Hypothyroidism Food List
Selenium supplementation may improve inflammatory activity in chronic autoimmune thyroiditis patients, as evidenced by a significant reduction in the concentration of thyroid peroxidase antibodies (TPO-Ab) to 63.8 in selenium-supplemented subjects versus 88 (P 0.95) in placebo subjects (Gartner et al 2002). The randomised study of 70 females (mean age 47.5 years) compared 200 jg sodium selenium daily orally for 90 days to placebo. A follow-up crossover study of 47 patients from the initial 70 was conducted for a further 6 months (Gartner & Gasnier 2003). The group that continued to take sodium selenite (200 g day) experienced further significant decreases whereas the group that ceased selenium use experienced a significant increase. The patients who received 200 jg sodium selenite after placebo also experienced a significant decrease in levels of TPO-Ab.
Myxedema coma results from extreme hypothyroidism and is characterized by impaired mentation, hypoventilation, hypothermia, hyponatremia, and CHF. Treatment is with iV thyroid hormones (300-500 mcg of levothyroxine sodium in patients without heart disease). Cortisol should also be given.
Preoperative patients with uncorrected severe hypothyroidism or myxedema coma should not undergo elective surgery. Mild to moderate hypothyroidism is not a absolute contraindication to surgery. Patients should be treated with histamine H2 blockers and metoclopramide because of their slowed gastric emptying times. B. Intraoperative ketamine is the induction agent of choice because of the exquisite sensitivity of hypothyroid patients to drug-induced myocardial depression. MAC requirements for inhaled agents are not changed with hypothyroidism. Maintenance usually with nitrous oxide plus supplementation (opioids, ketamine, etc). Monitoring directed toward early recognition of CHF and hypothermia. Other potential problems include hypoglycemia,
Thyroid disorders can be a diagnostic trap in family practice and early diagnosis is a real challenge. A family practice of 2500 patients can expect one new case of thyroid disorder each year and ten 'cases' in the practice with a slight preponderance of hyperthyroid patients compared with hypothyroid patients. 1 The diagnosis of an overactive or underactive thyroid can be difficult as the early clinical deviations from normality can be subtle. The clinical diagnosis of classical Graves' disease is usually obvious with the features of exophthalmos, hyperkinesis and a large goitre but if the eye and neck signs are absent it can be misdiagnosed as an anxiety state. Elderly patients may present with only cardiovascular signs such as atrial fibrillation and tachycardia or with unexplained weight loss. The hypothyroid patient can be very difficult to diagnose in the early stages, especially if the patient is being seen frequently. Hypothyroidism often has a gradual onset with general...
Table 6-6 lists the major causes of hypothyroidism. Hashimoto's disease is an autoimmune thyroid disease in which the subject has circulating thyroid antibodies. It is not known whether these antibodies functionally contribute to the state of hypothyroidism. The typical patient with Hashimoto's disease is a middle-aged woman with an enlarged, but firm nodular goiter who is euthyroid or hypothyroid, that is, presenting an appearance of mild myxedemas. The thyroglobulin antibodies usually are of the IgG type. They are highly species-specific. Complexes of antibody and thyroglobulin frequently are deposited in the thyroid. Hypothyroidism in elderly patients is usually considered to be an inactive phase of Hashimoto's disease and the major cause of idiopathic hypothyroidism. Without question, in many sections of the world the prime cause of hypothyroidism is dietary insufficiency TABLE 6-6 Major Causes of Hypothyroidism Loss of functional thyroid tissue Chronic autoimmune thyroiditis...
Congenital hypothyroidism (cretinism Figure 11-5 F) occurs when a thyroid deficiency exists during the early fetal period due to either a severe lack of dietary iodine, thyroid agenesis, or mutations involving the biosynthesis of thyroid hormone. Figure 11-5. (A) Treacher Collins syndrome is characterized by underdevelopment of the zygomatic bones, mandibular hypoplasia (double arrows), lower eyelid colobomas, and malformed external ears (arrow). (13) Pharyngeal fistula. A radiograph after injection of a contrast medium demonstrating the course of the fistula through the neck (arrow). The fistula may begin inside the throat near the tonsils, travel through the neck, and open to the outside near the anterior border of the sternocleidomastoid muscle. (C) Pharyngeal cyst. A fluid-filled cyst (dotted circle) near the angle of the mandible (arrow). (D, E) Ectopic thyroid tissue. A sublingual thyroid mass (dotted circle) is seen in a 5-year-old euthyroid girl. A mTc pertechnetate scan...
