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Turkish Archives of Pediatrics Oct 2023Mercury poisoning is a condition with multiple-organ dysfunction that has effects on the central nervous system, gastrointestinal system, cardiovascular system, skin,...
OBJECTIVE
Mercury poisoning is a condition with multiple-organ dysfunction that has effects on the central nervous system, gastrointestinal system, cardiovascular system, skin, lungs, and kidneys. It can be fatal or may result in sequelae such as neurological disturbances, if treated late or left untreated. The endocrinological effects of mercury exposure are not well-known. We aimed to evaluate patients with mercury poisoning.
MATERIALS AND METHODS
A total of 6 cases of mercury poisoning from 3 families were included in the study. Clinical, laboratory, and follow-up data were recorded.
RESULTS
Thyroid dysfunction was presented as high thyroid hormones and normal thyrotropin level (unsuppressed) in 5 cases (83.3%). On the other hand, pheochromocytoma-like syndrome was detected in 5 cases (83.3%) with hypertension. The 4 cases were the first to use methimazole for mercury poisoning due to tachycardia and hypertension despite antihypertensive treatment due to catecholamine excess and thyroid dysfunction. Hyponatremia was detected in 3 cases (50%).
CONCLUSION
Mercury poisoning is difficult to diagnose because it is rare and presents with nonspecific physical and laboratory findings. Early diagnosis and providing appropriate treatment are essential in order to prevent sequelae. Mercury poisoning should be considered in patients with unexplained hypertension and tachycardia suggesting the involvement of thyroid hormones and catecholamines.
PubMed: 37818842
DOI: 10.5152/TurkArchPediatr.2023.23150 -
Bioorganic Chemistry Dec 2023Lactoperoxidase was previously used as a model enzyme to test the inhibitory activity of selenium analogs of anti-thyroid drugs with...
Lactoperoxidase was previously used as a model enzyme to test the inhibitory activity of selenium analogs of anti-thyroid drugs with 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) as a substrate. Peroxidases oxidize ABTS to a metastable radical ABTS, which is readily reduced by many antioxidants, including thiol-containing compounds, and it has been used for decades to measure antioxidant activity in biological samples. We showed that anti-thyroid drugs 6-n-propyl-2-thiouracil, methimazole, and selenium analogs of methimazole also reduced it rapidly. This reaction may explain the anti-thyroid action of many other compounds, particularly natural antioxidants, which may reduce the oxidized form of iodine and/or tyrosyl radicals generated by thyroid peroxidase thus decreasing the production of thyroid hormones. However, influence of selenium analogs of methimazole on the rate of hydrogen peroxide consumption during oxidation of ABTS by lactoperoxidase was moderate. Direct hydrogen peroxide reduction, proposed before as their mechanism of action, cannot therefore account for the observed inhibitory effects. 1-Methylimidazole-2-selone and its diselenide were oxidized by ABTS to relatively stable seleninic acid, which decomposed slowly to selenite and 1-methylimidazole. In contrast, oxidation of 1,3-dimethylimidazole-2-selone gave selenite and 1,3-dimethylimidazolium cation. Accumulation of the corresponding seleninic acid was not observed.
Topics: Antioxidants; Cations; Hydrogen Peroxide; Lactoperoxidase; Methimazole; Oxidation-Reduction; Selenious Acid; Selenium; Propylthiouracil
PubMed: 37788560
DOI: 10.1016/j.bioorg.2023.106891 -
International Journal of Molecular... Sep 2023Mood alterations, anxiety, and cognitive impairments associated with adult-onset hypothyroidism often persist despite replacement treatment. In rodent models of...
