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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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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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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.

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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