scholarly journals A Rare Case of a Plurihormonal Pituitary Adenoma

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A565-A565
Author(s):  
Alisha Hossain ◽  
Emily Skutnik ◽  
Arjan Ahluwalia ◽  
Lindor Gelin ◽  
Sonum Singh ◽  
...  

Abstract Background: Pituitary adenomas are usually benign tumors that arise from adenophypophyseal cells and produce one or two types of hormones. Plurihormonal adenomas are a rare subtype that produce two or more hormones and represent less than 1% of all pituitary adenomas. Clinical Presentation: A 76-year-old female presented for evaluation of abnormal thyroid function test results. She was found to have an elevated free T4 of 1.92 ng/dL and total T4 of 14.4 ug/dL with an inappropriately normal TSH of 2.11 uIU/mL. Physical examination was significant for tachycardia, tremors, diaphoresis, coarse facial features, and enlarged hands. Further biochemical evaluation of her pituitary hormone levels demonstrated an elevated prolactin (PRL) of 237.2 ng/mL, elevated insulin-like growth factor 1 (IGF-1) of 787 ng/mL, normal morning ACTH of 47 pg/mL, normal morning cortisol of 17.0 ug/dL, an inappropriately suppressed FSH of <5.0 mIU/mL, an elevated alpha subunit of pituitary glycoprotein hormones (PGH) of 6.9 ng/mL, and an elevated free T4 of 3.5 ng/dL by equilibrium dialysis. She underwent an MRI of the pituitary and brain which demonstrated a pituitary adenoma measuring 1.2 x 1.3 x 1.8 cm with a portion herniating into the sella turcica with no mass effect of the optic chiasm. A formal visual field examination was normal. The patient underwent workup for Cushing’s Disease with a low dose overnight dexamethasone suppression test, resulting in an appropriate response with an 8 AM cortisol of <1.0 ug/dL. Glucose suppression test confirmed the diagnosis of acromegaly with growth hormone at 120 minutes of 19.90 ng/mL. Neurosurgery performed a trans-sphenoidal pituitary adenoma resection. Thyroid function tests on post-operative day 4 demonstrated a suppressed TSH of 0.01 uIU/mL and an elevated free T4 of 2.30 ng/dL. Histological evaluation revealed dual expression of transcription factors pituitary-specific positive transcription factor 1 (PIT1) and steroidogenic factor 1 (SF1) as well as PRL, GH, TSH and FSH expression. Immunostaining for LH and ACTH were negative. Post-operative IGF-1 and GH levels were 106 ng/mL and 0.51 ng/mL at 17 weeks, respectively. Post-operative TSH normalized to 0.82 uIU/mL, free T4 normalized to 1.04 ng/dL, and PRL normalized to 8.1 ng/mL at 12 weeks. The patient remained symptom free after successful surgical resection. Discussion: Our case demonstrates the clinical course of a unique patient with clinical and biochemical manifestations of thyroid dysfunction and acromegaly with a pituitary adenoma immunoreactive for GH, TSH, FSH, and PRL. The co-secretion of GH, TSH, PRL, and FSH as well as positivity for the alpha-subunit is extremely unusual. This case emphasizes the importance of considering pituitary abnormalities as a cause for abnormal thyroid function tests.

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Robert P McEvoy ◽  
Anthony O’Riordan ◽  
Mark J Hannon

