scholarly journals Clinical case of gestational diabetes insipidus

2021 ◽  
Vol 17 (1) ◽  
pp. 98-100
Author(s):  
N.O. Abramova ◽  
N.V. Pashkovska ◽  
N.I. Stankova ◽  
M.S. Khangarot
Keyword(s):  
Gestational Diabetes ◽  
Diabetes Insipidus ◽  
Laboratory Data ◽  
Liver Function Tests ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Total Blood ◽  
Free Cortisol ◽  
History Of ◽  
Total Urine

Diabetes insipidus is a rare endocrinological disease and occurs in 2–4 per 100,000 pregnancies. Diagnosis of gestational diabetes insipidus is very difficult because it develops against the background of physio­logical mechanisms that accompany pregnancy: thirst threshold decreases leading to polydipsia and plasma osmolarity decreases causing hypotonic polyuria. Understanding of pathophysiology of the disorder is very important for further management of these vulnerable patients. A 32-year-old patient at 36 weeks of gestation, primigravida, was referred to an endocrinologist with complaints of polyuria (6.5 l/day), nocturia — up to 5 times, severe polydipsia. At 12 weeks of gestation, there was a risk of abortion for prevention of which the patient received progesterone 100 mg intravaginally twice a day until 34 weeks. She has a history of subacute thyroiditis, with no family history of endocrine pathology. Physical examination revealed a decrease in skin turgor, blood pressure 110/85 mm Hg. Heart rate 115 bpm, weight 71 kg (body mass index 26.9 kg/m2). The patient was at high risk of developing preeclampsia. Laboratory data: analysis of urine according to Zimnitsky: volume per day — 6.8 l, specific gravity in portions: 1.012; 1.008; 1.010; 1.005; 1.012; 1.014; 1.010. Total blood count, total urine test, serum sodium and potassium, liver function tests, level of thyroid-stimulating hormone, free thyroxine, thyroid peroxidase antibodies and morning free cortisol level were normal. The patient was administered desmopressin 10 μg intranasally twice daily. Six weeks after delivery, desmopressin was stopped and she had no further evidence of polyuria, polydipsia or nocturia.

scholarly journals High levels of maternal total tri-iodothyronine, and low levels of fetal free L-thyroxine and total tri-iodothyronine, are associated with altered deiodinase expression and activity in placenta with gestational diabetes mellitus

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0242743
Author(s):  
Sebastián Gutiérrez-Vega ◽  
Axel Armella ◽  
Daniela Mennickent ◽  
Marco Loyola ◽  
Ambart Covarrubias ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Normal Glucose Tolerance ◽  
Thyroid Stimulating Hormone ◽  
Third Trimester ◽  
Total Blood ◽  
Normal Glucose ◽  
Low Levels ◽  
Expression And Activity

Gestational Diabetes Mellitus (GDM) is characterized by abnormal maternal D-glucose metabolism and altered insulin signaling. Dysregulation of thyroid hormones (TH) tri-iodethyronine (T3) and L-thyroxine (T4) Hormones had been associated with GDM, but the physiopathological meaning of these alterations is still unclear. Maternal TH cross the placenta through TH Transporters and their Deiodinases metabolize them to regulate fetal TH levels. Currently, the metabolism of TH in placentas with GDM is unknown, and there are no other studies that evaluate the fetal TH from pregnancies with GDM. Therefore, we evaluated the levels of maternal TH during pregnancy, and fetal TH at delivery, and the expression and activity of placental deiodinases from GDM pregnancies. Pregnant women were followed through pregnancy until delivery. We collected blood samples during 10–14, 24–28, and 36–40 weeks of gestation for measure Thyroid-stimulating hormone (TSH), Free T4 (FT4), Total T4 (TT4), and Total T3 (TT3) concentrations from Normal Glucose Tolerance (NGT) and GDM mothers. Moreover, we measure fetal TSH, FT4, TT4, and TT3 in total blood cord at the delivery. Also, we measured the placental expression of Deiodinases by RT-PCR, western-blotting, and immunohistochemistry. The activity of Deiodinases was estimated quantified rT3 and T3 using T4 as a substrate. Mothers with GDM showed higher levels of TT3 during all pregnancy, and an increased in TSH during second and third trimester, while lower concentrations of neonatal TT4, FT4, and TT3; and an increased TSH level in umbilical cord blood from GDM. Placentae from GDM mothers have a higher expression and activity of Deiodinase 3, but lower Deiodinase 2, than NGT mothers. In conclusion, GDM favors high levels of TT3 during all gestation in the mother, low levels in TT4, FT4 and TT3 at the delivery in neonates, and increases deiodinase 3, but reduce deiodinase 2 expression and activity in the placenta.