Mood alterations, anxiety, and cognitive impairments associated with adult-onset hypothyroidism often persist despite replacement treatment. In rodent models of hypothyroidism, replacement does not bring 3-iodothyronamine (TAM) brain levels back to normal. TAM is a thyroid hormone derivative with cognitive effects. Using a pharmacological hypothyroid mouse model, we investigated whether augmenting levothyroxine (L-T) with TAM improves behavioural correlates of depression, anxiety, and memory and has an effect on hippocampal neurogenesis. Hypothyroid mice showed impaired performance in the novel object recognition test as compared to euthyroid mice (discrimination index (DI): 0.02 ± 0.09 vs. 0.29 ± 0.06; t = 2.515, = 0.02). L-T and L-T+TAM rescued memory (DI: 0.27 ± 0.08 and 0.34 ± 0.08, respectively), while TAM had no effect (DI: -0.01 ± 0.10). Hypothyroidism reduced the number of neuroprogenitors in hippocampal neurogenic niches by 20%. L-T rescued the number of neuroprogenitors (mean diff = 106.9 ± 21.40, t = 4.99, p = 0.003), while L-T+TAM produced a 30.61% rebound relative to euthyroid state (mean diff = 141.6 ± 31.91, t = 4.44, p = 0.004). We performed qPCR analysis of 88 genes involved in neurotrophic signalling pathways and found an effect of treatment on the expression of , , , , , , and . Our data confirm that L-T is necessary and sufficient for recovering memory and hippocampal neurogenesis deficits associated with hypothyroidism, while we found no evidence to support the role of non-canonical TH signalling.
Topics: Mice; Animals; Thyroxine; Hypothyroidism; Hippocampus; Dietary Supplements; Nerve Tissue Proteins; Basic Helix-Loop-Helix Transcription Factors
PubMed: 37762153
DOI: 10.3390/ijms241813845 -
BMC Endocrine Disorders Aug 2023Insulin autoimmune syndrome (IAS) is a rare cause of hypoglycemia characterized by high levels of blood insulin autoantibodies. It has been documented that drugs...
Long-term follow-up after discharge witnesses a slow decline of insulin autoantibodies in patients with insulin autoimmune syndrome complicated with Grave's disease: a report of two cases.
BACKGROUND
Insulin autoimmune syndrome (IAS) is a rare cause of hypoglycemia characterized by high levels of blood insulin autoantibodies. It has been documented that drugs containing sulfhydryl groups may result in IAS. In this study, we present two cases of IAS induced by methimazole, along with their corresponding treatments and a long-term follow-up after hospitalization.
CASE PRESENTATION
We report two patients with Grave's disease (GD), carrying the HLA-DRB1 04:06 genotype, who experienced hypoglycemic episodes after taking methimazole. Inpatient treatments helped return their blood glucose levels to normal. Although no recurrences of hypoglycemia were present in the two cases studied, insulin autoantibodies remained positive for the previous follow-up sessions, which turned negative only three years after discharge.
CONCLUSIONS
GD patients who carry the HLA-DRB1 04:06 genotype are prone to IAS if they take drugs containing sulfhydryl groups. It may take time for the elimination of insulin autoantibodies after the recovery from the hypoglycemic episode in IAS patients.
Topics: Humans; Follow-Up Studies; Patient Discharge; HLA-DRB1 Chains; Methimazole; Autoimmune Diseases; Graves Disease; Autoantibodies; Hyperinsulinism; Hypoglycemia; Sulfhydryl Compounds; Hypoglycemic Agents; Insulins
PubMed: 37587407
DOI: 10.1186/s12902-023-01410-6 -
Cureus Jul 2023Hyperthyroidism is more common in women and the sensitivity of thyroid function changes during pregnancy. Excess levels of thyroid hormones and thioamides have a major... (Review)
Review
Hyperthyroidism is more common in women and the sensitivity of thyroid function changes during pregnancy. Excess levels of thyroid hormones and thioamides have a major impact on maternal and fetal outcomes. Our aim was to perform an extensive literature review and provide relevant details concerning the analytical and clinical aspects of the potential effects of the two main drugs used (methimazole and propylthiouracil) in newborns. A thorough literature review was conducted using PubMed and Google Scholar databases. In total, 10 relevant studies were identified and data from these studies were extracted and then extrapolated into results after analysis. Three out of four studies that used methimazole and carbimazole, one and two, respectively, showed adverse fetal outcomes requiring surgical management for congenital anomalies like aplasia cutis, patent vitellointestinal duct, and gastroschisis. Out of the three studies that used propylthiouracil, one baby underwent surgery for bilateral pyelectasis, vesicovaginal fistula, anal stenosis, and polydactyly. The findings of the aforementioned studies provide enough evidence to imply that the use of methimazole and carbimazole to treat antenatal hyperthyroidism has worse fetal outcomes than the use of propylthiouracil. Also, given the paucity of data in the existing literature regarding propylthiouracil's effects on newborns, further studies in this demographic are needed.
