Diagnosis and Treatment > Signs and Symptoms
Search for other papers by Frank Gao in
Google Scholar
PubMed
Search for other papers by Stephen Hall in
Google Scholar
PubMed
Department of Medicine (Alfred), Monash University, Melbourne, Australia
Search for other papers by Leon A Bach in
Google Scholar
PubMed
Summary
Sodium/glucose co-transporter 2 (SGLT2) inhibitors are novel oral hypoglycaemic agents that are increasingly used in the management of type 2 diabetes mellitus (T2DM). They are now recommended as second-line pharmacotherapy (in conjunction with metformin) in patients with type 2 diabetes and established atherosclerotic heart disease, heart failure or chronic kidney disease due to their favourable effects on cardiovascular and renal outcomes. We report a case of a 69-year-old man who developed muscle pain, weakness and wasting after commencing the SGLT2 inhibitor empagliflozin. This persisted for 1 year before he underwent resistance testing, which confirmed muscle weakness. His symptoms resolved within weeks of ceasing empagliflozin, with improvement in muscle strength on clinical assessment and resistance testing and reversal of MRI changes. No other cause of myopathy was identified clinically, on biochemical assessment or imaging, suggesting that empagliflozin was the cause of his myopathy.
Learning points:
-
Empagliflozin, a commonly used SGLT2 inhibitor, was associated with myopathy.
-
A high degree of suspicion is required to diagnose drug-induced myopathy, with a temporal relationship between starting the medication and symptom onset being the main indicator.
-
Recognition of drug-induced myopathy is essential, as discontinuation of the offending drug typically improves symptoms.
Search for other papers by Ayanthi A Wijewardene in
Google Scholar
PubMed
Kolling Institute of Medical Research
Sydney Medical School, University of Sydney, Sydney, Australia
Search for other papers by Sarah J Glastras in
Google Scholar
PubMed
Sydney Medical School, University of Sydney, Sydney, Australia
Search for other papers by Diana L Learoyd in
Google Scholar
PubMed
Sydney Medical School, University of Sydney, Sydney, Australia
Search for other papers by Bruce G Robinson in
Google Scholar
PubMed
Sydney Medical School, University of Sydney, Sydney, Australia
Search for other papers by Venessa H M Tsang in
Google Scholar
PubMed
Summary
Medullary thyroid cancer (MTC) is a rare neuroendocrine tumour that originates from the parafollicular cells of the thyroid gland. The most common presentation of MTC is with a single nodule; however, by the time of diagnosis, most have spread to the surrounding cervical lymph nodes. Cushing’s syndrome is a rare complication of MTC and is due to ectopic adrenocorticotrophic hormone (ACTH) secretion by tumour cells. Cushing’s syndrome presents a challenging diagnostic and management issue in patients with MTC. Tyrosine kinase inhibitors (TKI) previously used for the management of metastatic MTC have become an important therapeutic option for the management of ectopic ACTH in metastatic MTC. The article describes three cases of ectopic ACTH secretion in MTC and addresses the significant diagnostic and management challenges related to Cushing’s syndrome in metastatic MTC.
Learning points:
-
Medullary thyroid cancer (MTC) is a rare neuroendocrine tumour.
-
Cushing’s syndrome is a rare complication of MTC that has a significant impact on patients’ morbidity and mortality.
-
Tyrosine kinase inhibitors (TKI) provide an important therapeutic option for the management of ectopic ACTH in metastatic MTC.