A third nutritionally related cause of MR is hypothyroidism during pregnancy. A genetic form of hypothyroidism (which, when untreated is referred to as cretinism), unrelated to iodine deficiency, can result in progressive neurological deficits after 3 months of age. In the United States, screening of all newborns is mandatory in all states and thus the occurrence of cretinism is rare. Cretinism can also result when there is maternal, fetal, or neonatal nutritional thyroid hormone deficiency the supplementation of iodine in the mother needs to occur prior to conception. Cretinism can result in neurodevelopmental deficits in the newborn, including MR and a number of other sensory and motor impairments. When both fetal and maternal hypothyroxinemia are present, such as in iodine-deficient regions of China, it has been shown that iodine replacement in the first trimester of pregnancy was necessary to prevent neurological deficits (Cao et al., 1994 Liu, Momotani, & Yoshimura, 1994...
Polyps and nodules mucosal polyps are uncommonly detected in the nasopharynx and oropharynx and are likely to represent florid lymphoid proliferations in association with adenoid or tonsillar enlargement. Localised thickenings of the vocal cords usually arise at the junction of the anterior and middle one-thirds and may be unilateral or bilateral. They are due to trauma or voice abuse (hence the alternative term singer's node) but are also associated with smoking. Nodules are broadly based sessile lesions that are usually bilateral and arise in females while the pedunculated polyps are unilateral and predominate in males. Myxoid degeneration of Reinke's space (Reinke's oedema) arises in older females, affects both cords along their length and is associated with smoking and not voice abuse. All are characterised by mild hyperplasia of the stratified squamous epithelium, accumulation of myxoid matrix in the lamina propria, increased vascularity and fibrin deposition. Similar lesions may...
Lymphoma involving the thyroid gland is rare, accounting for only 2 to 3 of all cases of lymphoma and less than 10 of thyroid malignancies. Women are affected more frequently than men are by a ratio of 2.7 1. The median age at presentation is over 60 years. The most common subtypes are DLBCL and follicular Grade-3 lymphoma, accounting for at least 80 of cases. A rare but interesting subtype is marginal zone B-cell lymphoma, which arises from MALT. In many cases, this lymphoma arises from a background lymphocytic infiltrate occurring in the setting of Hashimoto's thyroiditis. MALT lymphomas are low grade and clinically indolent. Hodgkin's disease may rarely involve the thyroid gland (10), sometimes as the only site of disease. Burkitt's lymphoma and follicular Grade-1 and -2 lymphomas occur less frequently (11,12).
Normally, as a result of the very rapid IRD of T4S and T3S and outer ring deiodination of rT3S and T2S, the plasma concentrations of these sulfated iodothyronines are low (Chopra et al., 1992, 1993 Eelkman Rooda et al., 1989 Wu et al., 1993). However, in conditions in which D1 activity is low, e.g., in selenium deficiency and after administration of iopanoic acid or propylthiouracil, iodothyronine sulfate levels are increased (Chopra et al., 1992 Rooda et al., 1989 Wu et al., 1995). Elevated serum T3S T3 ratios have also been reported in patients with nonthyroidal illness and in hypothyroid patients, in whom D1 activity is known to be decreased (Chopra et al., 1992).
Chronic thyroiditis (Hashimoto's disease, hypothyroidism) is a self-limiting disease with a probable genetic basis that affects mainly women. a. Chronic thyroiditis is characterized by autoantibodies and CMI to thyroglobu-lin or thyroid peroxidase. This reactivity causes progressive destruction of the thyroid gland.
