Graves’ disease presenting with psychosis crisis: A case report

BACKGROUNDNeuroendocrine dysfunction, especially involving the hypothalamic-pituitary-thyroid axis, plays a critical role in the onset and progression of schizophrenia. Alterations in thyroid stimulating hormone (TSH), triiodothyronine (T3), free T3 (FT3), thyroxine (T4), and free T4 have been implicated in this process. Although previous studies have established an association between thyroid function and psychiatric symptoms, how thyroid hormone levels vary with disease duration remains underexplored.AIMTo investigate duration stage-specific associations between thyroid hormones and psychotic symptoms among inpatients with stable schizophrenia.METHODSThis cross-sectional study was conducted at Zigong Mental Health Center, China, and included 237 hospitalized patients with stable schizophrenia. Participants were stratified into three groups based on disease duration: 0-10 years, 10.1-20 years, and over 20 years. Peripheral blood samples were collected to measure serum thyroid hormone levels. Psychotic symptoms were assessed using the Positive and Negative Syndrome Scale. Covariate-adjusted linear regression analyses were performed to assess the relationships between thyroid hormone levels and Positive and Negative Syndrome Scale sub-scale scores.RESULTSThe relationship between thyroid hormones and psychotic symptoms varied by disease duration. In patients with a disease course of 0-10 years, T4 [β = -0.848; 95% confidence interval (CI): -1.564 to -0.133; P = 0.021] and FT3 (β = -2.483; 95%CI: -4.693 to -0.273; P = 0.028) levels were significantly inversely associated with general psychopathology scores. Among those with 10.1-20 years of disease, only TSH showed a significant negative correlation with general psychopathology (β = -1.429; 95%CI: -2.348 to -0.509; P = 0.003). No significant correlations were found in the > 20 years group.CONCLUSIONThe associations between thyroid hormones and psychotic symptoms vary according to the duration of schizophrenia (T4/FT3 early; TSH mid), enabling the development of stage-adapted models and management.

Antidepressant-Resistant Depression in Patients With Comorbid Subclinical Hypothyroidism or High-Normal TSH Levels.

Heart failure (HF) is a major public health and economic problem in Western countries and is one of the most common causes of hospitalization and death. Coronary artery disease is the underlying cause in more than two thirds of chronic HF patients. By 2020, the World Health Organization projects that ischemic heart disease alone will be the most important global cause of morbidity and mortality. The estimated increases in HF-related morbidity and mortality suggest that our understanding of the pathophysiological mechanisms of this syndrome is inadequate. Interest in the role of thyroid hormones (THs) in HF has increased in recent years. The driving considerations can be summarized as follows: (1) the known effects of THs on contractile and relaxation properties of the heart; (2) experimental findings offering strong support for the hypothesis that TH signaling is critical in preserving cardiac structure and performance under normal conditions and after cardiac injury; and (3) evidence that mildly altered TH function is strongly associated with a worsening prognosis in cardiac patients in general and in HF patients in particular. Diastolic function and systolic function are clearly influenced by THs.1 Ventricular contractile function is also influenced by changes in hemodynamic conditions secondary to TH effects on peripheral vascular tone.1 TH homeostasis preserves positive ventricular-arterial coupling, leading to a favorable balance for cardiac work. A study in rats demonstrated that chronic hypothyroidism alone can eventually lead to HF.2 Other studies suggest reduced cardiac tissue triiodothyronine (T3) levels after myocardial infarction (MI) or with development of hypertension by upregulating type 3 deiodinase (D3), which leads to deactivation of T3 and T4 (thyroxine).3–6 This review highlights a growing body of evidence from animal studies and small-scale clinical trials suggesting that low cellular thyroid activity at the cardiac tissue level may adversely affect HF …

IntroductionAuditory 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.CaseThe 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.ConclusionThis 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.

