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Journal articles on the topic 'Dysthyroidie'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Khouri, Charles, Elodie Jean Bart, Sophie Logerot, Amandine Decker-Bellaton, Hervé Bontemps, and Michel Mallaret. "Dysthyroidie sous anti-VEGF, effet indésirable de classe ? À propos d’un cas." Therapies 69, no. 6 (November 2014): 521–24. http://dx.doi.org/10.2515/therapie/2014063.

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2

Grecescu, Mihai Leonard C. "COMPUTED TOMOGRAPHY FOR DIAGNOSING GRAVES OPHTALMOPATHY." Romanian Medical Journal 68, no. 2 (June 30, 2021): 268–72. http://dx.doi.org/10.37897/rmj.2021.2.21.

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Graves ophtalmopathy (GO), thyroid eye disease (TED) and thyroid - associated orbitopathy (TAO) are terms referring to an autoimmune inflammatory process that affects the adipogenesis of orbital fat and periorbital tissue, associated with dysthyroidism. On imaging, such as computed tomography (CT) thyroid -associated orbitopathy (or thyroid -associated ophtalmopathy) is characterised by symmetrical and bilateral proptosis, secondary to extra-ocular muscle (EOM) enlargement and expansion of orbital fat. Imaging studies ca be useful in identifying patients risk to develop dysthyroid optic neuropathy and initiating early treatment of the condition, avoiding permanent visual loss. The purpose of this study was to reveal the prevalence of thyroid ophtalmopathy imaging considerations in Graves disease patients. A total of 19 patients were evaluated on computed tomography scanning the diameters and density of extra-ocular muscles, muscular index, proptosis, width of the optic nerve, width of superior ophthalmic vein and lacrimal gland position.

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3

Kintu-Luwaga, Ronald, Timothy Makumbi, Cathy Kilyewala, and Jane O. Fualal. "Pattern of sub-clinical dysthyroidism in a postthyroidectomy cohort: Implications for supplementary treatment." East and Central African Journal of Surgery 23, no. 3 (December 31, 2018): 95–99. http://dx.doi.org/10.4314/ecajs.v23i3.2.

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Background: Defective thyroid functioning is referred to as dysthyroidism. Despite incomplete thyroidectomy or thyroxine supplementation, post-thyroidectomy patients may still experience dysthyroidism. Many times, this may be sub - clinical. This study aimed to assess the prevalence and pattern of sub-clinical dysthyroidism following thyroid surgery. Methods: In this prospective cohort study, 40 patients were consecutively recruited following conventional thyroidectomy and followed up to 12months. All patients were euthyroid at surgery. At 12 months serum TSH, T4 and T3 levels were measured and the patients clinically assessed. The prevalence and pattern of dysthyroidism was analysed statistically against the patient demographics, clinical and peri-operative variables for significance, using stata version 13. The confidence interval was at 95% and the statistical significance at a p-value of <0.05. Results: The mean age was 44.3 years (M:F= 1: 12.3). 20% of the patients had medical comorbidities. The types of surgery performed were sub-total thyroidectomy (55%), near total thyroidectomy (25%) and total thyroidectomy (20%). The prevalence of postoperative dysthyroidism was 52.5%. 22.7% of patients who underwent sub-total thyroidectomy had dysthyroidism. Most patients (90%) who were on thyroxine supplement (following total or near total thyroidectomy) still developed dysthyroidism (P= 0.017). The type of resection done had the greatest significance (P= 0.000). Other factors associated with dysthyroidism albeit non-significantly were history of pre-operative hyperthyroidism, middle age (40 - 60 years), and female gender. Conclusions: The prevalence of dysthyroidism in this cohort was high which may reflect the broader picture among post - thyroidectomy patients in this setting. Regular biochemical testing in post-thyroidectomy patients is important to identify and correct dysthyroidism early. This requires frequent follow-up and accurate dose adjustment, based on objective assessments like weight or body mass index. Keywords: post-thyroidectomy; dysthyroidism; hypothyroidism; hyperthyroidism; sub-clinical dysthyroidism; prospective; cohort

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4

Giordanetti, Stefano. "Dysthyroidism and heart failure: from clinical case to pathophysiology." Clinical Management Issues 4, no. 3S (October 13, 2015): 37–42. http://dx.doi.org/10.7175/cmi.v4i3s.1152.

