The incidence of Addison’s disease (AD) is rare. One of the most common causes of AD in developed countries is autoimmune. On the other hand, in developing countries, infective causes still predominate. The symptoms are mostly insidious in onset and non-specific, making it challenging to diagnose AD. The delay in starting the right treatment predisposes to high mortality due to Addison’s crisis. Hence, biochemical parameters play a vital role in diagnosing AD since they usually will present with prominent hyponatraemia, hyperkalaemia and hypoglycaemia. Here, we report a case of a 66-year-old man with multiple co-morbidities and disseminated histoplasmosis who presented with asymptomatic hyponatraemia and hyperkalaemia and was eventually diagnosed with Addison’s disease. Although the non-specific symptoms from his multiple co-morbidities obscured the diagnosis of AD, comprehensive biochemical tests have helped in establishing the diagnosis.

Discordant TFT in Lupus Nephritis Patients: A Case Report and Comprehensive Literature Review The thyroid function test (TFT) is usually easy to interpret, but only if the clinical assessment, thyroid-stimulating hormone (TSH), and free-T4 (fT4) levels are consistent with each other. However, there are cases where TFT results are inconsistent, which may be due to assay interference. In this regard, we presented a case study of a patient with discordant TFT results which was likely caused by assay interference. A 43-year-old woman with underlying lupus nephritis for 20 years presented with painless anterior neck swelling over three years duration. Clinically, she was euthyroid without any symptoms of thyroid gland compression. A series of TFT was requested to rule out hyperthyroidism, showing low normal fT4 ranging between 9.83 - 12.76 pmol/L (9 - 19.05 pmol/L) with suppressed TSH of 0.05 - 0.18 μIU/ml (0.35 - 4.94 μIU/ml), biochemically consistent with subclinical hyperthyroidism. The reflex free-triiodothyronine (fT3) test was normal at 3.85 pmol/L (2.63-5.7pmol/L) with negative anti-thyroglobulin and anti-thyroperoxidase antibodies. A neck ultrasound revealed four insignificant thyroid nodules. No hyperthyroid treatment was commenced except prolonged steroid therapy and azathioprine for the underlying autoimmune disease. An initial clinical assumption was made that the TFT result might be possibly due to assay interference. The TFT results led to several differential diagnoses: subclinical hyperthyroidism, nonthyroidal illness (NTI), recent hyperthyroid treatment, drug, or assay interference (biotin, anti streptavidin antibodies, macro-TSH, anti-ruthenium antibodies, thyroid hormone autoantibodies, and heterophilic antibodies) . The patient’s normal fT3 ruled out NTI. Furthermore, the patient was not on any anti-hyperthyroid medications to explain it as the cause. Chronic glucocorticoid therapy reduces TSH secretion and inhibits thyroxine-binding globulin (TBG) synthesis, but steroids rarely result in thyroid dysfunction. Our laboratory method was a non-biotinylated chemiluminescent assay using the Abbott Allinity system, devoid of biotin-streptavidin interaction. The patient's results disagreed with other assay interference (macro-TSH, anti-ruthenium antibodies, thyroid hormone autoantibodies, and heterophilic antibodies), as they resulted in falsely high TSH and fT4 in most literature. Nonetheless, sample treatment with heterophile binding receptors can help to confirm further whether the patient's TFTs were consistent with true subclinical hyperthyroidism.