Abstract The population attending the Medical Assessment Unit at our hospital comprises patients attending electively for investigation and acutely unwell patients presenting for unscheduled care. The standard panel of blood tests taken on arrival includes thyroid function tests (TFTs, i.e. TSH and free-T4), despite a recent review questioning the clinical utility of this practice [1]. We performed a retrospective audit to determine what proportion of our patients had abnormal thyroid function on presentation, and whether these abnormal test results were being followed up. Using the iSoft Clinical Manager software, a list was generated of all patients who attended the hospital between January 2018 and June 2018 inclusive. For each attendance, we recorded the date, medical record number, patient age, gender, and TFT result. Abnormal TFT results were classified as overt or subclinical hyper- or hypothyroid, or non-thyroid illness syndrome (NTIS), based on their admission TSH and free-T4. We then examined the hospital and primary care records of patients with abnormal TFTs to determine if they had ongoing thyroid follow up post discharge. In total, 2,298 patients attended over the 6-month study period. The mean patient age was 67.2 years, and 49% were female. Thyroid function tests were ordered on the day of attendance for 1,688 patients (73%). Of these, 181 results (11%) were abnormal: 20 overt hyperthyroid (11%), 72 subclinical hyperthyroid (40%), 12 overt hypothyroid (7%), 35 subclinical hypothyroid (19%), and 42 NTIS (23%). Twenty of these patients died within 3 months of the abnormal TFT result (4 overt hyperthyroid, 3 subclinical hyperthyroid, 3 overt hypothyroid, 6 subclinical hypothyroid, and 4 NTIS). Of the remaining 161 patients, 74 (46%) had not been followed up within 3 months (4 overt hyperthyroid, 34 subclinical hyperthyroid, 3 overt hypothyroid, 15 subclinical hypothyroid, and 18 NTIS). The low percentage of abnormal TFTs (11%) in this audit is in keeping with similar studies where thyroid function testing was performed on unselected hospital populations [1]. Subclinical hyperthyroidism was by far the most common abnormality found. A high percentage of abnormal tests (46%) were not followed up, with poor compliance with thyroid management guidelines [2]. Future work will investigate adoption of an ‘opt-in’ order system [3] and electronic alerts to flag abnormal results for follow-up. [1] Premawardhana LD. Thyroid testing in acutely ill patients may be an expensive distraction. Biochemia medica. 2017; 27(2): 300-307. [2] Ross DS et al. 2016 American Thyroid Association Guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016 Oct; 26(10):1343-1421. [3] Leis B et al. Altering standard admission order sets to promote clinical laboratory stewardship: a cohort quality improvement study. BMJ Qual Saf. 2019; 28(10): 846-52.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A940-A941
Author(s):  
Nyembezi Dhliwayo ◽  
Rana Wajahat ◽  
Andriy Havrylyan ◽  
Alvia Moid ◽  
Walid Khayr ◽  
...  

Abstract There is considerable evidence that some Borrelial (Lyme spirochetal) proteins share significant antigenic properties with several thyroid-related proteins (e.g. TSH receptor, thyroglobulin, thyroid peroxidase) and can induce thyroid autoimmunity, sometimes associated with Hashimoto’s thyroiditis and perhaps also a “destructive thyroiditis” such as “silent” thyroiditis or “Hashitoxicosis.” As an acute illness, Lyme disease may also constitute a “non-thyroidal illness” capable of perturbing thyroid function tests without causing thyroid dysfunction. We report a 22-year old woman admitted with an acute paranoid schizophrenia, thyroid function tests consistent with autoimmunity, transient thyrotoxicosis (tachycardia, lid-lag, brisk DTR’s) and a greatly reduced radioiodine uptake. The thyroid was not palpably enlarged, nodular or tender. On screening assay, reactivity was demonstrated to 4 of 13 Borrelial proteins. Anti-Lyme IgM but not IgG, antibodies, were positive. This was consistent with recent Lyme disease infection. Serum TSH (NL: 0.358-3.74 mcU/ml), Free T4 (NL: 0.76-1.46 ng/dl), and Free T3 (NL: 2.18-3.98 pg/ml) were, respectively: Day1: 0.087 mcU/ml (suppressed), 1.52 ng/dl (slightly elevated), 2.07 pg/ml (slightly reduced); Day2: 0.148 (suppressed), 1.18 (normal), no FT3; Day4: 0.827 (normal), no FT4 or FT3; Day5: 1.66 (normal), 0.89 (normal), 1.77 (low). Anti-Tg and Anti-Peroxidase antibodies were both moderately elevated. Thyroid Stimulating Immunoglobulins were not elevated. The radioactive iodine uptake on Day4 was 2.8% (NL: 15-30% at 24 hr). Thyroid ultrasonogram was normal. An attractive explanation is that Lyme disease triggered a “destructive thyroiditis,” perhaps but not necessarily mediated by thyroid autoimmunity. This would account for the brief interval of thyrotoxicosis accompanied by a very low radioiodine uptake. Alternatively, Lyme disease, as an acute process, would expectedly be capable of eliciting the thyroid function abnormalities of “non-thyroidal illnesses” in general, as would acute psychosis, well-known to often resemble Graves’ disease at admission.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Jorge Pedro ◽  
Vanessa Gorito ◽  
Cristina Ferreras ◽  
Ferreira João Silva Maria ◽  
Sofia Ferreira ◽  
...  