Chronic mucocutaneous candidiasis is a highly specific T cell disorder that is characterized by an absence of immunity to Candida. Patients have apparently normal T cell absolute numbers and functions. Approximately 50 of patients with this disorder also have endocrine dysfunctions (e.g., hypothyroidism).
Hashimoto thyroiditis is the most common cause of goitrous hypothyroidism. 3. It is characterized clinically by goiter and hypothyroidism. In some variants of Hashimoto thyroiditis, only hypothyroidism and no goiter exists. D. Primary hypothyroidism 1. Primary hypothyroidism is most commonly idiopathic, whereby TSH receptor-blocking autoantibodies are present. E. Secondary hypothyroidism is relatively uncommon and caused by a deficiency in the adenohypophysis (low TSH secretion) or hypothalamus flow thyrotropin-releasing factor (TRF) secretion . 2. Wherever endemic goiter is prevalent, endemic cretinism occurs. A severe iodine deficiency during fetal development results in growth retardation and severe mental retardation.
Health histories of a nationwide sample of centenarian offspring (n 176) and controls (n 166). The controls consisted of offspring whose parents were born in the same years as the centenarians but at least one of whom died at age 73, the average life expectancy for that birth cohort. The average age at death of the other parent was 77 years, the same as the spouses of the centenarians. Centenarian offspring were found to have a 56 reduced relative prevalence of heart disease, a 66 reduced relative prevalence of hypertension, and a 59 reduced relative prevalence of diabetes in multi-variate analyses that controlled for age, gender, years of education, annual income, IADL score, ethnicity, marital status, exercise, smoking, and alcohol use. There were no significant differences in the prevalence of a number of other age-related diseases including cancer, stroke, dementia, osteoporosis, cataracts, glaucoma, macular degeneration, depression, Parkinson's disease, thyroid disease, and COPD....
Hypopituitarism may present in the newborn in a nonspecific fashion. Signs and symptoms include apnea, cyanosis, pallor, lethargy, jitteriness, and seizures. The differential diagnosis of hypogylcemia includes GHD and hypopituitarism, which could include cortisol deficiency. Prolonged hyperbilirubinemia may be owing to TRH or TSH deficiency, causing hypothyroidism in a neonate with multiple hormone deficiency. Patients with congenital hypopituitarism may have a turbulent neonatal course, generally more characteristic of a full-term infant because of the frequency of neonatal problems in preterm infants. Neonatal glucocorticoid deficiency can present as hyponatremia.
Sometimes, GHAD will first be suspected when there is severe neonatal hypoglycemia or other signs of hypopituitarism (hypothyroidism, small phallus in male babies, or neonatal hepatitis). During early childhood, children with GHAD are detected when they demonstrate short stature and subnormal rates of growth. Often these children will have proportionally small limbs, increased body fat, and a cherubic appearance.
Adverse effects delayed wound healing, seizures, osteoporosis, hyperglycemia, diarrhea, nausea, GI bleeding, cushingoid effects. Comments use with caution in patients with hypothyroidism, cirrhosis, hypertension, CHF, ulcerative colitis, thromboembolic disorders may cause adrenocortical insufficiency (Addison's crisis) with abrupt withdrawal.
Differential Diagnosis Inadequate caloric intake, peptic ulcer, depression, anorexia nervosa, dementia, hy-per hypothyroidism, cardiopulmonary disease, narcotics, diminished taste, diminished olfaction, poor dental hygiene (loose dentures), cholelithiasis, malignancy (gastric carcinoma), gastritis, hepatic or renal failure, infection, alcohol abuse, AIDS.
Past Medical History Past episodes of heart failure hypertension, excess salt or fluid intake noncompliance with diuretics, digoxin, antihypertensives alcoholism, drug use, diabetes, coronary artery disease, myocardial infarction, heart murmur, arrhythmias. Thyroid disease, anemia, pulmonary disease.
Hypothyroidism, histologic section. High magnification of a myocyte showing basophilic degeneration of the cytoplasm (Hematoxylin and Eosin, IOOX). Figure 43. Hypothyroidism, histologic section. High magnification of a myocyte showing basophilic degeneration of the cytoplasm (Hematoxylin and Eosin, IOOX).
