scholarly journals MASSIVE THYMIC HYPERPLASIA SECONDARY TO GRAVES DISEASE

2020 ◽  
Vol 6 (3) ◽  
pp. e144-e146
Author(s):  
WingYee Wan ◽  
Jeffrey A. Colburn

Objective: Graves disease (GD) has a well-known association with thymic hyperplasia, which is seen histo-logically in up to 38% of patients with GD. However, there have only been approximately 100 documented cases of Graves-associated massive thymic hyperplasia. Potential mechanisms of thymic pathology are reviewed. Methods: A 24-year-old female presented to the emergency department with dyspnea, palpitations, tachycardia, anxiety, and weight loss. She was evaluated for hyperthyroidism using labs (thyroid-stimulating hormone, free thyroxine, thyroid-stimulating immunoglobulins) and imaging (radioactive iodine uptake [RAIU] scan), leading to treatment with radioiodine. A computed tomography angiogram of the chest was also performed to evaluate for pulmonary embolism given the patient's presenting symptoms. Results: Our patient was found to have undetectable thyroid-stimulating hormone, elevated free thyroxine (2.9 ng/dL), and elevated thyroid-stimulating immunoglobulins (399%). Diagnosis of GD was confirmed on RAIU scan. The computed tomography chest angiogram demonstrated a significant anterior mediastinal mass (7.9 × 6.9 × 6.3 cm). Treatment with radioiodine led to reduction of the mass by 76% in volume. Conclusion: While the patient's thyroid labs and RAIU scan were consistent with GD, the presence of massive thymic hyperplasia was atypical. However, the resolution of thymic hyperplasia after radioiodine therapy, without the use of thymectomy, was similar to other reported cases.

2019 ◽  
Vol 5 (6) ◽  
pp. e388-e392 ◽  
Author(s):  
Jonathan C. Li ◽  
Deepika Nandiraju ◽  
Serge Jabbour ◽  
Alan A. Kubey

Objective: In rare instances, cytopenias manifest as a complication of thyrotoxicosis. Here, we report a case of Graves disease (GD) thyrotoxicosis presenting as pancytopenia that resolved with antithyroid therapy. Methods: A 35-year-old male presented with fever and chills following an outpatient colonoscopy. Initial blood work revealed pancytopenia. Workup included viral antigen titers, blood cultures, rheumatologic antibodies, inflammatory markers, immunocompetency, nutrient deficiency, metal toxicity, and malignancy. Bone marrow aspirate was analyzed by microscope, flow cytometry, fluorescence in situ hybridization, and genetic analysis. Computed tomography scan of the chest, abdomen, and pelvis was obtained. Thyroid labs included thyroid-stimulating hormone, total triiodothyronine, free thyroxine, thyroid-stimulating immunoglobulin, anti-thyroid peroxidase antibody, and radioiodine uptake scan. Results: All workup above was non-revelatory except as follows. Imaging revealed thymic hyperplasia and splenomegaly. Thyroid labs revealed thyroid-stimulating hormone <0.02 μIU/mL (reference range is 0.30 to 5.00 μIU/mL), free thyroxine of 4.7 ng/dL (reference range is 0.7 to 1.7 ng/dL), total triiodothyronine of 191 pg/mL (reference range is 90 to 180 pg/mL), thyroid-stimulating immunoglobulin of 522% (reference range is <140%). Bone marrow biopsy was consistent with a reactive process suggesting an infectious or autoimmune process. Radioiodine uptake scan confirmed GD. He was discharged on antithyroid medication. Two-month follow-up labs revealed improved cell counts; his absolute neutrophil count was 1.94 × 109 cells/L (reference range is 1.50 to 8.00 × 109 cells/L), hemoglobin was 12.9 g/dL (reference range is 14.0 to 17.0 g/dL), and platelets were 153 × 109 cells/L (reference range is 140 to 400 × 109 cells/L). Definitive treatment was obtained with 12 mCi of 131-iodine. Conclusion: Pancytopenia and lymphoid organ hyperplasia (splenomegaly, thymic hyperplasia, and lymphadenopathy) have been previously reported to be associated with thyrotoxicosis secondary to GD, rarely simultaneously, and manifest from both thyrotoxic and immunologic mechanisms. After excluding alternative life-threatening pathologies, in such presentations, GD should be considered and treated if confirmed.


2017 ◽  
Vol 1 ◽  
pp. 3-9
Author(s):  
Orysia Lishchuk ◽  
Olesya Kikhtyak ◽  
Khrystyna Moskva