scholarly journals Pediatric toxic polycystic thyroid

2017 ◽  
Vol 30 (7) ◽  
Author(s):  
Janeil M. Belle ◽  
Nektarios Vasilottos ◽  
Todd D. Nebesio ◽  
Benjamin C. James
Keyword(s):  
Thyroid Disease ◽  
Pediatric Population ◽  
Receptor Gene ◽  
Hormone Replacement ◽  
Gene Mutations ◽  
Rare Condition ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Autoimmune Thyroid ◽  
History Of

AbstractBackground:Polycystic thyroid disease (PCTD) is a rare condition and has been described in adults in the setting of subclinical and clinical hypothyroidism. We present the first known case of a pediatric patient with diffuse macrocystic degeneration of the thyroid.Clinical presentation:A 6-year-old previously healthy patient was evaluated after presenting with a 16-month history of an enlarging polycystic thyroid and hyperthyroidism. Markers of autoimmune thyroid disease including thyroid stimulating immunoglobulin (TSI), thyroid stimulating hormone (TSH) receptor antibody, thyroid peroxidase antibody and thyroglobulin antibody were negative. No family history of benign or malignant thyroid or cystic disease was present. The patient underwent a total thyroidectomy without perioperative complication. She remains euthyroid with thyroid hormone replacement therapy.Summary:To our knowledge, this is the first report of PCTD in the pediatric population associated with hyperthyroidism without evidence of autoimmune disease. Somatic activating thyrotropin-receptor gene mutations are known to cause non-autoimmune hyperthyroidism in children, however it is unknown if similar mechanisms are responsible for pediatric PCTD.Conclusions:Polycystic thyroid degeneration can occur in children and may result in a hyperthyroid state.

scholarly journals The Prevalence of Thyroid Dysfunction and Autoimmunity in Women With History of Miscarriage or Subfertility

2020 ◽  
Vol 105 (8) ◽  
pp. 2667-2677 ◽  
Author(s):  
Rima K Dhillon-Smith ◽  
Aurelio Tobias ◽  
Paul P Smith ◽  
Lee J Middleton ◽  
Kirandeep K Sunner ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Thyroid Disease ◽  
Thyroid Dysfunction ◽  
Significant Proportion ◽  
Thyroid Stimulating Hormone ◽  
Overt Hypothyroidism ◽  
Thyroid Peroxidase ◽  
Regression Analyses ◽  
Asian Ethnicity ◽  
History Of

