Diagnosis and Treatment > Signs and Symptoms
Search for other papers by Sulaiman Haji Ali in
Google Scholar
PubMed
Search for other papers by K Aljenaee in
Google Scholar
PubMed
Search for other papers by W A Wan Mahmood in
Google Scholar
PubMed
University College Dublin, Dublin, Ireland
Search for other papers by M Hatunic in
Google Scholar
PubMed
Summary
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.
Search for other papers by Michael Dick in
Google Scholar
PubMed
Search for other papers by Sarah R Catford in
Google Scholar
PubMed
Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University, Clayton, Victoria, 3168, Australia
Search for other papers by Kavita Kumareswaran in
Google Scholar
PubMed
Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University, Clayton, Victoria, 3168, Australia
Search for other papers by Peter Shane Hamblin in
Google Scholar
PubMed
Department of Medicine, Faculty of Medicine, Nursing and Health Sciences, Alfred Hospital, Monash University, Clayton, Victoria, 3168, Australia
Search for other papers by Duncan J Topliss in
Google Scholar
PubMed
Summary
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur following traumatic brain injury (TBI), but is usually transient. There are very few case reports describing chronic SIADH and all resolved within 12 months, except for one case complicated by meningo-encephalitis. Persistent symptomatic hyponatremia due to chronic SIADH was present for 4 years following a TBI in a previously well 32-year-old man. Hyponatremia consistent with SIADH initially occurred in the immediate period following a high-speed motorbike accident in 2010. There were associated complications of post-traumatic amnesia and mild cognitive deficits. Normalization of serum sodium was achieved initially with fluid restriction. However, this was not sustained and he subsequently required a permanent 1.2 l restriction to maintain near normal sodium levels. Multiple episodes of acute symptomatic hyponatremia requiring hospitalization occurred over the following years when he repeatedly stopped the fluid restriction. Given the ongoing nature of his hyponatremia and difficulties complying with strict fluid restriction, demeclocycline was commenced in 2014. Normal sodium levels without fluid restriction have been maintained for 6 months since starting demeclocycline. This case illustrates an important long-term effect of TBI, the challenges of complying with permanent fluid restrictions and the potential role of demeclocycline in patients with chronic hyponatremia due to SIADH.
Learning points
-
Hyponatraemia due to SIADH commonly occurs after TBI, but is usually mild and transient.
-
Chronic hyponatraemia due to SIADH following TBI is a rare but important complication.
-
It likely results from damage to the pituitary stalk or posterior pituitary causing inappropriate non-osmotic hypersecretion of ADH.
-
First line management of SIADH is generally fluid restriction, but hypertonic saline may be required in severe cases. Adherence to long-term fluid restriction is challenging. Other options include oral urea, vasopressin receptor antagonists and demeclocycline.
-
While effective, oral urea is poorly tolerated and vasopressin receptor antagonists are currently not licensed for use in Australia or the USA beyond 30 days due to insufficient long-term safety data and specific concerns of hepatotoxicity.
-
Demeclocycline is an effective, well-tolerated and safe option for management of chronic hyponatraemia due to SIADH.