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Dysthyroidism affects cardiovascular function in many ways and can cause heart failure. The physiopathological mechanisms underlying the development of heart failure involve both direct intranuclear transcriptional effects of thyroid hormones and specific haemodynamic consequences of vascular modifications induced by dysthyroidism. Phospholamban regulatory action on diastolic ventricular function appears to play a pivotal role in mediating both direct T3 action and adrenal effects on myocardial contractility, possibly explaining the way dysthyroidism mimics sympathoadrenergic alterations on cardiovascular function. Therapeutical approach to cardiovascular disorders in dysthyroidism should focus on both thyroid hormones dysregulation and sympathoadrenergic activity, to attempt a reversal of the associated derangements.

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5

Jacobson, Daniel M. "Dysthyroid Orbitopathy." Seminars in Neurology Volume 20, Number 1 (2000): 0043–54. http://dx.doi.org/10.1055/s-2000-6832.

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6

Dresner, S. C., and J. S. Kennerdell. "Dysthyroid orbitopathy." Neurology 35, no. 11 (November 1, 1985): 1628. http://dx.doi.org/10.1212/wnl.35.11.1628.

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7

Luz, Inês Romão, João Rio Martins, Mónica Jerónimo, Joana Serra Caetano, Rita Cardoso, Isabel Dinis, and Alice Mirante. "Neonates Born to Mothers with Graves’ Disease: 15 Year Experience of a Pediatric Endocrinology Department." Acta Médica Portuguesa 33, no. 7-8 (July 1, 2020): 483. http://dx.doi.org/10.20344/amp.12279.

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Introduction: Graves disease is characterized by the existence of autoantibodies directed to the thyrotropin receptor, which can have a stimulatory/inhibitory action, in women with the condition, their fetus or neonate. Our aim was to review the case series of these neonates in order to establish neonatal thyroid function predictors.Material and Methods: Retrospective cohort study of the database of the Department of Pediatric Endocrinology, including patients born to mothers with Graves’ disease, between 2002 and 2017. Clinical and biochemical data were collected from mothers and offspring.Results: Fifty newborns, from 46 women with a median of 3.5 years after diagnosis, were included. During all trimesters of pregnancy, more than half of women had positive autoantibodies directed to the thyrotropin receptor. Not every woman had a complete thyroid function evaluation every trimester. In 32 newborns, cord blood screening was done. During the neonatal period, there were three cases of hypothyroidism and two of hyperthyroidism. The mothers of these five newborns had higher levels of free thyroid hormones during the second trimester (p = 0.03). The level of antibodies directed to the thyrotropin receptor was significantly higher in the cord blood (p = 0.03) and in the first neonatal test (p = 0.03) of these dysthyroid newborns.Discussion: Our results reinforce the need for every pregnant woman with Graves’ disease to be subject to thyroid function and autoantibodies evaluation during every trimester, as well as the importance of evaluating these antibodies in cord blood.Conclusion: High levels of free thyroid hormones during the second trimester of pregnancy and antibodies directed to the thyrotropin receptor value in cord blood are predictors of dysthyroidism in neonates born from women with Grave’s disease.

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8

Signorelli, Diego, Maria Silvia Cona, Milena Vitali, Giuseppe Lo Russo, Claudia Proto, Martina Imbimbo, Nicoletta Zilembo, et al. "Correlation between dysthyroidism and efficacy in patients treated with anti PD-1 or anti PDL-1 agents." Journal of Clinical Oncology 35, no. 7_suppl (March 1, 2017): 67. http://dx.doi.org/10.1200/jco.2017.35.7_suppl.67.