Abstract Objective To describe the prevalence of and factors associated with different thyroid dysfunction phenotypes in women who are asymptomatic preconception. Design Observational cohort study. Setting A total of 49 hospitals across the United Kingdom between 2011 and 2016. Participants Women aged 16 to 41years with history of miscarriage or subfertility trying for a pregnancy. Methods Prevalences and 95% confidence intervals (CIs) were estimated using the binomial exact method. Multivariate logistic regression analyses were conducted to identify risk factors for thyroid disease. Intervention None. Main Outcome Measure Rates of thyroid dysfunction. Results Thyroid function and thyroid peroxidase antibody (TPOAb) data were available for 19213 and 19237 women, respectively. The prevalence of abnormal thyroid function was 4.8% (95% CI, 4.5-5.1); euthyroidism was defined as levels of thyroid-stimulating hormone (TSH) of 0.44 to 4.50 mIU/L and free thyroxine (fT4) of 10 to 21 pmol/L. Overt hypothyroidism (TSH > 4.50 mIU/L, fT4 < 10 pmol/L) was present in 0.2% of women (95% CI, 0.1-0.3) and overt hyperthyroidism (TSH < 0.44 mIU/L, fT4 > 21 pmol/L) was present in 0.3% (95% CI, 0.2-0.3). The prevalence of subclinical hypothyroidism (SCH) using an upper TSH concentration of 4.50 mIU/L was 2.4% (95% CI, 2.1-2.6). Lowering the upper TSH to 2.50 mIU/L resulted in higher rates of SCH, 19.9% (95% CI, 19.3-20.5). Multiple regression analyses showed increased odds of SCH (TSH > 4.50 mIU/L) with body mass index (BMI) ≥ 35.0 kg/m2 (adjusted odds ratio [aOR] 1.71; 95% CI, 1.13-2.57; P = 0.01) and Asian ethnicity (aOR 1.76; 95% CI, 1.31-2.37; P < 0.001), and increased odds of SCH (TSH ≥ 2.50 mIU/L) with subfertility (aOR 1.16; 95% CI, 1.04-1.29; P = 0.008). TPOAb positivity was prevalent in 9.5% of women (95% CI, 9.1-9.9). Conclusions The prevalence of undiagnosed overt thyroid disease is low. SCH and TPOAb are common, particularly in women with higher BMI or of Asian ethnicity. A TSH cutoff of 2.50 mIU/L to define SCH results in a significant proportion of women potentially requiring levothyroxine treatment.

scholarly journals Lenvatinib-Induced Destructive Thyroiditis in a Patient With Hepatocellular Carcinoma

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A939-A940
Author(s):  
Anjani Pandya ◽  
Jawairia Shakil
Keyword(s):  
Hepatocellular Carcinoma ◽  
Thyroid Gland ◽  
Thyroid Function ◽  
Kinase Inhibitor ◽  
Previous History ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Thyroid Function Tests ◽  
Normal Range ◽  
History Of

Abstract Lenvatinib is an antineoplastic oral agent that acts as a multi-kinase inhibitor against vascular endothelial growth factor (VEGF). This drug is commonly known for its use against radioiodine-refractory differentiated thyroid cancer, but it is also approved for unresectable hepatocellular carcinoma (HCC). Side effects such as fatigue, hypertension, palmar-plantar erythrodysesthesia, diarrhea, decreased appetite, and hypothyroidism are frequently reported adverse effects. However, the incidence of hyperthyroidism is a less known phenomenon. This case describes a patient with HCC on lenvatinib therapy who develops destructive thyroiditis. A 69-year-old man with hepatitis c cirrhosis complicated by progressive hepatocellular carcinoma (Child-Pugh class A6) presented with generalized weakness, unintentional weight loss, heat intolerance, palpitations, and tremors. He had been started on chemotherapy with lenvatinib 12 mg/day four weeks prior to presentation. Endocrinology was consulted due to abnormal thyroid function tests (TFTs). He had no previous history of thyroid function abnormalities or family history of thyroid disease. Laboratory tests revealed a hyperthyroid state [total thyroxine (T4), 14.3 µg/dL (normal range 4.5-11.7); free thyroxine (FT4), 1.9 ng/dL (normal range 0.9-1.7); thyroid-stimulating hormone (TSH), 0.07 µIU/mL (normal range 0.27-4.20), and negativity for antibodies [anti-thyroid peroxidase antibody (TPO Ab), 0.8 IU/mL (normal range 0.0-9.0); thyroglobulin antibody (Tg Ab), < 0.9 IU/mL (normal range 0.0-4.0); thyroid stimulating immunoglobulin (TSI), 90% (normal range < 122)]. Ultrasonography revealed a mildly prominent thyroid gland, a homogenous echo texture, and no suspicious thyroid nodules. In addition, a 99m-technetium (99mTc) scintigraphy demonstrated reduced radioactive uptake that was consistent with thyroiditis. Therefore, this patient was diagnosed with lenvatinib-induced destructive thyroiditis. Palpitations improved with a beta-blocker and the patient was resumed on a lower dose of lenvatinib, 8 mg/day, one week later. About six weeks after the initial dose of lenvatinib, his TFT results normalized. Lenvatinib disrupts cell proliferation which can affect many organs, including the thyroid gland. Although several theories have been proposed, the exact underlying mechanism by which this occurs remains unknown. It is important to note that in addition to hypothyroidism, lenvatinib may also cause hyperthyroidism in the form of a transient destructive thyroiditis. This emphasizes the need to routinely check TFTs prior to the initiation of lenvatinib and throughout the course of therapy.