PubMed: 37551246
DOI: 10.7759/cureus.41505 -
Foods (Basel, Switzerland) Jul 2023Tea plants absorb chromium-contaminated soil and water and accumulate in tea leaves. Hexavalent chromium (Cr) is a very toxic heavy metal; excessive intake of tea...
Tea plants absorb chromium-contaminated soil and water and accumulate in tea leaves. Hexavalent chromium (Cr) is a very toxic heavy metal; excessive intake of tea containing Cr can cause serious harm to human health. A reliable and sensitive surface-enhanced Raman spectroscopy (SERS) method was developed using Au@Ag nanoparticles as an enhanced substrate for the determination of Cr in tea. The Au@AgNPs coated with carbimazole showed a highly selective reaction to Cr in tea samples through a redox reaction between Cr and carbimazole. The Cr in the contaminated tea sample reacted with methimazole-the hydrolysate of carbimazole-to form disulfide, which led to the decrease in the Raman intensity of the peak at 595 cm. The logarithm of the concentration of Cr has a linear relationship with the Raman intensity at the characteristic peak and showed a limit of detection of 0.945 mg/kg for the tea sample. The carbimazole functionalized Au@AgNPs showed high selectivity in analyzing Cr in tea samples, even in the presence of other metal ions. The SERS detection technique established in this study also showed comparable results with the standard ICP-MS method, indicating the applicability of the established technique in practical applications.
PubMed: 37509765
DOI: 10.3390/foods12142673 -
Frontiers in Psychiatry 2023Auditory hallucinations are the most common type of hallucinations observed in schizophrenia; however, visual hallucinations are not uncommon. In Graves' disease,...
INTRODUCTION
Auditory hallucinations are the most common type of hallucinations observed in schizophrenia; however, visual hallucinations are not uncommon. In Graves' disease, depression, hypomania, and psychosis can occur. While the association between Graves' disease and psychosis has been explored, understanding of the specific impact of thyroid dysfunction severity on psychiatric symptom severity is limited. Here, we present a case report of a patient with schizophrenia comorbid with Graves' disease whose psychotic symptoms were impacted by hyperthyroidism.
CASE
The patient was a 32-year-old Japanese woman who presented with auditory and visual hallucinations, agitation, and pressured speech. The patient was diagnosed with schizophrenia comorbid with Graves' disease and thyroid storm. The patient's psychotic symptoms were found to be associated with fluctuations in thyroid hormone levels, and visual hallucinations were observed only during thyroid storms. Treatment involved dexamethasone, potassium iodide, bisoprolol fumarate, and methimazole for thyrotoxicosis, and a blonanserin transdermal patch, paliperidone, and paliperidone palmitate for psychotic symptoms. The patient's auditory and visual hallucinations improved with antipsychotic treatment and decreased thyroid hormone levels.
CONCLUSION
This case highlights the importance of monitoring thyroid function in patients with schizophrenia, particularly those with comorbid Graves' disease. The correlation between psychiatric symptoms and thyroid hormone levels was demonstrated on an individual level over time, with symptoms worsening as thyroid hormone levels increased. Additionally, our case suggests that abnormally high thyroid hormone levels may trigger visual hallucinations in individuals with schizophrenia. Further studies are needed to elucidate the underlying mechanisms and potential treatment implications of this association.