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67 Background: Immune checkpoints inhibitors have clearly improved patients’outcomes in different tumors, but definitive predictive biomarkers are still missing. Since thyroiditis have been reported, we have evaluated whether clinical responses are more frequent in patients who underwent anti PD-1 or anti PDL-1 agents and experienced dysthyroidism. Methods: We retrospectively evaluated 135 metastatic solid tumor patients, treated at our Institute with anti PD-1/PDL-1 antibodies since 2013. Thyroid toxicity was defined according to CTCAE version 4.0 and disease control (DC: CR+PR+SD) was chosen as efficacy endpoint. Correlation between dysthyroidism and DC rate was assessed by Fisher’s exact test. Results: Of 135 patients, 76 (56.3%) were treated by anti PD-1 and 59 (43.7%) by anti PDL-1 agents. Population was heterogeneous, including patients from the 1st to the 9th line of therapy, affected by the following cancers: 57 (42.2%) NSCLC, 18 (13.3%) melanoma, 13 (9.6%) RCC, 7 (5.2%) bladder and urothelial, 6 (4.5%) mesothelioma, 5 (3.7%) SCLC, 5 (3.7%) sarcoma, 5 (3.7%) biliary tract, 5 (3.7%) head and neck, 3 (2.2%) gastric, 3 (2.2%) colon, 2 (1.5%) Merkel cells and one each for thyroid, HCC, ovary, cervix, anal carcinoma and germ cells tumor. Median follow up was 8.6 months. Best responses were: 5 CR, 30 PR, 51 SD and 49 PD; 86 (63.7%) patients achieved DC. Overall, 38 patients developed dysthyroidism (subclinical, G1, G2 hypo/hyperthyroidism): 18/76 (23.7%) in anti PD-1, 20/59 (33.9%) in anti PDL-1 group; 31/38 (81.6%) of them achieved DC. The median time of dysthyroidism appearance was the 6th cycle of therapy (range 1st-22th). Of 97 patients who did not develop thyroid toxicity, 55 (56.7%) achieved DC. Dysthyroidism significantly correlated with DC rate (p=0.009). Conclusions: We found a significant correlation between dysthyroidism and clinical responses in solid tumor metastatic patients treated by anti PD-1 or anti PDL-1 antibodies. Our observation suggests that evaluation of thyroid function should be regularly performed during therapy with these agents. These retrospective findings must be confirmed in a prospective trial powered to see whether thyroid dysfunction is a surrogate marker of response.

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9

Elouazzani, H., K. Sirajedine, M. Aladib, and H. Colomb. "Les dysthyroidies chez l’hémodialysé chronique." Néphrologie & Thérapeutique 7, no. 5 (September 2011): 309–10. http://dx.doi.org/10.1016/j.nephro.2011.07.104.

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10

Desailloud, R. "Dysthyroidies des traitements par cytokines." Annales d'Endocrinologie 74, no. 4 (September 2013): 244. http://dx.doi.org/10.1016/j.ando.2013.07.035.

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11

Ha, Jerome How Ing, James Leong, Peter Martin, Raf Ghabrial, and Ross Benger. "Outcomes following orbital decompression surgery for dysthyroid optic neuropathy associated with Graves’ ophthalmopathy." Asian Journal of Ophthalmology 14, no. 3 (August 4, 2015): 97–107. http://dx.doi.org/10.35119/asjoo.v14i3.138.