scholarly journals Prevalence of postpartum thyroiditis in women with gestational diabetes mellitus in Ardabil: North West of Iran

2016 ◽  
Vol 2 (6) ◽  
pp. 116
Author(s):  
Manouchehr Iranparvar-Alamdari ◽  
Hosein Ghorbani Behrooz ◽  
Mostafa Alidousti
Keyword(s):  
Diabetes Mellitus ◽  
Family History ◽  
Gestational Diabetes ◽  
Gestational Diabetes Mellitus ◽  
Thyroid Stimulating Hormone ◽  
Cross Sectional ◽  
Family History Of Diabetes ◽  
Postpartum Thyroiditis ◽  
Pregnancy And Postpartum ◽  
History Of

<p class="abstract"><strong>Background:</strong> Gestational diabetes is the most common metabolic disorder during pregnancy and postpartum thyroiditis is a destructive thyroiditis that can cause serious complications for the mother and her child. The purpose of this study was to determine the prevalence of postpartum thyroiditis in women with gestational diabetes.</p><p class="abstract"><strong>Methods:</strong> In this cross-sectional study, 86 cases satisfy inclusion criteria and gestational diabetes mellitus (GDM) and were evaluated for postpartum thyroiditis with thyroid stimulating hormone (TSH), T4, anti-TPO, T3RU tests. The groups with and without thyroiditis were compared and data was analyzed by statistical methods.</p><p class="abstract"><strong>Results:</strong> There were 17 patients (19.8%) with postpartum thyroiditis, of whom 4 patients (23.5%) had hyperthyroidism, 9 patients (52.9%) were in the age group of 21 to 30 years, and 9 patients (52.9%) had a family history of diabetes.  Five patients (29.4%) with high anti-TPO level (P=0.022) and mean TSH and anti-TPO respectively, 2.8 (4.8) and 17.2 (35.9).</p><p><strong>Conclusions:</strong> The results showed that higher level of anti TPO titer and family history of diabetes can be associated with a higher rate of postpartum thyroiditis, so it is recommended that postpartum thyroiditis to be examined in women with gestational diabetes who have these mentioned items.</p>

scholarly journals Switching of Hashimoto Thyroiditis Into Graves’ Disease: A Case Report and Literature Review

2021 ◽  
Vol 10 (2) ◽  
pp. 82-85
Author(s):  
Rajab Maksoud ◽  
Nour Maksoud ◽  
Lubana Wannous ◽  
Samaher Almousa
Keyword(s):  
Laboratory Tests ◽  
Hashimoto Thyroiditis ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Graves Disease ◽  
Free Triiodothyronine ◽  
Full Remission ◽  
History Of ◽  
Tsh Levels

