Delayed diagnosis of severe secondary hypothyroidism in a patient presenting with mixed hyperlipidaemia and a metabolic myositisA 51 year old South Asian woman was referred by her GP to the outpatient endocrine clinic with diffuse musculosksletal pains in her lower limbs, lethargy and weight gain in the context of a previous hemithyroidectomy
Social historyWorks in customer services 2 school-age children
Further history of presenting complaintFurther history revealed intermittent pains in both lower limbs for several months; primarily left knee and right ankle. This was associated with 5kg of unintentional weight gain.. The patient also had a new diagnosis with hypercholesterolaemia from her GP 9 months ago that was being managed with lifestyle interventions in the first instance. She reported feeling increasingly lethargic for many months but this hasn't affected her ability to undertake her job or activities of daily living
Diagnosis and managementDiagnosis: Panhypopituitarism with a metabolic myositis and dyslipidaemia Commenced on thyroid hormone replacement which was subsequently uptitrated to 100 micrograms per day and hydrocortisone replacement therapy (10mg, 5mg, 5mg)Over the following 9-12 months there was almost a complete resolution of the metabolic myositis and dyslipidaemia as shown on the graphs below Subsequently, the patient experienced exertional chest pains prompting a cardiology referral. Work-up has revealed stenosis within the LAD awaiting percutaneous intervention.
Hypothyroid myositis Hypothyroid dyslipidaemia TSH and T4 -paired testingThis patient demonstrates a mild hypothyroid myositis with gradual normalisation of CK upon initiation of exogenous thyroid hormone. Musculoskeletal complaints are very common in patients with hypothyroidism; up to 79% as reported by Duyff and colleagues in a prospective cohort study although only 38% had clinical signs of weakness.[1] Elevation of serum CK is also common in hypothyroidism with between 37%-60% having values above the upper limit of the reference range [2]. There is a poor correlation between the extent of the rise of the CK and clinical symptomology (both subjective and objective). Generally, a CK >10 times the upper limit of normal (~2000iU/L) is thought to be of clinical significance and warrant further investigation or therapy rather than just monitoring. Without a clear aetiology for the hyperCKaemia a serum TSH would always be advised to screen for thyroid dysfunction.The pathophysiology underlying the muscle changes in hypothyroidism are well documented. Lack of bioavailable T3 leads to intracellular changes in glycogen metabolism and oxidative phosphorylation and alterations of the actin-myosin unit. Ultrastructurally changes are also seen in the membrane permeability of myocytes leading to increased enzymatic release. [2] Dyslipidaemia is a common abnormality in patients with thyroid disease. It is the end result of thyroid hormones playing a role in multiple aspects of lipid metabolism including synthesis, mobilisation and degrada...