The differential diagnosis includes hypothyroidism, anemia, perimenopause, drug and alcohol abuse, and affective disorders. Common alternative diagnoses in patients complaining of PMS include affective or personality disorder, menopausal symptoms, eating disorder, and alcohol or other substance abuse. A medical condition such as diabetes or hypothyroidism, is the cause of the symptoms in 8.4 , and 10.6 have symptoms related to oral contraceptive (OC) use.
Concentrations will decrease when hepatic retinol stores become inadequate, and this usually occurs when there is insufficient dietary intake of vitamin A for a prolonged period. Plasma retinol concentrations will increase to high levels above the normal range when vitamin A intake is excessive. Various disease states can decrease plasma retinol concentrations, including protein-energy malnutrition (213,214), hypothyroidism (215), zinc status (216), and inflammation and infection (217), or increase plasma retinol concentrations, such as renal disease (218).
Even more surprising was Weigle's observation that hapten conjugation could break natural tolerance (3). The injection of rabbits with homologous thyroglobulin in incomplete Freund's adjuvant produced, as expected, little or no antibody to thyroglobulin. However, rabbits injected with thyroglobulin that had been modified with arsanilic acid plus SA or with trinitrophenyl (TNP) produced precipitating antibody to both modified and native thyroglobulin. Moreover, some of the rabbits developed histological evidence of autoimmune thyroiditis. Once the animals had been immunized, the height of their antibody titers and the severity of the thyroiditis could be increased by administering booster injections of native thyroglobulin.
Hashimoto thyroiditis, normal thyroid, and Graves disease (Figure 21-2) Figure 21-2. (A) Light micrograph of Hashimoto thyroiditis (HT). HT is characterized by a high lymphocytic infiltration that may form lymphoid follicles with germinal centers (L). Normal thyroid follicles (TF) also are observed. (B) Light micrograph of a normal thyroid gland showing numerous thyroid follicles (TF) containing colloidal material. The follicles are lined by follicular cells arranged as a simple cuboidal epithelium. (C) Light micrograph of Graves disease (GD). Graves disease is caused by a diffuse, hyperplastic goiter. The follicular cells are increased in number (hyperplasia) and arranged as a simple tall columnar epithelium. In addition, the follicular cells can form buds that encroach into the colloidal material (arrow). (A and C Reprinted with permission from East Carolina University, School of Medicine, Department of Pathology slide collection.) Figure 21-2. (A) Light micrograph of Hashimoto...
Thyroid cancer Risk factors for thyroid carcinoma include irradiation (particularly in first two decades of life), underlying thyroid disease (especially Hashimoto's thyroiditis), family history of thyroid cancer including rare inherited syndromes such as Multiple Endocrine Neoplasia syndromes 2A and 2B, or non-MEN familial medullary thyroid carcinoma. Primary malignant lymphoma a rare neoplasm in the thyroid gland (1-2 ), presenting in elderly patients with a rapidly enlarging mass, stridor and dysphagia. There is a strong association with pre-existing Hashimoto's thyroiditis (MALToma). The tumour is large, replaces much of the thyroid gland and is usually of diffuse, large B-cell type (although other types may occur). The tumour cells infiltrate between follicles, produce lymphoepithelial lesions and extend into the perithyroid soft tissues. In contrast to anaplastic carcinoma, it responds well to radiotherapy and chemotherapy, although the long-term prognosis depends on the stage.
Unilateral, pink colored, bloody or non-milky discharge, or discharges associated with a mass are the discharges of most concern. Milky discharge can be caused by oral contraceptive agents, estrogen replacement therapy, phenothiazines, prolactinoma, or hypothyroidism. Nipple discharge secondary to malignancy is more likely to occur in older patients.
FIGURE 6-4 Biosynthetic pathway for the production of thyroglobulin. TSH initiates the process via stimulation of the cAMP pathway. The mature mRNA is translated into the 2748-amino acid subunit of 330 kDa. The mature Tg is a dimer of two subunits. Before Tg is secreted, extensive glycosylation occurs. Modified with permission from Medeiros-Neto, G., Targovnik, H. M., and Vassart, G. (1993). Defective thyroglobulin synthesis and secretion causing goiter and hypothyroidism. Endocr. Rev. 14, 165-183.
