Browsing by Subject "Hypothyroidism"

Now showing 1 - 7 of 7
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    Dietary Patterns and Hypothyroidism in U.S. Adult Population
    (MDPI, 2024-01-28) Alkhatib, Dana; Shi, Zumin; Ganji, Vijay; Nutrition and Dietetics, School of Health and Human Sciences
    The thyroid gland produces hormones that are essential for various body functions. Hypothyroidism is defined as insufficient thyroid hormone production. Several studies have found associations between specific micronutrients and overall thyroid function; however, the amount of evidence regarding the relationship between dietary patterns and hypothyroidism among the U.S. population is limited. Data from three cycles of National Health and Nutrition Examination Surveys (NHANES), 2007–2008, 2009–2010, and 2011–2012, were used (n = 8317). Subjects with serum thyroid stimulating hormone >4.5 mIU/L or on levothyroxine were considered to have hypothyroidism. Age, sex, race/ethnicity, body mass index, and several lifestyle factors were considered as covariates. Three patterns were extracted using factor analysis. These were labeled as fat–processed grains–sugars–meats (FPSM), oils–nuts–potatoes–low-fat meats (ONPL), and fruits–whole grains–vegetables–dairy (FWVD) patterns. In a weighted multiple logistic regression, FPSM and ONPL were inversely associated with hypothyroidism (OR, 0.75; 95% CI, 0.57–1; p = 0.049 and OR, 0.81; 95% CI, 0.67–0.97; p = 0.025, respectively). However, FWVD demonstrated no association with hypothyroidism (p = 0.63). In conclusion, FPSM and ONPL patterns but not FWVD patterns were associated with hypothyroidism in U.S. adults. Nutrient deficiencies and their interactions may be linked to hypothyroidism.
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    Hepatic hypoglycogenosis in the hyperthyroid rat
    (1976) Pruden, Elizabeth L.
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    A Histologic Investigation of Orthodontic Tooth Movement in Hypothyroid Macaque Speciosa Monkeys
    (1974) Davis, Steven L.; Garner, LaForrest D.; Barton, Paul; Tomich, Charles E.; Mitchell, David F.; Chalian, Varoujan
    This study was undertaken to histologically evaluate orthodontic tooth movement in hypothyroid and in normal Macaque speciosa monkeys. The experimental animals were rendered hypothyroid by radiosurgically altering the thyroid gland. A clinically acceptable orthodontic force was delivered to the anterior teeth of the monkeys. After the desired movement, a histologic investigation was made to correlate tissue responses with pressure, tension and root resorption. There was no significant difference among the three experimental animals. Likewise, there was no significant difference between the control animal and the three experimental animals. Osteoblastic and osteoclastic activity occurred to a comparable degree in both the experimental and control animals and was within normal limits for the amount of orthodontic tooth movement achieved. Root resorption was evident in both orthodontically treated and non-treated teeth in both the experimental and control animals. The root resorption observed was not significantly different, quantitatively or strategically, between the experimental and the control animals. Repair of root resorption was evident in both the experimental and control animals.
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    Hypothyroidism is a rare cause of isolated constipation
    (Wolters Kluwer, 2012-02) Bennett Jr., William E.; Heuckeroth, Robert O.; Department of Pediatrics, IU School of Medicine
    The prevalence of constipation in children is high and accounts for a large percentage of pediatric and pediatric gastroenterology visits. Thyroid testing is frequently ordered to evaluate constipation and other gastrointestinal complaints in children. We reviewed all patients with thyroid testing ordered by our pediatric gastroenterology division over a five-year period. We found 873 patients on whom thyroid testing was performed, and 56 had evidence of hypothyroidism. Nine patients had constipation and clinically significant hypothyroidism in this group. However, only one child had constipation as their sole presenting symptom. The contribution of occult hypothyroidism to isolated constipation in children may have been previously overestimated.