Thyroid bone disease

Visual and Auditory Hallucinations During Normal Use of Paroxetine for Treatment of Major Depressive Disorder

Persistent Auditory Hallucinations That Are Unresponsive to Antipsychotic Drugs

Purpose: Nonalcoholic fatty liver disease (NAFLD) is associated with dyslipidemia, metabolic syndrome, and hypothyroidism. It is unknown if serum thyroid hormone (TH) levels are associated with NAFLD disease severity. We wished to evaluate differences in serum TH levels and liver expression of TH-associated genes between early and advanced NAFLD. Methods: RNA was extracted and microarray performed from liver tissue of 70 patients with biopsy-proven NAFLD (42 early (F:0-1), 28 advanced (F:3-4)). Serum collected on the same day as biopsy was analyzed for thyroid stimulating hormone (TSH), free T4 (fT4), free T3 (fT3), and reverse T3 (rT3). TH levels were compared between early vs advanced NAFLD using Wilcoxon rank-sum analysis. Logistic regression models using a stepwise algorithm were built with histologic severity as the outcome and TH serum markers as the primary predictors, with and without adjusting for potential confounders including: age, gender, BMI, ethnicity, HgBA1C, history of hypertension, and history of hyperlipidemia. Differential gene expression was determined on normalized data by an empirical Bayes method with a 5% False Discovery Rate control. Results: Free T3 was significantly lower (p=0.03) and rT3 significantly higher (p=0.005) in patients with advanced disease as compared to early disease. Free T3 and rT3 remained significant predictors of advanced fibrosis in the final stepwise logistic regression model after adjusting for potential confounders (p=0.034 and 0.032). The fT3/rT3 ratio, previously reported as a positively-associated surrogate test for intracellular fT4 uptake, was lower in those with advanced NAFLD (p=0.001). Both univariate and multivariate logistic regression analysis confirmed that a reduced fT3/rT3 ratio was a strong predictor of advanced fibrosis (p values<0.005). Area under the curve (AUC) for fT3/rT3 ratio as a predictor of fibrosis was 0.72. In addition to serum TH levels, we evaluated gene expression levels of potential regulators of intracellular hepatic TH uptake. Analysis revealed increased expression of THRSP in early NAFLD and increased expression of tissue remodeling genes in advanced NAFLD (IGFBP6, RCAN2, and ITGAV). Spearman's rank correlations indicate a significant positive relationship between serum fT3 and fT3/rT3 ratio, with RAC3 expression (ρ=0.55, ρ=0.46) (p <0.001), a gene important in morphogenesis and tissue remodeling. Conclusion: Advanced NAFLD is associated with lower fT3 and higher rT3 levels vs. those with early NAFLD. Thyroid-specific gene expression differences in early vs. advanced NAFLD suggest that TH levels and/or hepatic responsiveness to TH are potential pathogenic mechanisms contributing to NAFLD disease severity.

When a patient presents with both psychotic and obsessive-compulsive symptoms, the clinician is faced with a differential diagnosis that includes comorbid schizophrenia and obsessive-compulsive disorder (OCD), OCD with poor insight, and schizophrenia with antipsychotic-induced obsessive-compulsive symptoms. If the psychotic symptoms are subthresh-old or attenuated in form, the individual may have OCD and putative prodromal schizophrenia. The authors present a case to outline a strategy for differentiating among these possible diagnoses and for optimizing treatment.

Thyroid storm as a result of functioning metastatic thyroid carcinoma is exceedingly rare. 1 We describe a patient with functioning distant metastases from adenocarcinoma of the thyroid in whom thyroid storm developed in the course of care for extensive burns.