Between 50 and 70 of carcinoid patients have tumors that will actively take up (therefore positive to) MIBG (34,35,37,105-107). The exact mechanism of MIBG therapy effects in the treatment of carcinoids remains unclear. Guanidine is a precursor of DOPA in the adrenergic catecholamine synthetic pathway (34). The uptake of MIBG by neuroendocrine tumors is probably mediated by vesicular monoamine transporters into the tumor cells (108), and interestingly the response to 131I-labeled MIBG is enhanced by pretreatment with nonlabeled MIBG (105,106). Good long-term symptomatic control, with decreased demand for somatostatin analog treatment has now been reported in a number of series (37,105-107,109,110), and this improvement is reportedly cost-effective (37). Toxicities include pancytopenia, thrombocytopenia, nausea, emesis, and hypothyroidism (as a consequence of 131I treatment) (37,105-107,109,110).
Benign thyroid lesions including adenomas, hamartomas, and multinodular goiter occur in 50 to 67 of all affected patients (16). It is suspected that Hashimoto thyroiditis occurs at an increased frequency in CS, especially in patients who are of non-Asian ancestry this belief is supported by early literature describing Hashimoto thyroiditis as a component of BRRS (8). Currently, functional disorders of the thyroid resulting in hyperthyroidism or hypothyroidism in the absence of adenomas or goiter are not considered components of CS.
Polymorphism of the apoE gene has been detected in all populations. The most common allele in Europe is apoE3 (frequency 0.75) followed by apoE4 (0.13) and apoE2 (0.1) (Motulsky et al., 2002). ApoE3 binds with high affinity to the LDLR, whereas apoE2 has much reduced binding. About 1 of the population are homozygous for apoE2 but only 1 of these individuals will have the additional genetic or acquired factors (obesity, diabetes, hypothyroidism, FCHL, alcohol abuse) that lead to type III hyperlipidaemia. This rare disorder, which results from the presence in the circulation of large amounts of CM remnants and VLDL remnants (collectively termed b VLDL) is characterized by markedly raised serum cholesterol
Values increase in diabetes mellitus and hypothyroidism. They decrease in pernicious anemia, hyperthyroidism, and acute infections. Values increase in diabetes mellitus, liver diseases, nephritis, hyperthyroidism, and pregnancy. They decrease in hyperinsulinism, hypothyroidism, and Addison disease. Values increase in hypothyroidism, diabetes mellitus, and nephritis. They decrease in hyperthyroidism. Values increase in renal failure, hypothyroidism, and Addison disease. They decrease in renal disease, liver disease, and pancreatitis.
Conventional multimodailty therapies have not altered the dismal prognosis of glioblastoma which has prompted alternative investigational approaches utilising biological modifiers of response.We review here interferon alpha (IFN-a) and beta (IFN-P), interleukin-2 (IL-2), tumor necrosis factor-a TNF, interleukin 4 (IL-4) , monoclonal antibodies to EGFR, EGFRvIII and radiolabeled anti-tenascin monoclonal antibody. A current novel approach is exploitation of some of the biological consequences of thyroid hormone deprivation on tumor biology. In a preliminary Phase I II trial significant improvement in survival and tumor regression rates in recurrent high grade glioma patients were observed following propylthiouracil induced mild (chemical) hypothyroidism combined with high dose tamoxifen.The background to this approach is reviewed. Key Words glioblastoma biological modifiers hypothyroidism tamoxifen
Raised autoantibodies (antimicrosomal or antithyroid peroxidase) are suggestive of Hashimoto's disease (autoimmune thyroiditis). Hypothyroidism (myxoedema) Hypothyroidism, which is relatively common, is more prevalent in elderly women (up to 5 ). 2 The term myxoedema refers to the accumulation of mucopolysaccharide in subcutaneous tissues. The early changes are Hypothyroidism (myxoedema)
High consumption of goitrogens can induce a secondary deficiency state. Goitrogens are substances that inhibit iodine metabolism and include thiocyanates found in the cabbage family (e.g. cabbage, kale, cauliflower, broccoli, turnips and Brussels sprouts) and in linseed, cassava, millet, soybean and competing entities, such as other members of the halogen family (e.g. bromine, fluorine and lithium, as well as arsenic) (Gropper et al 2005). Most researchers agree, however, that moderate intake of goitrogens in the diet is not an issue, except when accompanied by low iodine consumption (Gropper 2005, Kohlmeier 2003). A very rare cause of secondary iodine deficiency and hypothyroidism isTSH deficiency. Low selenium intake Low dietary intake of selenium is a factor that exacerbates the effects of iodine deficiency. Selenium is found in the thyroid gland in high concentrations, and while iodine is required for thyroid hormone synthesis, selenium-dependent enzymes are required for the...