Aim. The number of patients with endocrine disorders in the world, in particular, Graves’ disease is continuously increasing. Recent studies have determined the fact of insulin resistance in thyroid disorders. On the one hand, numerous researches prove correlation of hypothyroidism with arterial hypertension, ischaemic heart disease and lipid metabolism disorder, on the other – carbohydrate metabolism disorder and hyper-sympathicotonia are closely associated with hyperthyroidism. The subject of the research was to study the correlation of insulin resistance, lipid and carbohydrate metabolism indices in patients with Graves’disease. Material and Methods. During the study 53 (37 female and 16 male) patients with Graves’ disease with noticed IR have been examined. At the beginning, after 3– and 6-months thyreostatic therapy with insulin sensitizers (metformin or pioglitazone) the following investigations have been performed: assessing thyroid-stimulating hormone levels, free thyroxine and triiodothyronine; assessing glycated haemoglobin, glucose, C-peptide and fasting insulin as primary IR markers; calculating НОМА-IR index for analysing tissue sensitivity to insulin; calculating НОМА-β index for evaluating the functional capacity of β-cells of islets of Langerhans; measuring Caro indices to monitor hyperinsulinemia, measuring total cholesterol level, low-density lipoproteins, very-low-density lipoproteins, high-density lipoproteins , triglycerides, for analysing IR in relation to lipid metabolism. Results. The research results found out that free thyroid hormones and thyroid-stimulating hormone are closely related to lipid metabolism. Thus, thyroid-stimulating hormone was characterized as having direct correlation with low-density lipoproteins, while the free thyroxine inversely correlated with total cholesterol, low-density lipoproteins, and high-density lipoproteins. The free triiodothyronine negatively correlated with high-density lipoproteins. The research has also determined the direct correlation between insulin and free thyroxine, as well as free triiodothyronine in patients with diffuse toxic goitre. Conclusions. The study proves the presence of insulin resistance in patients with Graves’ disease that generates interest to further study of the changes in insulin sensitivity, relation of insulin resistance to thyroid-stimulating hormone, thyroid hormones and looking for the ways to correct these disorders.


2021 ◽  
Vol 53 (04) ◽  
pp. 272-279
Author(s):  
Chaochao Ma ◽  
Xiaoqi Li ◽  
Lixin Liu ◽  
Xinqi Cheng ◽  
Fang Xue ◽  
...  

AbstractThyroid hormone reference intervals are crucial for diagnosing and monitoring thyroid dysfunction during early pregnancy, and the dynamic change trend of thyroid hormones during pregnancy can assist clinicians to assess the thyroid function of pregnant women. This study aims to establish early pregnancy related thyroid hormones models and reference intervals for pregnant women. We established two derived databases: derived database* and derived database#. Reference individuals in database* were used to establish gestational age-specific reference intervals for thyroid hormones and early pregnancy related thyroid hormones models for pregnant women. Individuals in database# were apparently healthy non-pregnant women. The thyroid hormones levels of individuals in database# were compared with that of individuals in database* using nonparametric methods and the comparative confidence interval method. The differences in thyroid stimulating hormone and free thyroxine between early pregnant and non-pregnant women were statistically significant (p<0.0001). The reference intervals of thyroid stimulating hormone, free thyroxine and free triiodothyronine for early pregnant women were 0.052–3.393 μIU/ml, 1.01–1.54 ng/dl, and 2.51–3.66 pg/ml, respectively. Results concerning thyroid stimulating hormone and free thyroxine reference intervals of early pregnancy are comparable with those from other studies using the same detection platform. Early pregnancy related thyroid hormones models showed various change patterns with gestational age for thyroid hormones. Early pregnancy related thyroid hormones models and reference intervals for pregnant women were established, so as to provide accurate and reliable reference basis for the diagnosing and monitoring of maternal thyroid disfunction in early pregnancy.


2009 ◽  
Vol 42 (7-8) ◽  
pp. 750-753 ◽  
Author(s):  
Rechelle Silvio ◽  
Karly J. Swapp ◽  
Sonia L. La'ulu ◽  
Kara Hansen-Suchy ◽  
William L. Roberts

Author(s):  
George M. Ziegler ◽  
Jonathan L. Slaughter ◽  
Monika Chaudhari ◽  
Herveen Singh ◽  
Pablo J. Sánchez ◽  
...  

2020 ◽  
Vol 6 (6) ◽  
pp. e290-e294
Author(s):  
Stephanie B. Lubchansky ◽  
Ruth McManus

Objective: Hirsutism and hyperandrogenism in premenopausal women are most often associated with polycystic ovarian syndrome. We present a case of progressive, severe hyperandrogenism with negative imaging identified on surgical histopathology as being due to a Leydig cell tumor (LCT), thus illustrating localization challenges associated with these small tumors. Methods: Laboratory investigations included testosterone, dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, 24-hour urine cortisol, and prolactin. Imaging included pelvic ultrasound, adrenal magnetic resonance imaging, and computed tomography. Ovarian vein sampling was not available. Results: A 42-year-old woman presented with frontal alopecia, voice deepening, coarse facial hair, and amenorrhea on a background of lifelong oligomenorrhea. Peak testosterone was 30.2 nmol/L (female normal range is <2.0 nmol/L) with normal dehydroepiandrosterone sulfate, 17-hydroxyprogesterone, prolactin, 24-hour urine cortisol, and thyroid-stimulating hormone. Transvaginal ultrasound, adrenal magnetic resonance imaging, and computed tomography of the thorax and abdomen revealed no androgen source. Testosterone failed to suppress with gonadotropin-releasing hormone agonist. Although no abnormality was seen during oophorectomy, surgical pathology documented a 1.8-cm, well-circumscribed hilar LCT. Postoperative testosterone was <0.5 nmol/L. Conclusion: Although this patient had testosterone levels well into the masculine range, multiple imaging results were negative with a LCT found only after oophorectomy. LCTs are rare ovarian stromal tumors and while 50 to 70% of these tumors produce androgen, size and clinical severity may not be well correlated. This case report illustrates that despite an association with substantially elevated androgen levels, the small size of LCTs can result in localization challenges.


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