ENDOCRINE TUMOURS: Thyrotropin-secreting pituitary adenoma: a structured review of 535 adult cases.

BACKGROUND AND AIMS: Thyrotropin-secreting pituitary adenomas (TSHomas) are a rare entity, occurring in one per million people. We performed a systematic review of 535 adult cases summarizing the clinical, biochemical, hormonal and radiological characteristics of TSHoma. Furthermore, we discussed the current guidelines for diagnosis and treatment. METHODS: A structured research was conducted using Pubmed and Web of Science with the following MeSH terms: 'thyrotropin secreting pituitary adenoma' OR 'TSHoma' OR 'thyrotropinoma.' RESULTS: Our analysis included 535 cases originating from 18 case series, 5 cohort studies and 91 case reports. The mean age at diagnosis was 46 years. At presentation, 75% had symptoms of hyperthyroidism, 55.5% presented with a goitre and 24.9% had visual field defects. The median TSH at diagnosis was 5.16 (3.20-7.43) mU/L with a mean FT4 of 41.5 ± 15.3 pmol/L. The majority (76.9%) of the TSHomas were macroadenoma. Plurihormonality was seen in 37.4% of the adenoma with a higher incidence in macroadenoma. Surgical resection of the adenoma was performed in 87.7% of patients of which 33.5% had residual pituitary adenoma. Post-operative treatment with a somatostatin analogue (SSA) led to a stable disease in 81.3% of the cases with residual tumour. We noticed a significant correlation between the diameter of the adenoma and residual pituitary adenoma (r = 0.490, P < 0.001). However, in patients preoperatively treated with an SSA, this correlation was absent. CONCLUSION: TSHomas are a rare cause of hyperthyroidism and are frequently misdiagnosed. Based on our structured analysis of case series, cohort studies and case reports, we conclude that the majority of TSHomas are macroadenoma being diagnosed in the fifth to sixth decade of life and presenting with symptoms of hyperthyroidism. Plurihormonalitiy is observed in one-third of TSHomas. Treatment consists of neurosurgical resection and SSA in case of surgical failure.

Misdiagnosis of Graves' hyperthyroidism due to therapeutic biotin intervention.

BACKGROUND: Lately, high dose of biotin is often given orally to patients with a primary progressive multiple sclerosis (PPMS). However, the molecule biotin is also a principle compound in various analytic immunoassays. CLINICAL CASE: An asymptomatic 60-year-old woman with PPMS on high dose of biotin therapy (3 × 100 mg/d) displayed abnormal thyroid function tests (TSH 0.02 mU/l, fT4 > 103 pmol/l, and fT3 > 46 pmol/l). TSH was determined by a homogeneous sandwich chemiluminescent immunoassay and fT4 and fT3 were both determined by a homogeneous, sequential, chemiluminescent immunoassay. TSH receptor antibodies were found to be markedly elevated (>40 IU/l) using a electrochemiluminescence immunoassay, suggestive for Graves' hyperthyroidism. Due to inconsistency between clinical presentation and laboratory results, thyroid function tests have been repeated with two other immunoassays. A direct, labeled antibody, competitive immunoassay to determine TSH and a luminescent immunometric immunoassay to determine fT4 and fT3 showed a subclinical hyperthyroidism (TSH < 0.02 mU/l, fT4 15.9 pmol/l, and fT3 4.7 pmol/l). Normal thyroid function tests (TSH 1.66 mU/l, fT4 15.3 pmol/l, and fT3 4.7 pmol/l) were obtained by a chemiluminescent microparticle immunoassay. All abnormal levels of TSH, fT4, fT3, and TSH-R-Ab were observed in immunoassays using biotin as a reagent. CONCLUSION: Abnormal thyroid function tests in this euthyroid patient were found to be false due to significant interference of supraphysiological levels of plasma biotin. Laboratory tests applying immunoassays using a biotin-containing reagent should be interpreted with caution in patients on biotin substitution.

An Intact Dopamine Sensitivity in the Brain: A Necessity to Recover Hyperprolactinemia and Galactorrhea in a Female Hemodialysis Patient?

A female hemodialysis patient with galactorrhea due to hyperprolactinemia was treated with different dialysis modalities to assess the effect on prolactin levels. A single session of both high-flux hemodialysis and hemodiafiltration resulted in decreased prolactin levels (16,6% and 77,2%, resp.). However, baseline prolactin levels measured immediately before the next dialysis session did not change markedly. After cabergoline treatment was started, prolactin levels normalized and galactorrhea disappeared. Thus, dopaminergic inhibition of prolactin secretion might be reduced in patients with end-stage renal disease. This dopaminergic resistance could be an important mechanism of hyperprolactinemia in hemodialysis patients and its subsequent treatment strategies.