AimsIn patients presenting with acute mania &amp; psychosis, it is important to rule out organic cause of their symptoms. Neuropsychiatric problems include affective disorders, disturbances in cognition and psychosis. Mania is commonly associated with hyperthyroidism, But hypothyroidism is a medical condition commonly encountered in a variety of the clinical settings. Patients with severe hypothyroidism may present with psychosis and less commonly with symptoms of mania. We report a case of 37 year old male presenting with acute mania &amp; psychosis, in context of severe hypothyroidism.Thyroid dysfunction is known to have a significant impact on mental health. Hypothyroidism, in particular, has been linked to mood disorders and acute psychosis. Though most commonly associated with depression, hypothyroidism has been linked to psychosis since the late 1800s, in reports of delusions and hallucinations in patients with myxedema. More recent literature highlights the incidence and coexistence of hypothyroidism and psychiatric disorders, describing possible mechanisms contributing to the pathophysiology of these disorders. The link between hypothyroidism and mania, however, is less clear, with few reports in the literature. We present a case report of a 37 year old male presenting with acute onset mania with psychosis and previously undiagnosed severe hypothyroidism.MethodsAB, a 37-year-old married male from a Telugu-speaking rural background, was brought to the psychiatric outpatient department with his family. The patient's attendants reported concerns about inappropriate talk, bizarre behavior, hyperactivity, sleeplessness, decreased appetite, and suspiciousness lasting for 10 days, indicative of acute psychosis. AB, with no previous psychiatric history, attributed his symptoms to stress related to business and property issues. Family members described him screaming in his apartment, displaying grandiose delusions of a divine presence within him, and exhibiting restlessness and aggression.Further exploration revealed a history of sleepless nights preceding these symptoms, during which AB initiated a fast, abstaining from eating or drinking to establish himself as a ‘spiritual advisor.’ He expressed paranoia, believing neighbors and family members were conspiring against him due to fictitious landownership claims. Upon examination, AB appeared conscious but restless, agitated, and inattentive for the past 15 days.Blood work unveiled thyroid abnormalities, with elevated thyroid-stimulating hormone (TSH) (&gt;100 mIU/L) and decreased free triiodothyronine (T3). AB denied prior hypothyroidism diagnoses, though his mother had a history managed with levothyroxine. Notably, no apparent physical symptoms of hypothyroidism were observed.AB's social history included occasional alcohol (30ml once in a blue moon) and tobacco use (3–4 cigarettes/day). Three days before admission, he ceased smoking, and his last social drink occurred a month earlier.Diagnosed with acute mania per ICD-10, AB commenced treatment with Tab. diazepam 5mg HS and levothyroxine 100 mcg daily. With this regimen, he showed improved goal-directed behavior and reduced grandiosity, although mild restlessness persisted. Continuing the treatment, the endocrinology team increased levothyroxine to 300 mcg daily, leading to stabilized restlessness. Remarkably, psychosis and mania resolved after two weeks without antipsychotics or mood stabilizers, accompanied by a downward trend in TSH (83.10 mIU/L) and an upward trend in free T3 (0.70 ng/mL) and free T4 (5.03 mg/dL). At discharge, AB showed no residual psychotic or manic symptoms, and levothyroxine was maintained at 300 mcg daily, with diazepam discontinued after a few days.ResultsIn the above case rare effect of hypothyroidism was observed. The coexistence of hypothyroidism with depression, bipolar disorder and psychosis has been reported, dating back to the late 1800s. In 1949, Asher reported 14 cases of psychosis with hypothyroidism, 9 of which recovered with thyroid hormone treatment alone. Numerous cases have since linked psychosis to hypothyroidism. The majority of these cases were managed with a combination of antipsychotic medication and thyroid replacement, however in some cases maintenance therapy included thyroid replacement alone. There was no correlation between the degree of hypothyroidism and the severity of psychiatric symptoms. Psychosis usually remits after 1 week of thyroid replacement, with earlier resolution with the addition of antipsychotic medications. Although psychosis is less commonly associated with hypothyroidism than depression, it is a possible manifestation of the disorder.Hypothyroidism is a common co-morbidity in bipolar disorder. The association between hypothyroidism and mania is less clear. Mania with concomitant hypothyroidism has been reported in patients previously undiagnosed with psychiatric illness. Patients presenting with acute manic episodes and hypothyroidism have improved clinically with a combination of psychotropic medications and thyroid hormone. But in this case patient’s manic condition improved with levothyroxine alone.Delineating aetiology of psychiatric symptoms in our patient is not difficult. AB's description of manic &amp; psychotic symptoms with no past or family history of bipolar illness would suggest the diagnosis of acute mania. It is possible that hypothyroidism aggravated an underlying psychiatric illness or induced a manic episode with psychotic features. Treatment with levothyroxine &amp; diazepam was considered for this patient to see whether the patient improves with levothyroxine alone &amp; to prove mania is secondary to hypothyroidism. It is possible that levothyroxine contributed to improvement of ABs psychotic and manic symptoms. It is surmised psychotic symptoms completely resolved when the TSH, T3, T4 levels returned to normal.ConclusionThyroid function should be investigated in all patients presenting with mania or psychotic symptoms. Without an underlying psychiatric illness, thyroid hormone replacement may suffice in the treatment of acute onset psychosis in the context of severe hypothyroidism. However, during an acute manic episode, treatment with thyroid hormone therapy alone may not suffice in some cases, and likely requires concomitant therapy with an antipsychotic or mood stabilizer.

