supportive medical management. A diagnosis of stress cardiomyopathy following radioactive iodine therapy was made. This is the second case reported in the literature so far to the best of our knowledge.

Learning points

  • Stress cardiomyopathy in the context of radiation thyroiditis is a rare complication following radioiodine therapy.

  • A degree of awareness is essential because the approach is multidisciplinary. Management is mainly supportive and cardiac dysfunction is completely reversible in most cases.

  • The pathogenesis of this condition remains unclear. Post-menopausal women and susceptible individuals appear to be pre-disposed.

Open access