1.Beta Blocker-Induced Raynaud Phenomenon in a Case of Graves' Disease
Lui Tjun Yew ; Gerard Jason Mathews
Journal of the ASEAN Federation of Endocrine Societies 2026;41(S1):109-
Introduction:
Beta-blockers are frequently used as adjunctive therapy in
hyperthyroidism to manage adrenergic symptoms, yet their
potential to precipitate secondary Raynaud’s phenomenon
remains under-recognized. This adverse effect is attributed
to β2-adrenoceptor blockade, which impairs peripheral
vasodilation and promotes reflex vasoconstriction. Nonselective agents such as propranolol carry this particular risk.
Case:
A 22-year-old female presented with a 6-month history of
palpitations, 11 kg weight loss, and fine tremors. There was
no personal or family history of autoimmune or connective
tissue disease. She denied any malar rash, joint swelling,
alopecia, myopathy, oral ulcers, or uveitis. She also
denied using any supplements or any herbal or traditional
remedies. Examination revealed tachycardia, fine tremors,
and Graves’ ophthalmopathy, but no acropachy or
organomegaly. Investigations confirmed Graves’ disease:
Free T4 of 73 pmol/L, thyroid-stimulating hormone <0.05
mIU/L, with elevated anti-thyroid peroxidase and antithyroglobulin antibodies. Full blood count, renal, and liver
function were unremarkable.
She was commenced on carbimazole 20 mg daily and
propranolol 40 mg three times daily. After 8 months
of treatment, she developed cold-induced digital color
changes and skin tightening consistently, suggestive of
Raynaud’s phenomenon. Dose reduction of propranolol to
20 mg BD only yielded partial improvement. Propranolol
was subsequently substituted with verapamil, a nondihydropyridine calcium channel blocker, resulting in
significant resolution of Raynaud’s phenomenon.
Conclusion
Propranolol-induced Raynaud’s phenomenon is an underrecognized complication in the management of Graves’
disease, and this case illustrates that it may develop
insidiously after months of therapy and can persist despite
dose reduction. Substitution with verapamil achieves rate
control without β2-adrenergic antagonism. Clinicians
should maintain a low threshold for recognizing this adverse
effect and consider early substitution with verapamil in
affected patients. While verapamil does not confer the
same adrenergic blockade as propranolol, its vasodilatory
properties make it a rational and effective alternative in
this context.
Raynaud Disease
;
Graves Disease


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