To compare serum concentrations of thyroid hormones--T4, T3, free T4 (FT4) and reverse T3 (rT3)--and thyroid-stimulating hormone (TSH) found in the umbilical cord blood of term newborns with and without asphyxia and those found in their arterial blood collected between 18 and 24 h after birth. A further aim of the study was to assess the association between severity of hypoxic-ischemic encephalopathy and altered thyroid hormone and TSH levels, and between mortality and FT4 levels in the arterial blood of newborns between 18 and 24 h of life. A case-control study was carried out. The case group comprised 17 term newborns (Apgar score < or = 3 and < or = 5 at the first and fifth minutes; umbilical cord blood pH < or = 7.15) who required bag and mask ventilation for at least one minute immediately after birth. The control group consisted of 17 normal, term newborns (Apgar score > or = 8 and > or = 9 at the first and fifth minutes; umbilical cord blood pH > or = 7.2). Cord blood and arterial blood samples were collected immediately after birth and 18 to 24 h after birth, respectively, and were used in the blood gas analysis and to determine serum concentrations of T4, T3, FT4, rT3 and TSH by radioimmunoassay. All newborns were followed-up until hospital discharge or death. Gestational age, birthweight, sex, size for gestational age, mode of delivery and skin color (white and non-white) were similar for both groups. No differences were found in mean levels of cord blood TSH, T4, T3 and FT4 between the groups. In the samples collected 18 to 24 h after birth, mean levels of TSH, T4, T3 and FT4 were significantly lower in the asphyxiated group than in the control group. Mean concentrations of arterial TSH, T4 and T3 between 18 and 24 h of life were lower than concentrations found in the cord blood analysis in asphyxiated newborns, but not in controls. In addition, asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy presented significantly lower mean levels of TSH, T4, T3 and FT4 than those of controls. None of the asphyxiated newborns with FT4 > or = 2.0 ng/dl died; 6 out of the 11 asphyxiated newborns with FT4 < 2.0 ng/dl died. Serum concentrations of TSH, T4, T3 and FT4 are lower in asphyxiated newborns than in normal newborns between 18 and 24 h of life; this suggests central hypothyroidism secondary to asphyxia. Asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy present a greater involvement of the thyroid function and consequently a greater risk of death.

Aim: To compare serum concentrations of thyroid hormones—T4, T3, free T4 (FT4) and reverse T3 (rT3)—and thyroid-stimulating hormone (TSH) found in the umbilical cord blood of term newborns with and without asphyxia and those found in their arterial blood collected between 18 and 24 h after birth. A further aim of the study was to assess the association between severity of hypoxic-ischemic encephalopathy and altered thyroid hormone and TSH levels, and between mortality and FT4 levels in the arterial blood of newborns between 18 and 24 h of life. Methods: A case-control study was carried out. The case group comprised 17 term newborns (Apgar score ≤3 and ≤5 at the first and fifth minutes; umbilical cord blood pH ≤7.15) who required bag and mask ventilation for at least one minute immediately after birth. The control group consisted of 17 normal, term newborns (Apgar score ≥8 and ≥9 at the first and fifth minutes; umbilical cord blood pH ≥7.2). Cord blood and arterial blood samples were collected immediately after birth and 18 to 24 h after birth, respectively, and were used in the blood gas analysis and to determine serum concentrations of T4, T3, FT4, rT3 and TSH by radioimmunoassay. All newborns were followed-up until hospital discharge or death. Results: Gestational age, birthweight, sex, size for gestational age, mode of delivery and skin color (white and non-white) were similar for both groups. No differences were found in mean levels of cord blood TSH, T4, T3 and FT4 between the groups. In the samples collected 18 to 24 h after birth, mean levels of TSH, T4, T3 and FT4 were significantly lower in the asphyxiated group than in the control group. Mean concentrations of arterial TSH, T4 and T3 between 18 and 24 h of life were lower than concentrations found in the cord blood analysis in asphyxiated newborns, but not in controls. In addition, asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy presented significantly lower mean levels of TSH, T4, T3 and FT4 than those of controls. None of the asphyxiated newborns with FT4 ≥2.0 ng/dl died; 6 out of the 11 asphyxiated newborns with FT4 < 2.0 ng/dl died. Conclusions: Serum concentrations of TSH, T4, T3 and FT4 are lower in asphyxiated newborns than in normal newborns between 18 and 24 h of life; this suggests central hypothyroidism secondary to asphyxia. Asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy present a greater involvement of the thyroid function and consequently a greater risk of death.