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Purpose: To investigate the outcomes of orbital decompression surgery for dysthyroid optic neuropathy associated with severe Graves’ ophthalmopathy. Design: Ten years (2000-2010) retrospective case series.Methods: Thirty-eight orbits (with dysthyroid optic neuropathy) of 119 surgical orbital decompressions. Patients with dysthyroid optic neuropathy associated with Graves’ ophthalmopathy, who underwent orbital decompression surgery at Sydney Eye Hospital (Sydney, Australia), were investigated for outcome measures.Results: Thirty-five orbits were eligible for data analysis. Orbital decompression surgery improved visual acuity in 29 orbits and maintained visual acuity in four orbits. In patients with dysthyroid optic neuropathy, there was a statistically significant mean improvement in visual acuity of 2.8 lines postoperatively (standard deviation = 3.2; 95% confidence interval 3.9 to 1.7, p-value < 0.05). There were no statistically significant differences invisual acuity amongst different combinations of orbital walls being decompressed, with the majority of orbits had the medial orbital wall decompressed. This may reflect the small number of decompressions performed in each subgroup. Orbital decompression surgery reduced proptosis by a mean of 3.2 mm (standard deviation = 2.9; 95% confidence interval -4.32 to -2.07; p-value < 0.05). Medial and lateral orbital walls decompression resulted in the greatest mean reduction in proptosis. There were no severe visual impairment cases postoperatively (VA worse than 6/60). There were two patients with new onset diplopia postoperatively. There were three orbits with bleeding and one orbit with CSF leakage, all without major sequelae postoperatively.Conclusion: Regardless of surgical access, orbital decompression surgery is effective and safe in the management of dysthyroid optic neuropathy and in reducing proptosis in patients with Graves’ ophthalmopathy.

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12

Neigel, Janet M., Jack Rootman, Rod I. Belkin, Robert A. Nugent, Stephen M. Drance, Craig W. Beattie, and John A. Spinelli. "Dysthyroid Optic Neuropathy." Ophthalmology 95, no. 11 (November 1988): 1515–21. http://dx.doi.org/10.1016/s0161-6420(88)32978-7.

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13

Wilkins, Robert B., and Rex A. Yannis. "Dysthyroid Optic Neuropathy." Ophthalmic Plastic & Reconstructive Surgery 5, no. 4 (December 1989): 297. http://dx.doi.org/10.1097/00002341-198912000-00025.

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14

Demba, Diedhiou, Diallo Ibrahima Mané, Gadji Fatou Kiné, Sow Djiby, Ndour Michel Assane, Barrage Ahmed Limane, Thioye Elhadji Mamadou Moussa, Ka-Cissé Mariama, Sarr Anna, and Ndour-Mbaye Maimouna. "Dysthyroidism in Elderly Subjects." Open Journal of Internal Medicine 10, no. 02 (2020): 181–89. http://dx.doi.org/10.4236/ojim.2020.102019.

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15

Jaafar, Jaafar, Eugenio Fernandez, Heba Alwan, and Jacques Philippe. "Programmed cell death-1 and programmed cell death ligand-1 antibodies-induced dysthyroidism." Endocrine Connections 7, no. 5 (May 2018): R196—R211. http://dx.doi.org/10.1530/ec-18-0079.

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Background Monoclonal antibodies blocking the programmed cell death-1 (PD-1) or its ligand (PD-L1) are a group of immune checkpoints inhibitors (ICIs) with proven antitumor efficacy. However, their use is complicated by immune-related adverse events (irAEs), including endocrine adverse events (eAEs). Purpose We review the incidence, time to onset and resolution rate of dysthyroidism induced by PD-1/PD-L1 Ab, and the clinical, biological and radiological findings. We aim to discuss the potential mechanisms of PD-1/PD-L1 Ab-induced dysthyroidism, and to propose a management algorithm. Methods We performed a literature search of available clinical trials regarding PD-1/PD-L1 Ab in the PubMed database. We selected all English language clinical trials that included at least 100 patients. We also present selected case series or reports, retrospective studies and reviews related to this issue. Findings In patients treated with PD-1 Ab, hypothyroidism occurred in 2–10.1% and hyperthyroidism occurred in 0.9–7.8%. When thyroiditis was reported separately, it occurred in 0.34–2.6%. Higher rates were reported when PD-1 Ab were associated with other ICI or chemotherapy. The median time to onset of hyperthyroidism and hypothyroidism after PD-1 Ab initiation was 23–45 days and 2–3.5 months, respectively. Regarding PD-L1 Ab, hypothyroidism occurred in 0–10% and hyperthyroidism in 0.5–2% of treated patients. The average time to onset of dysthyroidism after PD-L1 Ab was variable and ranged from 1 day after treatment initiation to 31 months. Conclusion Dysthyroidism occurs in up to 10% of patients treated with PD-1/PD-L1 Ab. Hypothyroidism and reversible destructive thyroiditis are the most frequent endocrine adverse events (eAE) in PD-1/PD-L1 treated patients. Immune and non-immune mechanisms are potentially involved, independently of the presence of thyroid antibodies.