Abstract Background: Impaired sensitivity to thyroid hormone refers to any process that negatively affects its action, including defects in its transport, metabolism and action on the receptor. Resistance to thyroid hormone due to beta-receptor mutations (RTH-beta) is the most common form of this entity and is characterized by reduced response of peripheral tissues to the action of thyroid hormone. The genetic variability of cofactors involved in the action of thyroid hormone explains the heterogeneity of resistance among affected individuals. Generally, patients with this disorder, have increased levels of free T4 and free T3 in association with normal or high TSH. Clinical case: 11-year-old boy, with personal history of Attention-deficit/hyperactivity disorder (ADHD). A pediatric endocrinology consultation was requested to evaluate abnormalities in his thyroid function tests. A few months earlier, his father was referred to endocrinology consultation because of thyroid function tests abnormalities: TSH - 3.01 μIU / mL (N: 0.35 - 4.94); Free T4 1.7 ng / dL (N: 0.7-1.48); Free T3 4.77 pg / mL (N: 1.71-3.71). Initially, two diagnostic hypotheses were considered: central hyperthyroidism or impaired sensitivity to thyroid hormone. The adult underwent pituitary magnetic resonance, which raised the hypothesis of a pituitary microadenoma, and TRH stimulation test, whose result was strongly suggestive of the second diagnostic possibility. A genetic study was requested and the presence of the c700 G> A variant (p. Ala 324 trh) in the THRB gene was identified, which confirmed the most likely hypothesis. At the time of the pediatric endocrinology consultation, the 11-year-old boy had the results of his lab tests: TSH - 6.67 μIU / mL (N: 0.35 - 5); T4L 2.27 ng / dL (N: 0.88-1.58); T3L 7.79 pg / mL (N: 2-4.20). Given his perfect height and weight evolution and the absence of symptoms suggestive of hypo or hyperthyroidism, it was decided not to start any medication, keeping only periodic surveillance. Conclusion: This case exemplifies unusual thyroid function tests. This discordance between serum thyroid hormone and TSH concentrations should raise the possibility of impaired sensitivity to thyroid hormone. In this condition, patients may present with symptoms of hypo or hyperthyroidism and the etiology of thyroid function tests abnormalities are not easily recognized. This can lead to misdiagnosis and consequently unnecessary treatment.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A948-A949
Author(s):  
Jordan Albrecht ◽  
Moeed Ahmed ◽  
Sudha Nandala ◽  
Saad Farooqi ◽  
Robert J Anderson

Abstract Introduction: Postpartum Thyroiditis (PPT) is an autoimmune disorder characterized by destruction of the thyroid gland within the first year after delivery. Systemic Lupus Erythematosus (SLE), another autoimmune disease, has been associated with a spectrum of thyroid disorders. While the prevalence of thyroid diseases in patients with SLE is increased, the association between SLE and PPT is not well known. The infrequency of encountering SLE and PPT makes abnormal thyroid tests in the postpartum period a diagnostic challenge. Clinical Case: A 27-year-old G1P1001 who was five months postpartum and not breast feeding was referred to Endocrinology clinic for evaluation of abnormal thyroid function tests. Past medical history was significant for SLE with renal and pericardial involvement. SLE was well controlled, treated with hydroxychloroquine. Family history was significant for hypothyroidism in her mother. She was asymptomatic and appeared clinically euthyroid. Vitals were stable and physical exam was negative for goiter, nodule or orbitopathy. Lab results at two months postpartum showed an elevated TSH of 3.87 UIU/mL (Normal 0.40-3.8 UIU/mL) and at four months postpartum TSH was low at 0.012 UIU/mL. Repeat labs at five months postpartum continued to show a low TSH at 0.007 UIU/mL with mildly elevated Free T4 at 1.7 ng/dL (Normal 0.6-1.6 ng/dL) and elevated Free T3 of 6.0 pg/mL (Normal 2.1-3.8 pg/mL). Anti-thyroid peroxidase antibodies (TPO), thyroid stimulating antibodies (TSI) and TSH receptor antibodies (TRAb) were negative. Thyroid Ultrasound with Doppler was within normal limits. Radioactive Iodine Uptake and Scan, obtained at 6 months postpartum, showed high normal uptake (17% and 32% at 4 hours and 24 hours respectively), suggestive of recovery phase of PPT. The most recent TSH was elevated at 8.5 UIU/mL and Free T4 was low at 0.7 ng/dL. Disease course was consistent with PPT. Conclusion: The Th1 (T-helper) lymphocyte immune predominance in autoimmune thyroid disease and SLE is the immune-pathogenetic base of the association between both diseases. Postpartum thyroiditis is a variant of chronic autoimmune thyroiditis. Serum anti-TPO antibodies vary during pregnancy and tend to increase early and may decline later. Immunologic tolerance increases during pregnancy, fades in the postpartum period and makes interpretation of thyroid function tests and disease process challenging. Pregnant and postpartum patients who have SLE have increased prevalence of thyroid disease. Causes are multifactorial with a higher prevalence of hypothyroidism and thyroid autoantibodies. Hyperthyroidism is much less likely. One comparable study found 6 of 43 (14%) women with SLE developed PPT and only one of these patients had positive thyroid antibodies. These reports and our patient illustrate the variability of thyroid function tests in patients with SLE.


