Factitious Graves' Disease Due to Biotin Immunoassay Interference-A Case and Review of the Literature.

CONTEXT: Biotin (vitamin B7) is an essential co-factor for four carboxylases involved in fatty acid metabolism, leucine degradation, and gluconeogenesis. The recommended daily intake (RDI) of biotin is approximately 30 µg per day. Low-moderate dose biotin is a common component of multivitamin preparations, and high-dose biotin (10 000 times RDI) has been reported to improve clinical outcomes and quality of life in patients with progressive multiple sclerosis. Biotin is also a component of immunoassays, and supplementation may cause interference in both thyroid and non-thyroid immunoassays. OBJECTIVE: To assess whether biotin ingestion caused abnormal thyroid function tests (TFTs) in a patient through assay interference. DESIGN: We report a patient with biotin-associated abnormal TFTs and a systematic review of the literature. SETTING: A tertiary endocrine service in Hamilton, New Zealand. RESULTS: The patient had markedly abnormal TFTs that did not match the clinical context. After biotin cessation, TFTs normalized far more rapidly than possible given the half-life of T4, consistent with assay interference by biotin. Multiple other analytes also tested abnormal in the presence of biotin. CONCLUSION: Biotin ingested in moderate to high doses can cause immunoassay interference. Depending on the assay format, biotin interference can result in either falsely high or low values. Interference is not limited to thyroid tests and has the potential to affect a wide range of analytes. It is important for clinicians to be aware of this interaction to prevent misdiagnosis and inappropriate treatment.

Retrospective investigation of testosterone undecanoate depot for the long-term treatment of male hypogonadism in clinical practice.

INTRODUCTION: Testosterone undecanoate depot (TUD) administered intramuscularly is an effective form of testosterone replacement therapy (TRT) for male hypogonadism. Because of the ease of administration, TUD therapy may be preferable to subcutaneously implanted extended release T pellet implants (TI). AIM: The primary objective was to retrospectively assess the efficacy and safety of long-term (≥ 2 years therapy) TUD therapy in the clinical setting. The secondary objective was to retrospectively compare TUD with TI therapy. METHODS: Retrospective data were collected from the Waikato Hospital Endocrine Database for 179 hypogonadal men treated with TUD for ≥ 2 years from 1998-2011, with 124 of these men receiving previous TI therapy. MAIN OUTCOME MEASURES: The main outcome measure for efficacy was serum trough total testosterone (TT), and for safety an increase in hemoglobin (Hb) and/or hematocrit (Hct), rise in prostate-specific antigen (PSA) and/or prostatic biopsy and alteration in body mass index and lipid profile. Additional outcome measures were changes in the dosing and/or interval regimens for TUD therapy. RESULTS: Overall, 72% of trough TT levels were in the normal range for TUD therapy compared with 53% of trough TT levels during TI therapy. TUD therapy was well tolerated with 162 men (90.5%) completing 2 years of treatment, and only seven men (3.9%) stopping TUD because of adverse effects. A rise in Hb and/or Hct occurred in 25 men (14%), and a significant rise in PSA in 20 men (13%) at some stage during TUD therapy. At 2 years, 91% of men received the standard 1,000 mg TUD dose with 66% at the standard dosing interval of 10-14 weekly. CONCLUSIONS: TUD is an efficacious, safe, and well tolerated form of TRT, and individual optimisation of the dose and/or interval is only required in the minority of men. Particularly given the ease of administration, TUD was the preferred TRT for both patients and clinicians.

Investigating the pathways in primary practice leading to the diagnosis of central hypothyroidism.

AIM: Clinical diagnosis of central hypothyroidism is not always obvious: patients may live for years with symptoms. Endocrinologists and biochemists have suggested that a first-line TSH strategy will lead to avoidable delays in diagnosis and treatment of patients with central hypothyroidism. In order to improve timely diagnosis, and thus decrease morbidity from a treatable disease, this study aimed to investigate the diagnostic journey of patients with central hypothyroidism in the Waikato region of New Zealand. METHOD: A retrospective convenience sample seeking note review and semi-structured interviews were carried out with 16 patients who had a diagnosis of central hypothyroidism that was not caused by pituitary surgery or radiotherapy to the pituitary or hypothalamus. RESULTS: Seventy-five percent of participants had tests performed in general practice with results suggesting either pituitary disease or that further investigation would be required. In 38% (6/16) of participants diagnosis was made by the general practitioner. Time to diagnosis ranged from 3 months to more than 12 months. Seven participants identified having 3-6 visits to their general practitioner and five participants made 6 to 12 visits to their general practitioner prior to diagnosis. Lethargy was the most common symptom in 94% of participants. This was followed by changes in skin texture and body hair distribution and texture in 75% of participants and headaches in 63% of participants. CONCLUSION: Due to the era during which these patients were diagnosed, we did not find that a delay in diagnosis was due to an absence of FT4 requests; which a first-line TSH strategy would imply. It is important to recognise that a normal TSH does not exclude central hypothyroidism. By raising awareness with general practitioners of pituitary disease, with potential for deficiency of other anterior pituitary hormones, would focus more specific questioning on related symptoms.