Pesticides can act as endocrine disruptors by different mechanisms including inhibition of iodine absorption, increases in thyroid hormone clearance, decreased cellular uptake of thyroid hormones, or changes in expression of thyroid hormone regulated genes. This study examined how exposure to pesticides impacts thyroid hormone levels, thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), free T3 (FT3), and free T4 (FT4) by comparing conventional (n = 195) and organic farmers (n = 222), and by evaluating which types of pesticides might be associated with changes in thyroid hormone levels. Questionnaires were used to collect information about farmer characteristics, self-reported stress, agricultural activities, and history of pesticide use. Conventional farmers were asked to report the type and quantity of pesticides used each day. The TSH, FT3, T3, and T4 levels of conventional farmers were 1.6, 1.2, 1.3, and 1.1 times higher than those of organic farmers, respectively, after adjusting for covariates. Several specific herbicides had a significant relationship between the amount applied and an increase in thyroid hormone levels, after covariate adjustment. They included: paraquat (TSH, FT3 and T3); acetochlor (FT4); atrazine (TSH, FT3 and T3); glyphosate (T4); diuron (TSH) and the “other” herbicides including alachlor, propanil, and butachlor (FT4 and T3). The most commonly used herbicide among conventional farmers was glyphosate, followed by paraquat, 2,4-dichlorophenoxyacetic acid (2,4-D). These findings suggest that exposure to pesticides could impact the development of metabolic diseases and other health outcomes by altering the endocrine system (the thyroid hormone levels) through the hypothalamic–pituitary–thyroid (HPT) axis. This work is a part of a longitudinal study which will evaluate the sub-chronic effects of repeated exposure to different types of pesticides on thyroid hormone levels.

Alcoholic liver disease affects almost all aspects of the thyroid gland including the thyroid hormone levels and the thyroid gland size. The altered thyroid hormone levels in alcoholic liver disease may affect alcohol abstinence in withdrawal period by changing hormone milieu in brain, increasing withdrawal dysphoria and increasing craving. The aim of the present study was to assess and compare the levels of thyroid hormones- free T3, free T4, Thyroid Stimulating Hormone (TSH) and Gamma Glutamyl Transferase (GGT) in chronic alcoholic liver disease patients before and after treatment. This study was conducted on 70 alcoholic liver disease patients. Two serum samples were taken from the patient once at the time of admission and the other at the time of discharge after atleast ten days of treatment. Serum free T3, free T4, TSH and GGT were assessed on auto analyzer Beckman Coulter. Statistical analysis is done by paired t-test and Pearson's Correlation test. In present study, serum GGT levels decreased significantly (before treatment-207.46±66.90 U/L; after treatment-78.47±19.71 U/L) and free T3 levels increased significantly with treatment (before treatment-2.54±0.48 pg/mL; after treatment-2.88±0.37 pg/mL). Free T4 levels are also increased with treatment (before treatment-0.78±0.19 ng/dL; after treatment-0.88±0.13 ng/dL) and TSH levels are not altered significantly with treatment (before treatment-3.34±1.62 μIU/mL; after treatment-3.32±1.51 μIU/mL). Additionally, free T3 showed a significant correlation with GGT before (p-value<0.001) and after treatment (p-value-0.003) and free T4 and TSH showed a significant correlation with GGT after treatment (free T4: p-value<0.001) (TSH: p-value <0.001) and a suggestive significance exists before treatment (free T4: p-value= 0.098) (TSH: p-value=0.062). Thyroid hormones levels, particularly free T3 and free T4, need to be evaluated in chronic alcoholic liver disease patients. Free T3 could be used as a marker of alcoholism and is very useful in assessing the treatment efficacy in chronic alcoholic liver disease. Also, assessing free thyroid hormones is necessary during the withdrawal and abstinent periods as decreased hormone levels may increase withdrawal effects and craving for alcohol.