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Hyperthyroidism occurs in 0.2–0.7% of pregnancies with the large majority due to Graves’ disease. Graves’ disease is an autoimmune condition where TSH-receptor antibodies stimulate the thyroid gland, leading to increased thyroid hormone and decreased TSH via negative feedback loop. Screening for thyroid disease is indicated in pregnant persons with personal or family history of thyroid disease, history of type 1 diabetes, or clinical features suspicious for thyroid disease. Hyperthyroidism in pregnancy is diagnosed by a low TSH and a high T4 or T3, based on trimester-specific and population-based reference ranges. Treatment is traditionally with PTU given in the first trimester to reduce risk of embryopathy and methimazole in the second and third trimester to reduce the risk of hepatotoxicity, but variation in practice exists. Thyroid hormone, not TSH, should be monitored every 2 to 4 weeks with the goal to keep T4 or T3 slightly above or within the high-normal reference range. While rare, thyroid storm is a potentially life-threatening condition requiring immediate recognition and management in a tertiary care setting.
Sinus tachycardia due to hyperthyroidism is generally treated with beta-blockers. But some patients do not respond to beta-blockers or may have non-tolerable side effects or have contraindications. We presented a case with persistent sinus tachycardia secondary to hyperthyroidism refractory to maximal doses of propranolol. After ivabradine treatment, her heart rate was < 100 bpm within 24 hours. There were no electrocardiogram changes or side effects. The use of ivabradine is promising and can be considered in cases where tachycardia cannot be controlled in children with hyperthyroidism.
A number of endocrinopathies may complicate pregnancy with significant adverse effects on the mother and fetus. Diagnosis may prove difficult because of a long differential, and pregnancy can mask or mimic signs and symptoms of endocrine disease. Thyroid disease and diabetes are relatively common during pregnancy; however, serious complications such as thyroid storm and diabetic ketoacidosis are rare. Uncommon complications of hyperthyroidism and diabetes are discussed in this chapter along with other rare endocrinopathies
Mental symptoms are the first manifestations of hyperthyroidism. They include anxiety, dysphoria, irritability, emotional lability, sleep disorders, intellectual dysfunction, mania or depression. Anxiety is the main symptom and requires more detailed study.
Objectives
The objective was to determine symptomatology of anxiety in patients with hyperthyroidism and compare with euthyroid patients.
Methods
The study included 56 patients with hyperthyroidism (high free T3 and free T4, suppressed TSH) and 32 euthyroid patients (normal free T3, free T4 and TSH) of the control group. For psychiatric assessment State-Trait Anxiety Inventory [STAI], Hamilton Depression Rating Scale [HAM-D], and Hamilton Anxiety Rating Scale [HAM-A] were used.
Results
Total scores obtained from STAI, HAM-D and HAM-A were significantly greater in the hyperthyroidism group than that of the euthyroid group (p<0.05). The level of state anxiety in patients with hyperthyroidism was 51.39 ± 0.95 (high level) compared with 41.59 ± 2.41 (moderate level) in the control group. The level of trait anxiety in patients with hyperthyroidism was 46.86 ± 0.69 (high level), and 44.16 ± 2.17 (moderate level) in the control group. Psychomotor agitation (HAM-D # 9), psychic anxiety (HAM-D # 10), insomnia (HAM-A # 4) and weight loss (HAM-D # 16) were typical for patients with hyperthyroidism, while in the control group predominate the feelings of fatigue, weakness and loss of interest in working (HAM-D # 7).
Conclusions
The prevalence of anxiety in patients with hyperthyroidism is significantly more frequent compared to euthyroid patients. Anxiety and other psychiatric symptoms should be considered by both endocrinologists and psychiatrists.
Psychological symptoms commonly occur as a result of both thyroid and parathyroid disorders. Epidemiological studies evaluating the association between thyroid function and mood are heterogeneous in design and report varying results. The larger studies demonstrate no effect or an increase in depression with decreasing thyroid-stimulating hormone concentrations. There is growing evidence supporting the fact that thyroid function in psychiatric patients may be affected by the mental disorder itself, as well as by the medications used to treat that illness. Biochemical assessment of thyroid function and calcium concentrations should form part of the baseline assessment in those who present with new psychological symptoms. Once an abnormality is confirmed, further workup and treatment of the underlying endocrine disorder can be expected to alleviate and even reverse the psychological symptoms.
Rarely, thyroid cancer can lead to hyperthyroidism. The link between dysthyroidism and psychiatric symptoms is well established, but cases of psychosis associated with hyperthyroidism are rarely reported in the literature.
Objectives
Identifying psychosis secondary to hyperthyroidism caused by a secreting tumor through a case and literature review.
Methods
We report the case of a patient with thyroid suspect tumor and chronic psychosis. We performed a literature review based on a PubMed search with the following keywords: “dysthyroidism psychosis”.
Results
Mr. S,32, with a personal psychiatric history of chronic psychosis evolving since 4 years, without notable pathological history, was hospitalized in psychiatry for psychomotor instability, verbal hetero-aggressiveness, subtotal insomnia and refusal of treatment. The psychiatric examination revealed the presence of a chronic delusional syndrome with a theme of persecution, mysticism,and an interpretive, intuitive and hallucinatory mechanism, without dissociative syndrome. The somatic examination objectified a cachectic patient with a bilateral symmetrical non-impulsive exophthalmos, a goiter with a thrill on palpation, dysphonia and sinus tachycardia.A laboratory workup revealed inflammatory syndrome, collapsed TSH (<0.05 mU / L) and an increased T4 to 37 pmol / L. Cervical ultrasound showed a strongly suspect left lobar heteronodular goiter and poorly structured peripheral lymphadenopathy (TI-RADS 4-B). Sedative diazepam therapy was started with antithyroid therapy and a beta blocker. The evolution was quickly favorable. The patient is referred for surgical treatement.