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    LBSAT311 Rhabdomyolysis: A Rare Presentation Of Hashimoto Thyroiditis In An Adolescent Boy
    (Oxford University Press, 2022-11-01) Saroufim, Rita; Eugster, Erica A.; Pediatrics, School of Medicine
    Introduction: Hashimoto thyroiditis is the most common cause of hypothyroidism and is associated with a wide range of clinical presentations in children and adolescents. Hypothyroidism-induced rhabdomyolysis without precipitating factors is extremely rare, particularly in pediatric patients. We describe a previously healthy adolescent boy who came to our institution with vague symptoms and was found to have rhabdomyolysis secondary to hypothyroidism due to Hashimoto thyroiditis. Clinical Case: A 16 year old boy presented to the emergency department at Riley Hospital for Children due to a two week history of bilateral eye and lip swelling. Additional symptoms included fatigue, sleepiness, slowing of speech, decreased attention span and weight gain. He was not on any medications and had no history of allergies. There was no family history of endocrine or neuromuscular disorders. Physical exam revealed a height of 177 cm (75th tile), weight of 118.4 kg (99th %tile) and BMI at the 99th %tile. Exam was significant for slow generalized movements, facial edema, and delayed deep tendon reflexes in all extremities. The thyroid gland was normal. Laboratory evaluation revealed Creatinine-1.46 mg/dL (0.3-1.2), ALT-88 Units/L (7-52), AST-254 Units/L (13-39), TSH-32.2 mcU/mL (0.4-4.2), fT4 <0.2 ng/dL (0.6-1.5) and CK 20,500 Units/L (30-223). Thyroid peroxidase antibody was elevated at 686.1 IU/mL. A renal and bladder ultrasound showed trace intra-abdominal ascites and decreased echogenicity of the bilateral psoas muscles favoring edema and consistent with rhabdomyolysis. He received IV hydration and was started on levothyroxine 25 mcg daily that was increased over a 10 month period to achieve euthyroidism. Genetic testing for rhabdomyolysis revealed two variants of unknown significance. Acyl carnitine and carnitine profiles were normal ruling out a metabolic myopathy. His symptoms improved significantly after treatment with levothyroxine although his CK levels plateaued around 1,000 Units/L. Liver and kidney function normalized during follow up. Conclusion: Rhabdomyolysis is a rare but serious complication of hypothyroidism, the pathogenesis of which is unclear. Proposed hypotheses include impaired mitochondrial oxidative metabolism, decreased muscle carnitine and switching of muscle fibers from fast-twitching type II to slow-twitching type I due to thyroxine deficiency ultimately leading to myolysis and release of intracellular muscle contents into the circulation. It is important for clinicians to have a high index of suspicion for hypothyroidism in children who present with muscle weakness and high creatinine kinase levels. The etiology of the disproportionately mild elevation of TSH in the setting of an unmeasurable free T4 and severe clinical hypothyroidism in our patient remains a mystery.
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    The Thyroid Hormone Axis and Female Reproduction
    (MDPI, 2023-06-06) Brown, Ethan D. L.; Obeng-Gyasi, Barnabas; Hall, Janet E.; Shekhar, Skand; Medicine, School of Medicine
    Thyroid function affects multiple sites of the female hypothalamic-pituitary gonadal (HPG) axis. Disruption of thyroid function has been linked to reproductive dysfunction in women and is associated with menstrual irregularity, infertility, poor pregnancy outcomes, and gynecological conditions such as premature ovarian insufficiency and polycystic ovarian syndrome. Thus, the complex molecular interplay between hormones involved in thyroid and reproductive functions is further compounded by the association of certain common autoimmune states with disorders of the thyroid and the HPG axes. Furthermore, in prepartum and intrapartum states, even relatively minor disruptions have been shown to adversely impact maternal and fetal outcomes, with some differences of opinion in the management of these conditions. In this review, we provide readers with a foundational understanding of the physiology and pathophysiology of thyroid hormone interactions with the female HPG axis. We also share clinical insights into the management of thyroid dysfunction in reproductive-aged women.
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    UBR7 functions with UBR5 in the Notch signaling pathway and is involved in a neurodevelopmental syndrome with epilepsy, ptosis, and hypothyroidism
    (Cell Press, 2021-01-07) Li, Chunmei; Beauregard-Lacroix, Eliane; Kondratev, Christine; Rousseau, Justine; Heo, Ah Jung; Neas, Katherine; Graham, Brett H.; Rosenfeld, Jill A.; Bacino, Carlos A.; Wagner, Matias; Wenzel, Maren; Al Mutairi, Fuad; Al Deiab, Hamad; Gleeson, Joseph G.; Stanley, Valentina; Zaki, Maha S.; Kwon, Yong Tae; Leroux, Michel R.; Campeau, Philippe M.; Medical and Molecular Genetics, School of Medicine
    The ubiquitin-proteasome system facilitates the degradation of unstable or damaged proteins. UBR1-7, which are members of hundreds of E3 ubiquitin ligases, recognize and regulate the half-life of specific proteins on the basis of their N-terminal sequences ("N-end rule"). In seven individuals with intellectual disability, epilepsy, ptosis, hypothyroidism, and genital anomalies, we uncovered bi-allelic variants in UBR7. Their phenotype differs significantly from that of Johanson-Blizzard syndrome (JBS), which is caused by bi-allelic variants in UBR1, notably by the presence of epilepsy and the absence of exocrine pancreatic insufficiency and hypoplasia of nasal alae. While the mechanistic etiology of JBS remains uncertain, mutation of both Ubr1 and Ubr2 in the mouse or of the C. elegans UBR5 ortholog results in Notch signaling defects. Consistent with a potential role in Notch signaling, C. elegans ubr-7 expression partially overlaps with that of ubr-5, including in neurons, as well as the distal tip cell that plays a crucial role in signaling to germline stem cells via the Notch signaling pathway. Analysis of ubr-5 and ubr-7 single mutants and double mutants revealed genetic interactions with the Notch receptor gene glp-1 that influenced development and embryo formation. Collectively, our findings further implicate the UBR protein family and the Notch signaling pathway in a neurodevelopmental syndrome with epilepsy, ptosis, and hypothyroidism that differs from JBS. Further studies exploring a potential role in histone regulation are warranted given clinical overlap with KAT6B disorders and the interaction of UBR7 and UBR5 with histones.