PubMed: 37496682
DOI: 10.3389/fpsyt.2023.1219049 -
Placenta Aug 2023Hypothyroidism during pregnancy is associated with fetal growth restriction (FGR). FGR is commonly caused by placental insufficiency and yet the role of hypothyroidism...
INTRODUCTION
Hypothyroidism during pregnancy is associated with fetal growth restriction (FGR). FGR is commonly caused by placental insufficiency and yet the role of hypothyroidism in placental regulation of fetal growth is unknown. This study aimed to investigate the effects of maternal hypothyroidism on placental nutrient transporter expression, placental morphology, and placental metabolism.
METHODS
Hypothyroidism was induced in female Sprague-Dawley rats by adding methimazole (MMI) to drinking water at moderate (MOD, MMI at 0.005% w/v) and severe (SEV, MMI at 0.02% w/v) doses from one week prior to pregnancy and throughout gestation. Maternal and fetal tissues were collected on embryonic day 20 (E20).
RESULTS
Hypothyroidism reduced fetal weight (P<0.001) despite causing fetal hyperglycaemia (P = 0.016). Placental weight was not affected by hypothyroidism however placental efficiency was reduced (P<0.001), as was the junctional zone (JZ):labyrinth zone (LZ) weight ratio (P = 0.005). LZ glycogen content was increased (P = 0.029) and while mRNA expression of glucose transporters was reduced by hypothyroidism, only GLUT1 protein expression was reduced in male LZs. Maternal hypothyroidism reduced mitochondrial content (P = 0.031), particularly in SEV males relative to CON males (P = 0.004). Protein expression of Complex V (P < 0.001) and Complex III (P = 0.002) of the electron transport chain were also reduced in males. Maternal hypothyroidism reduced LZ (P<0.001) and fetal plasma triglycerides (P = 0.019) while fetal free fatty acids and the expression of LZ lipid transporters was not affected.
DISCUSSION
Overall, maternal hypothyroidism may lead to FGR through reduced maternal T4 availability, changes to placental morphology, altered nutrient transporter expression and sex-specific effects on placental metabolism. Changes to LZ glycogen and triglyceride stores as well as mitochondrial content suggest a metabolic shift from oxidative phosphorylation to anaerobic glycolysis in males. These changes also likely impact fetal substrate availability and therefore fetal growth.
Topics: Animals; Female; Male; Pregnancy; Rats; Fetal Development; Fetal Growth Retardation; Glycogen; Hypothyroidism; Nutrients; Placenta; Rats, Sprague-Dawley
PubMed: 37406552
DOI: 10.1016/j.placenta.2023.06.010 -
Internal Medicine (Tokyo, Japan) Feb 2024A 20-year-old woman with a 10-month history of treatment for Graves' disease (GD), developed hypothyroidism with a high level of thyrotropin (TSH) receptor-blocking...
Shift in Dominance from Blocking to Stimulating Type of Thyrotropin Receptor Antibodies, Resulting in Conversion from Hypothyroidism to Hyperthyroidism during Late Pregnancy.
A 20-year-old woman with a 10-month history of treatment for Graves' disease (GD), developed hypothyroidism with a high level of thyrotropin (TSH) receptor-blocking antibodies (TBAbs). She conceived at 28 years old and was clinically euthyroid in the first and second trimester, while taking L-thyroxine. However, at 28 weeks she became hyperthyroid with an unexpected rise in TSH receptor-stimulating antibody (TSAb) levels. She was diagnosed with GD, and methimazole was initiated. Her thyroid function normalized, but the neonate became hyperthyroid. We herein report the first case of a shift in dominance from TBAbs to TSAbs in late pregnancy.
Topics: Infant, Newborn; Female; Pregnancy; Humans; Young Adult; Adult; Long-Acting Thyroid Stimulator; Receptors, Thyrotropin; Hyperthyroidism; Hypothyroidism; Graves Disease; Thyrotropin; Autoantibodies
PubMed: 37380454
DOI: 10.2169/internalmedicine.1929-23