Conclusions
The severity of the hyperthyroidism,neoplastic origin, the improvement in psychotic signs with antithyroid treatment are arguments in favor of the thyroid origin by thyroid neoplasia.
In this overview of success stories in veterinary clinical nutrition topics in cats and dogs reviewed include the dietary management of chronic kidney disease, dissolution of urinary tract uroliths by dietary modification, the recognition that taurine and L-carnitine deficiencies can cause dilated cardiomyopathy; that clinical signs associated with feline hyperthyroidism (caused by a benign adenoma) can be controlled by a low-iodine diet alone; that dietary management of canine osteoarthritis can also reduce non-steroidal anti-inflammatory drug doses; and that disease-free intervals and survival times can be statistically longer in dogs with Stage III lymphoma managed with diet. As we discover more about nutrigenetics and nutrigenomics, and as we expand our basic understanding of idiopathic diseases we are bound to identify more nutritionally related causes, and be able to develop novel dietary strategies to manage disease processes, including the formulation of diets designed to alter gene expression to obtain beneficial clinical outcomes.
Hypokalemic periodic paralysis is the most common form of periodic paralysis and is characterized by attacks of muscle paralysis associated with a low serum potassium (K+) level due to an acute intracellular shifting. Thyrotoxic periodic paralysis (TPP), characterized by the triad of muscle paralysis, acute hypokalemia, and hyperthyroidism, is one cause of hypokalemic periodic paralysis. The triggering of an attack of undiagnosed TPP by β2-adrenergic bronchodilators has, to our knowledge, not been reported previously. We describe two young men who presented to the emergency department with the sudden onset of muscle paralysis after administration of inhaled β2-adrenergic bronchodilators for asthma. In both cases, the physical examination revealed an enlarged thyroid gland and symmetrical flaccid paralysis with areflexia of lower extremities. Hypokalemia with low urine K+ excretion and normal blood acid-base status was found on laboratory testing, suggestive of an intracellular shift of K+, and the patients' muscle strength recovered at serum K+ concentrations of 3.0 and 3.3 mmol/L. One patient developed hyperkalemia after a total potassium chloride supplementation of 110mmol. Thyroid function testing was diagnostic of primary hyperthyroidism due to Graves disease in both cases. These cases illustrate that β2-adrenergic bronchodilators should be considered a potential precipitant of TPP.
Many patients who require anaesthesia have coincidental disease of their thyroid gland. The thyroid gland is situated in the anterior region of the neck just deep to the strap muscles at the level of the C5 to T1 vertebrae. The structural units of the thyroid gland consist of round follicles, or acini, filled with colloid and surrounded by a single layer of epithelial thyroid cells. The signs and symptoms of hypothyroidism are predictable consequences of the physiological effects of the lack of thyroid hormones. Thyrotoxicosis affects approximately 2% of women and 0.2% of men in the general population. The prevalence of hyperthyroidism in iodine-sufficient areas is 2:1000 for overt and 6:1000 for sub-clinical hyperthyroidism. The indications for thyroidectomy include thyroid malignancy, obstructive symptoms, retrosternal goitre, Graves' disease unresponsive to medical treatment, recurrent hyperthyroidism, occasionally Hashimoto's disease and for cosmetic reasons.
Thyroid disorders become more common with advancing age. Clinical features of hypothyroidism overlap with signs and symptoms often present in euthyroid older people and there is high likelihood of misdiagnosis. Conversely, there may be a relative paucity of signs and symptoms in hyperthyroid older people. A large number of patients may have subclinical disease. High suspicion and confirmation by laboratory assay is the key to correct diagnosis, though thyroid function tests should be interpreted with caution during acute illnesses. There is a reduced requirement for levothyroxine replacement in elderly hypothyroid patients and dosage should be titrated up cautiously as it can unmask symptoms of ischaemic heart disease. Drug interactions should be taken into account because a number of drugs interfere with levothyroxine absorption and metabolism. Radioactive iodine ablation of overactive thyroid tissue is the preferred treatment of hyperthyroidism in older people.
The objective of the present review is to assess the impact of universal salt iodisation in Nigeria during the last five years, with reference to some of the sentinel sites studied previously during a 1995 multi-centre study.
Design, setting and subjects:
The method of goitre classification by palpation was employed using the new internationally accepted method in which the classification is simply graded as 0, 1 or 2. The multistage random sampling method was used and states and local government areas were already selected by virtue of their known status for iodine deficiency disorders (IDD). Schools were randomly chosen in each local government area and children aged 8–12 years in each school were determined. A percentage of the children was then included in the study to give a sample size greater than the minimum number allotted to the school. A total of 2372 schoolchildren (1420 males and 952 females) in 11 local government areas were examined; urine samples were collected from 537 children and analysed for urinary excretion of iodine. The method known as the Sandell–Kolthoff reaction was adopted, in which the iodide in the urine samples catalyses the reduction of ceric ammonium sulphate (yellow colour) to the cerous form (colourless) in the presence of arsenious acid. The degree of reduction in colour intensity of the yellow ceric ammonium sulphate is proportional to the iodine content in the urine sample.
Results:
The results from this study show that the median urinary iodine excretion for this sampled population in Nigeria, drawn mostly from IDD-endemic areas, is 14.65 μg dl−1 with a mean value of 13.39 μg dl−1.
Conclusion:
This finding would suggest that Nigeria, in general terms, has achieved the goal of universal salt iodisation and should now focus its attention on constant monitoring in order to sustain this iodisation level.
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