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16

Koay, Boon, Grant Bates, and John Elston. "Endoscopic orbital decompression for dysthyroid eye disease." Journal of Laryngology & Otology 111, no. 10 (October 1997): 946–49. http://dx.doi.org/10.1017/s0022215100139039.

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AbstractOrbital decompression for dysthyroid eye disease is traditionally performed either through an external approach or transantrally. The introduction of endoscopic sinus surgery over the last decade has led to a better understanding of the intranasal surgical landmarks of orbital walls and the development of endoscopic orbital decompression. We have adopted the endoscopic technique as the treatment of choice for orbital decompression in dysthyroid eye disease for the last two years. The surgical technique is described and illustrated, and the results of our first series of 15 patients (30 orbits) are presented.

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17

Ebner, Roberto. "Dysthyroid optic neuropathy (DON)." Seminars in Ophthalmology 17, no. 1 (January 2002): 18–21. http://dx.doi.org/10.1076/soph.17.1.18.10289.

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18

Akoum, Riad, Michel Saade, Wafic Tabbara, Emile Brihi, Marwan Masri, Khaled Habib, and Gerard Abadjian. "Dysplastic hematopoiesis and underlying dysthyroidism." Journal of Cancer Research and Therapeutics 4, no. 1 (2008): 50. http://dx.doi.org/10.4103/0973-1482.39609.

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19

Conte-Devolx, Bernard, and Bernard Vialettes. "Can stress induce dysimmune dysthyroidism?" Annales d'Endocrinologie 74, no. 5-6 (December 2013): 483–86. http://dx.doi.org/10.1016/j.ando.2013.09.001.

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20

Schmidt, E. D., G. van Hogerwou, R. van der Gaag, W. M. Wiersinga, G. Asmussen, and L. Koornneef. "Site-dependent effects of experimental hypo- and hyperthyroidism on resident macrophages in extraocular muscles of rats: a quantitative immunohistochemical study." Journal of Endocrinology 135, no. 3 (December 1992): 485—NP. http://dx.doi.org/10.1677/joe.0.1350485.

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ABSTRACT It has been suggested that the effects of dysthyroidism on resident immunocompetent cells of the extraocular muscles may play a role in the pathogenesis of Graves' ophthalmopathy. The distribution of such cells was therefore studied in extraocular muscles of rats that were made hyper- or hypothyroid by the oral administration of thyroxine or propylthiouracil respectively. Skeletal muscles were studied for comparison. The cell distributions were analysed in cryostat cross-sections subjected to a two-step immunoperoxidase method using well-characterized monoclonal antibodies against T cells, B cells, macrophages and MHC class II antigens. The extraocular muscles of control (euthyroid) rats contained numerous macrophages, fewer MHC-II positive cells and T cells and no B cells. Differences in the distribution of immunocompetent cells were found in control rats, between skeletal and extraocular muscles as well as within the various recti eye muscles. This particular tissue distribution resembles that previously reported for human extraocular and skeletal muscles. Quantitative analysis showed that experimental dysthyroidism only affected cell populations in the extraocular muscles. Significant effects on the number of macrophages were observed in the inferior rectus muscle of both hypo- and hyperthyroid rats, this was most pronounced in the orbital layer of the muscles. Both hyper- and hypothyroidism appear to affect local cell distributions in a tissue-specific manner. The presently observed site-dependent effects of dysthyroidism on local immunocompetent cell populations may have relevance for the differential involvement of muscular tissues in Graves' ophthalmopathy. Journal of Endocrinology (1992) 135, 485–493

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21

Haddam, A. E. M., N. S. Fedala, S. Ouahid, N. Fafa, L. Kedad, and D. Meskine. "Les dysthyroidies chez les patients avec Trisomie 21." Annales d'Endocrinologie 74, no. 4 (September 2013): 375–76. http://dx.doi.org/10.1016/j.ando.2013.07.477.