Background: Hashimoto thyroiditis (HT) and Graves’ disease (GD) are autoimmune inflammatory thyroid disorders. The evolution from GD into HT is the most common scenario while the conversion from HT into GD seems to be less common. Case Presentation: A 20-year-old female patient referred to the endocrinology clinic with a three-month history of fatigue, lethargy, lack of appetite, constipation, menorrhagia, cold intolerance, and 5 kg weight gain in the last two months. Clinical examination showed dry skin, scalp hair loss, and painless hard goiter whereas thyroid ultrasound revealed generalized homogeneous hypoechoic thyroid hypertrophy. Laboratory tests demonstrated increased serum thyroid-stimulating hormone (TSH) 210 µIU/L (normal: 0.25-4.50), decreased free thyroxine (FT4) 0.37 ng/L (normal: 0.8-1.8) and free triiodothyronine (FT3) 1.94 pg/mL (normal: 1.8-4.6), and finally, increased thyroid peroxidase antibodies (anti-TPO) 462 IU/mL (normal: up to 34). Based on observations, HT was diagnosed and thus daily treatment with levothyroxine 75 mcg was started for the patient. Two months later, she referred with symptoms suggestive of hyperthyroidism with reduced TSH levels, which did not improve after levothyroxine cessation, thus more laboratory tests were conducted and revealed decreased TSH levels, increased T3 and T4, and TSH receptor stimulating antibody (TSAb)levels, and increased radioactive iodine uptake at 24 hours. Therefore, the diagnosis of GD was made. Five weeks after treatment, she was in full remission. Conclusion: Although the switch from HT into GD is rare, it can occur at any time during the disease. Nonetheless, early diagnosis and treatment would improve the quality of care.

scholarly journals Assessment of the simultaneous effect of hypothyroidism and thyroid autoimmunity with gestational diabetes on the incidence of type 2 diabetes

2020 ◽  
Author(s):  
Maryam zahedi ◽  
Elham Kazemian ◽  
Fahimeh Ramezani Tehrani ◽  
Maryam tohidi ◽  
Fereidoun azizi ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gestational Diabetes ◽  
Incidence Rate ◽  
Thyroid Autoimmunity ◽  
Thyroid Peroxidase ◽  
Thyroid Disorders ◽  
Thyroid Peroxidase Antibody ◽  
Term Delivery ◽  
History Of

Abstract Introduction: Despite the evidence available on the adverse impact of gestational diabetes (GDM) and thyroid disorders on developing type 2 diabetes (T2DM), the concurrent influence of these disorders on the incidence of T2DM has not been reported yet. Methods: In this prospective study, 1894 non-diabetic women aged 20 to 60 years, with a history of at least one term delivery, without diagnosed hyperthyroidism were selected at the initiation of the Tehran Thyroid Study (TTS). Pooled logistic regression analyses were used to investigate the association of GDM, thyroid disorders i.e., hypothyroidism and/or thyroid peroxidase antibody (TPOAb) positivity and interaction between GDM and thyroid disorders with the risk of incident T2DM. Results: Of the 1894 participants of the present study, 346 (18.3%) had a history of GDM, and 832 (43.9%) had thyroid disorders. The total cumulative incidence rate of T2DM at the median follow-up time of ~ 12 years was overall 12/1000 person-years (95% confidence interval (CI): 10/1000–13/1000), with an incidence rate of 16/1000 (95%CI: 13/1000–20/1000) in women with GDM; and 11/100,000 (95%CI: 9/100,000–12/1000) among those without GDM. After adjustment for age, the risk of incident T2DM increased among individuals with the previous GDM compared to women without a history of GDM (odds ratio (OR): 1.54, 95%CI: 1.06, 2.25). No significant associations were found between either thyroid disorders or the interaction between GDM and thyroid disorders with the development of T2DM; (OR: 1.14, 95%CI: 0.82, 1.58) and (OR: 1.27, 95%CI: 0.66, 2.43), respectively.Conclusion: GDM and thyroid disorders have no concurrent impacts on the incidence of T2DM.

scholarly journals SAT-569 Management of Severe Gestational Hypertriglyceridemia

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Anne Borja ◽  
Meena Khandelwal ◽  
Farah Morgan
Keyword(s):  
Fatty Acids ◽  
Abdominal Pain ◽  
Gestational Diabetes ◽  
Triglyceride Level ◽  
Liver Function Tests ◽  
Ethyl Esters ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Limited Data ◽  
History Of