2019 ◽  
Vol 152 (Supplement_1) ◽  
pp. S4-S5
Author(s):  
Jeannie M Stubblefield ◽  
Jessica Becker ◽  
Jennifer Wallace ◽  
Uyen Vong ◽  
Dina Greene ◽  
...  

Abstract Introduction While biotin is widely used as a health and beauty supplement, patients rarely report the use of biotin supplements to clinicians. This can negatively impact patient care since biotin can falsely elevate or lower results in immunoassays that use biotinylated components. On the Beckman DxI platform, total T3 (T3), free T3 (FT3), and free T4 (FT4) assays are falsely elevated by excess biotin, while TSH and total T4 (T4) are unaffected. The goals of this study were to develop a method to measure serum biotin, to determine biotin concentrations in samples submitted for thyroid function testing, and to correlate biotin concentrations with immunoassay result patterns suggestive of biotin interference. Methods We developed and validated a targeted LC-MS/MS method to measure serum biotin (AMR: 5.4-500 mcg/L). Two collections of patient samples were tested using automated Beckman DxI assays for TSH (RR: 0.4-5.0 μIU/mL), T3 (RR: 73-178 ng/dL), FT3 (RR: 2.4-4.1 pg/mL), T4 (RR: 4.8-10.8 mcg/dL), and FT4 (RR: 0.6-1.2 ng/dL). The first collection included consecutive samples submitted for TSH and FT4 testing. To increase the probability of identifying samples with biotin interference, a middleware preselection algorithm was used to identify samples with a results pattern suggestive of biotin interference (normal to high TSH with elevated T3, FT3, and/or FT4). Results Two of the 94 samples consecutively submitted for thyroid function tests demonstrated biotin levels >AMR. TSH and FT4 were within normal ranges for one, while the other had normal TSH and elevated FT4 (biotin: 26 mcg/L). The preselection algorithm targeting normal to high TSH with elevated T3, FT3, and/or FT4 results flagged 83 samples, 21.7% of which had measurable biotin (5.71-194.3 mcg/L). Immunoassay results for TSH, T3, FT3, T4, and FT4 were obtained where there was sufficient volume for testing. Of these 38 samples, all samples with biotin >24 mcg/L had elevated results for 2(+) affected assays. Conclusions In this study, a targeted LC-MS/MS method to measure biotin in serum samples was developed and used to estimate the distribution of biotin concentrations in samples submitted for thyroid function testing. Comparison of immunoassay result patterns with biotin concentrations suggested an interference threshold around 24 mcg/L. The evaluation of consecutively submitted samples showed that biotin in excess of this interference threshold in patients receiving thyroid function tests on the Beckman DxI platform is rare. However, combining the preselection algorithm with quantitative biotin measurement by LC-MS/MS demonstrated that biotin interference does occur in these patient samples and should be evaluated when there are confounding results or result patterns suggestive of interference. In addition, the biotin LC-MS/MS method described here has additional clinical utility in the evaluation of suspected interference in any immunoassay that utilizes biotinylated components.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Samer El-Kaissi ◽  
Laila AbdelWareth ◽  
Ruba Dajani ◽  
Terrence Lee St John ◽  
Sherry Ann Santarina ◽  
...  