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22

Mehmet, Aysel, Eirini Kanella Panagiotopoulou, Aristeidis Konstantinidis, Charalampos Papagoras, Panagiotis Skendros, Doukas Dardabounis, Athanasia Maria Mikropoulou, and Georgios Labiris. "Α Case of Severe Thyroid Eye Disease Treated with Tocilizumab." Acta Medica (Hradec Kralove, Czech Republic) 64, no. 1 (2021): 64–69. http://dx.doi.org/10.14712/18059694.2021.12.

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This is a case report describing a patient with severe thyroid eye disease complicated with dysthyroid optic neuropathy that was unresponsive to intravenous steroids and orbital radiotherapy but responded well to intravenous tocilizumab.

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23

Igarashi, Yasuo, Kazuo Ogasawara, Hiroshi Maekawa, Hiroaki Ohyachi, and Masahiro Ohba. "Mechanical Properties in Dysthyroid Myopathy." Ophthalmologica 208, no. 4 (1994): 201–6. http://dx.doi.org/10.1159/000310488.

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24

Banerjee, S., and C. B. James. "Amiodarone and dysthyroid eye disease." British Journal of Ophthalmology 80, no. 9 (September 1, 1996): 851–52. http://dx.doi.org/10.1136/bjo.80.9.851.

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25

CHOU, PING-I., and STEVEN E. FELDON. "Late Onset Dysthyroid Optic Neuropathy." Thyroid 4, no. 2 (January 1994): 213–16. http://dx.doi.org/10.1089/thy.1994.4.213.

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26

Ludgate, Marian. "Fibrosis in dysthyroid eye disease." Eye 34, no. 2 (December 16, 2019): 279–84. http://dx.doi.org/10.1038/s41433-019-0731-5.

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27

Chu, Eugene A., Neil R. Miller, Michael P. Grant, Shannath Merbs, Ralph P. Tufano, and Andrew P. Lane. "Surgical treatment of dysthyroid orbitopathy." Otolaryngology–Head and Neck Surgery 141, no. 1 (July 2009): 39–45. http://dx.doi.org/10.1016/j.otohns.2009.04.004.

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28

FELLS, PETER, NICHOLAS F. LAWTON, BRIAN SHINE, and BERNADETTE McCARRY. "MANAGEMENT OF DYSTHYROID EYE DISEASE." Australian and New Zealand Journal of Ophthalmology 16, no. 1 (February 1988): 37–43. http://dx.doi.org/10.1111/j.1442-9071.1988.tb01198.x.

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29

Inoue, Yoichi, Toshikazu Tsuboi, Ai Kouzaki, Toshine Maeda, and Toyoko Inoue. "Ophthalmic Surgery in Dysthyroid Ophthalmopathy." Thyroid 12, no. 3 (March 2002): 257–63. http://dx.doi.org/10.1089/105072502753600241.

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30

Fells, Peter. "Systemic management of dysthyroid ophthalmopathy." Eye 2, no. 2 (March 1988): 198–200. http://dx.doi.org/10.1038/eye.1988.36.

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31

Hedin, A. "Eyelid surgery in dysthyroid ophthalmopathy." Eye 2, no. 2 (March 1988): 201–6. http://dx.doi.org/10.1038/eye.1988.37.

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32

Fells, P. "Management of dysthyroid eye disease." British Journal of Ophthalmology 75, no. 4 (April 1, 1991): 245–46. http://dx.doi.org/10.1136/bjo.75.4.245.

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33

Salonia, Andrea, Giliola Calori, Francesco Montorsi, Rossella Nappi, Elisa Gatti, Giulia Molteni, Patrizio Rigatti, and Roberto Lanzi. "Sexual dysfunction in italian dysthyroidal women." European Urology Supplements 1, no. 1 (January 2002): 63. http://dx.doi.org/10.1016/s1569-9056(02)80237-8.