Abstract Background: Severe gestational hypertriglyceridemia is a dangerous and life threatening illness. Management can be difficult due to the limited data on safety of medical therapy during pregnancy. We present a case of severe gestational hypertriglyceridemia. Case Presentation: A 29 year old woman, G4P2012 at 23w3d, with a past medical history of gestational diabetes, nontoxic thyroid nodule, and hypertriglyceridemia presented to the emergency room for abdominal pain and nausea. She has no known family history of lipid disorders. Her last pregnancy was complicated by acute pancreatitis due to hypertriglyceridemia. Between pregnancies, her triglyceride level was &gt;900 mg/dL and gemfibrozil therapy was advised, however reported nonadherence. In current pregnancy and after counseling, she was prescribed omega-3 acid ethyl esters (Lovaza) 2 grams twice a day and referred to maternal fetal medicine. Triglyceride level on admission was 3640 mg/dL, and she admitted to poor adherence to Lovaza. Liver function tests were within normal limits. She was started on an insulin drip, as well omega-3 fatty acids 4g daily. However, the triglyceride level remained elevated despite 72 hours on the insulin drip and it was subsequently discontinued. Plasmapheresis was discussed but deferred given no evidence of pancreatitis. Gemfibrozil 600mg twice a day was added to the omega-3 fatty acids which were titrated up to 2g three times a day. On her day of discharge, her triglyceride level was 2200 mg/dL and abdominal pain had resolved. She was maintained on gemfibrozil and Omega-3 fatty acids, with plans to increase them by 1g per week to reach a goal of 10g per day with a goal triglyceride level &lt;1000mg/dL. Pre-gestational diabetes was tightly controlled with insulin. She was also seen by the nutritionist for counseling of a low fat diet and was followed very closely as an outpatient. Although the omega-3 fatty acids were titrated to 8g per day, the triglyceride level remained ~2000mg/dL. She remained asymptomatic and delivered a healthy baby boy weighing 3446 grams at 36 weeks 4 days, with no complications. She continues follow up with endocrinology with triglycerides 6 months later being 1618 mg/dl. Conclusion: We present a patient with severe gestational hypertriglyceridemia with a known history of pancreatitis. Due to the rarity of this condition, there is limited data on the safety of treatments for hypertriglyceridemia in pregnant women. This case demonstrates the use of gemfibrizol is appropriate when the hypertriglyceridemia threatens the health of the mother and baby. Further studies are needed to establish efficacy and safety of the use of these treatments in pregnant patients.

scholarly journals Thyroid function in pregnant females carrying thyroid peroxidase antibodies

2003 ◽  
Vol 49 (5) ◽  
pp. 23-29
Author(s):  
V. V. Fadeyev ◽  
S. V. Lesnikova ◽  
G. A. Melnichenko
Keyword(s):  
Odds Ratio ◽  
Thyroid Stimulating Hormone ◽  
Control Group ◽  
Thyroid Peroxidase ◽  
Second Trimester ◽  
Early Gestation ◽  
Pregnant Females ◽  
Thyroid Peroxidase Antibodies ◽  
History Of ◽  
High Level

То define risk factors for gestational hypothyroxinemia in females carrying thyroid peroxidase antibodies (TPO Ab) during preg­nancy, a study was performed, which included 73 females at dif­ferent periods of pregnancy in accordance with the following cri­teria: the lack of impaired dysfunction of the thyroid gland (TG) on primary examination; elevated TPO Ab levels (more than 100 mEU/l; no history of TG pathology. The control group comprised 128 pregnant females without TG pathology. Evaluation of TG function in females with TPO Ab who received and did not the physiological doses of iodine revealed that the function did not differ by the end of pregnancy. The odds ratio for hypothyrox­inemia in pregnant females with more than 100 mEU/l of TPO Ab was 3.14. In a subgroup of females with TPO Ab and the en­larged TG in the second trimester, the level of fT4 was signifi­cantly lower and that of thyroid-stimulating hormone (TSH) was significantly higher than those in the control group. Logistic re­gression analysis indicated that a relatively high level of TSH in early gestation was most significant in females with TPO Ab. It is concluded that it is expedient to consider whether preventive levothyroxine therapy is performed in females who carry TPO Ab with the enlarged TG and with TSH level that is relatively high (more than 2 mMe/l) for early pregnancy.

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