Abstract Background and Aim: We previously showed in a retrospective analysis that the plasma TSH rises significantly post-Ramadan in levothyroxine-treated hypothyroid patients, possibly as a result of changes in the eating habit during the non-fasting period from dusk until dawn. The aim of this study is to determine the best time for taking levothyroxine during Ramadan in order to minimize changes in thyroid function tests. Methods: in a randomized prospective design, hypothyroid patients taking levothyroxine for greater than 6-months were randomized to take levothyroxine at one of the following 3 times during Ramadan: (group 1) at dusk after a prolonged fast and 30-minutes before the Iftar meal, (group 2) ≥ 3-hours after the Iftar meal, or (group 3) at dawn 30-minutes before Suhur meal. Patients were instructed to allow a minimum of 3-hours between the last meal and levothyroxine and to refrain from eating and drinking for at least 30-minutes after taking levothyroxine. Thyroid function tests were performed within 3-months before Ramadan and within 6-weeks post Ramadan. To estimate intent-to-treat effects, we examined pre- and post-Ramadan thyroid function tests in relation to the assigned levothyroxine administration times. Results: 147 patients were randomized into the study and the respective number of patients in groups 1, 2 and 3 were 50, 46 and 51. The mean age of participants was 43.5±12.4 years [range 21.0-86.0] and 78% were females with no statistical differences in the mean age or gender distribution between the 3 groups. The respective pre-Ramadan mean TSH values for the 3 groups were 2.49 mIU/L, 2.16 mIU/L and 3.37 mIU/L with no significant differences at baseline. Post-Ramadan mean TSH values were 2.47 mIU/L, 4.26 mIU/L and 3.85 mIU/L for groups 1, 2 and 3 respectively. The pre- and post-Ramadan mean TSH differences were significant only for group 2, who took levothyroxine 3-hours post-Iftar (P-value 0.041). There were no significant differences in the free-T4 levels across the 3-groups before and after Ramadan. In a subset of 85 patients, the preferred times for levothyroxine administration during Ramadan were 44.7% before Iftar, 50.6% post-Iftar and only 4.7% were in favor of taking the medication before Suhur meal. Conclusions: Levothyroxine-treated hypothyroid patients who took levothyroxine 3-hours after the main Iftar meal showed a significant increase in plasma TSH post-Ramadan, possibly reflecting a reduced time period between levothyroxine administration and the previous meal. There was no significant change in the mean plasma TSH for patients taking levothyroxine at dusk before Iftar or at dawn before Suhur. The least patient-preferred time for taking levothyroxine was at dawn before Suhur possibly due to time constraints before the start of fasting.


2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Mohammed Al Tameemi ◽  
Janice L Gilden

Abstract Background: Many causes of abnormal thyroid function tests (TFTs) occur that may or may not reflect a true thyroid disorder. The most common include: immune check point inhibitors therapies (ICI) used to treat various types of cancers; biotin supplements, which may interfere with thyroid function test assays; euthyroid sick syndrome; as well as amiodarone therapy for cardiac disorders. Clinical Case: A 67-year old female patient with type 2 diabetes mellitus, taking insulin and oral antihyperglycemic agents, with hyperlipidemia, hypertension and coronary artery disease, who had abnormal TFTs (TSH was 3.7 to 4.9 uIIu/ml; ref range 0.27-4.2 uIU/mL), and Free T4 was 0.92 to 1.06 ng/dL; ref range 0.55-1.6 ng/dl) prior to the diagnosis of metastatic adenocarcinoma of the lungs. She was initially treated with radiation. TFTs were unchanged. Her CEA was noted to be 129.5 (0-3.0 ng/mL). However, following chemotherapy with Tarceva (Erlotinib) 50 mg po daily, the TSH increased to 7.6 uIU/ml with Free T4 of 3.19 ng/dL. She remained clinically euthyroid. A thyroid ultrasound showed 1 -small sub centimeter nodule in each thyroid lobe. The patient later admitted to also taking biotin for an unknown period of time. TSH antibodies and TSI were both negative. Free T4 by dialysis was normal. While still taking Tarceva her TSH was noted to be 2.5 to 3.8 uIU/ml and both Free T4 and Free T3 were elevated and was 6.57 pg/ml;ref range=2.52-4.34 pg/mL). Six months later, the Free T4 decreased to 1.08 ng/dL. Thyroid antibodies and thyroglobulin remain normal. The patient remained clinically euthyroid. Conclusion: It is important to note that several factors can cause abnormal thyroid function tests, such as Immune check point inhibitors therapy, with the exact mechanism for abnormal TFTs unknown, and can also be associated with either Grave’s hyperthyroidism or Hashimoto’s hypothyroidism,as well as other autoimmune endocrine disorders. Biotin, a common supplement, has also been reported to interfere with the thyroid function test assays for free thyroxine (T4), total T4, free triiodothyronine (T3), total T3, TSH, and various cancer markers. However, It is important to clinically evaluate the patient for thyroid disorders, and recognize that therapy may not always be required, when discrepant and fluctuating thyroid function tests are obtained, such as in this patient. References: (1) Holmes EW, Samarasinghe S, Emanuele MA, Meah. Biotin interference in clinical immunoassays: a cause for concern. . Arch Pathol Lab Med. 2017;141:1459-1460. (2) Rossi E, Sgambato, De Chaira G, et al. Thyroid-induced toxicity of check-point inhibitors immunotherapy in the treatment of advance non-small cell lung cancer. J. Endocrinol Diabetes 2016;3:1-10.


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