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34

M, Zerrik, Echchachoui H, Iloughmanez Z, El Ghazi M, Bennanis F, and Chemsi M. "Dysthyroidia in aircrew: flight safety impairment and aptitude management." Endocrinology&Metabolism International Journal 8, no. 4 (July 22, 2020): 86–88. http://dx.doi.org/10.15406/emij.2020.08.00285.

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35

Kazim, Michael, and John S. Kennerdell. "Elevated intraocular pressure and dysthyroid orbitopathy." Orbit 10, no. 4 (January 1991): 211–15. http://dx.doi.org/10.3109/01676839109087666.

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36

Rootman, J. "Retrobulbar pressures in dysthyroid optic neuropathy." British Journal of Ophthalmology 80, no. 12 (December 1, 1996): 1034. http://dx.doi.org/10.1136/bjo.80.12.1034.

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37

BREMNER, F. D., M. D. SANDERS, and M. R. STANFORD. "Gaze evoked amaurosis in dysthyroid orbitopathy." British Journal of Ophthalmology 83, no. 4 (April 1, 1999): 501. http://dx.doi.org/10.1136/bjo.83.4.501.

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38

Currie, Z. I., S. Lewis, and L. G. Clearkin. "Dysthyroid eye disease masquerading as glaucoma." Ophthalmic and Physiological Optics 11, no. 2 (April 1991): 176–79. http://dx.doi.org/10.1111/j.1475-1313.1991.tb00218.x.

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39

Grusha, Y. O., D. S. Ismailova, P. A. Kochetkov, and N. A. Andreeva. "Dysthyroid optic neuropathy: surgical treatment potential." Vestnik oftal'mologii 136, no. 4 (2020): 193. http://dx.doi.org/10.17116/oftalma2020136042193.

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40

Chung, Sophia M. "Ocular Neuromyotonia in Graves Dysthyroid Orbitopathy." Archives of Ophthalmology 115, no. 3 (March 1, 1997): 365. http://dx.doi.org/10.1001/archopht.1997.01100150367009.

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41

Lyons, C. J., S. F. Vickers, and J. P. Lee. "Botulinum toxin therapy in dysthyroid strabismus." Eye 4, no. 4 (July 1990): 538–42. http://dx.doi.org/10.1038/eye.1990.74.

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42

A. May, U. Fries, I. Reimold, A. We. "Microsurgical Endonasal Decompression in Dysthyroid Orbitopathy." Acta Oto-Laryngologica 119, no. 7 (January 1999): 826–31. http://dx.doi.org/10.1080/00016489950180496.

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43

BORRUAT, FX. "Dysthyroid optic neuropathy: diagnosis and treatment." Acta Ophthalmologica 89, s248 (September 2011): 0. http://dx.doi.org/10.1111/j.1755-3768.2011.3343.x.

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44

Seiff, Stuart R., Jose Luis Tovilla, Susan R. Carter, and Phillip H. Choo. "Modified Orbital Decompression for Dysthyroid Orbitopathy." Ophthalmic Plastic and Reconstructive Surgery 16, no. 1 (January 2000): 62–66. http://dx.doi.org/10.1097/00002341-200001000-00014.

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45

Malins, T. J., R. P. Ward-Booth, and E. D. Allen. "Orbital decompression of dysthyroid eye disease." British Journal of Oral and Maxillofacial Surgery 28, no. 1 (February 1990): 29–33. http://dx.doi.org/10.1016/0266-4356(90)90007-8.

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46

Puymirat, J. "Effects of dysthyroidism on central catecholaminergic neurons." Neurochemistry International 7, no. 6 (January 1985): 969–77. http://dx.doi.org/10.1016/0197-0186(85)90145-7.

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47

Amiri, Fateme Shamekhi, and Ariana Kariminejad. "Juvenile nephronophthisis and dysthyroidism: a rare association." CEN Case Reports 6, no. 1 (March 13, 2017): 98–104. http://dx.doi.org/10.1007/s13730-017-0252-7.

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DRĂGAN, Eleonora, Maria Suzana GUBERNA, Cătălina Liliana ANDREI, and Crina-Julieta SINESCU. "Evolutionary and prognostic implications in patient with acute coronary syndrome and dysthyroidism." Romanian Journal of Medical Practice 16, no. 2 (June 30, 2021): 225–33. http://dx.doi.org/10.37897/rjmp.2021.2.20.

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Abstract:

Purpose. The study aims to determine the impact of dysthyroidism on the severity and type of coronary lesion, on vascular function, as well as on the morbidity and mortality of patients with acute coronary syndrome, by finding predictive markers that can be translated into preventive measures that contribute substantially to reduce the number of newly diagnosed patients with coronary heart disease. Methods. We introduced in the study 100 patients recently diagnosed with acute coronary syndrome, without history of ischemic heart disease or thyroid disease, hospitalized in the Cardiology Clinic of the “Bagdasar-Arseni“ Emergency Clinical Hospital Bucharest, for the interventional treatment of acute coronary syndrome. The studied patients were hospitalized between November 2014 and April 2015, with regular follow-up of up to 5 years (telephone or direct interview, conducted at 6 months, 12 months, 24 months, 36 months, 48 months, 60 months), with an average period follow-up of 1006 days, evaluated clinically, bio-humorally, by echocardiography, explored with coronary angiography with the calculation of the SYNTAX score and with the performance of electrocardiogram and pulse wave. The obtained data were integrated in Excel sheets and statistically processed with the Python program. Results. The mortality rate in the patient group was 7% (7 deaths). Descriptively, of the deceased, 6 patients (86%) were male, and as thyroid status 1 hyperthyroid patient (14%), 3 hypothyroid patients (43%) and 3 patients (43%) normothyroid. There were 4 deaths (8%) in the group of patients with unstable angina and 3 deaths (8%) in the group of patients with myocardial infarction without ST-segment elevation. There were no deaths in the group of patients with acute myocardial infarction with ST-segment elevation. At follow-up, 41 patients (41%) were readmitted. Re-hospitalization was influenced by elevated values of mean blood pressure, diastolic blood pressure and C-reactive protein, unicoronary atherosclerotic disease and unstable angina at admission. At follow-up, the development of noncardiac events was noted in the evolution of patients, diabetes mellitus occurring in the majority, in almost a quarter of patients (22 patients, respectively 24% developed diabetes over time), 34% (19 patients) in euthyroidism and 8% (3 patients) dysthyroidism. Discussions. Predictive factors for the readmission of the patient with acute coronary syndrome are highlighted the following: increased level of C-reactive protein (p = 0.017), tricoronary vascular damage (p = 0.01), diastolic blood pressure greater than 80 mmHg (p = 0.025), and euthyroid status (p = 0.04). The probability of death for the patient with acute coronary syndrome rises to 66% in the presence of severe systolic dysfunction of the left ventricle (p = 0.006), and to 61% in the case of elevated values of hs troponin I (p = 0.008). In our study, the presence of dysthyroidism in the patient with acute coronary syndrome has a protective role in the development of diabetes in the first 5 years (p = 0.025). Conclusion. Dysthyroidism is associated with increased morbidity and mortality from cardiovascular disease.

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Perry, Julian D., Anish Kadakia, and Jill A. Foster. "Transcaruncular Orbital Decompression for Dysthyroid Optic Neuropathy." Ophthalmic Plastic & Reconstructive Surgery 19, no. 5 (September 2003): 353–58. http://dx.doi.org/10.1097/01.iop.0000083645.19368.99.

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Giaconi, JoAnn A., Michael Kazim, Tae Rho, and Charles Pfaff. "CT Scan Evidence of Dysthyroid Optic Neuropathy." Ophthalmic Plastic & Reconstructive Surgery 18, no. 3 (May 2002): 177–82. http://dx.doi.org/10.1097/00002341-200205000-00005.

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