Iodine deficiency is accepted as the most common cause of brain damage worldwide, with IDD affecting 740 million people (Higdon 2003). Although it is well accepted that severe deficiency is responsible, evidence is now emerging that mild deficiency during pregnancy is also important and can have subtle effects on brain development, lowering intellectual functioning and inducing psychomotor deficits in early childhood. Preliminary data are also emerging to suggest an association between iodine deficiency hypothyroidism of pregnancy and the incidence of ADHD in the offspring however, this still requires confirmation in larger studies (Soldin et al 2002, Vermiglio et al 2004).
Evidence of iodine deficiency is not limited to pregnant women and newborns and has also been demonstrated in Australian schoolchildren (Li et al 2006). Iodine status in schoolchildren is based on median UIE values and is categorised as normal (UIE 100 jg L) or as mild (UIE 50-99 jg L), moderate (UIE 20-49 jg L) and severe deficiency (UIE
In 1958, the National Institutes of Health organized a conference on beriberi, iodine deficiency, and vitamin A deficiency (92). At the conference, H.A.P.C. Oomen (19021986), who had spent many years working in the field, reported that children with xerophthalmia in Indonesia often had intestinal and respiratory disease, and made an impassioned plea
And thyroiditis (Hogg et al., 1981 Engel et al., 1986 Gupta et al., 1992 Knowles et al., 1999 Sekine et al., 2001 Fujino et al., 2002). Clinical hematological involvement is observed in lymphadenopathy and hepatosplenomegaly. Biological hematological abnormalities include hypereosinophilia, atypical lymphocytes, neutropenia, thrombocytopenia, hemolytic anemia, pancytopenia, and hemophagocytic syndrome.
Amounts required vary from the order of grams per day for sodium and calcium, through milligrams per day (eg, iron) to micrograms per day for the trace elements. In general, mineral deficiencies are encountered when foods come from one region, where the soil may be deficient in some minerals, eg, iodine deficiency. Where the diet comes from a variety of different regions, mineral deficiencies are unlikely. However, iron deficiency is a general problem because if iron losses from the body are relatively high (eg, from heavy menstrual blood loss), it is difficult to achieve an adequate intake to replace the losses. Foods from soils containing high levels of selenium cause toxicity, and increased intakes of common salt (sodium chloride) cause hypertension in susceptible individuals.
GHRs are also regulated by thyroid hormones. The growth-promoting effects of exogenously administered GH are blunted in hypothyroid rats, hepatic GH binding sites are reduced in hypothyroidism, and elevated binding is observed in hyperthyroid rats (54). The authors have recently observed reduced GHR mRNA expression in the ARC in response to thyroidectomy, an effect that is rapidly restored by thyroid hormone replacement (P. A. Bennett, unpublished observations).
Traditionally, when surgery is advised in Graves' disease, subtotal thyroidectomy has been carried out although, because of recurrent hyperthyroidism in 5-10 of cases, there is an increasing tendency to perform total thyroidectomy. On the few occasions when operation is required for aesthetics and or obstructive symptoms in Hashimoto's thyroiditis, total thyroidectomy is the operation of choice. Likewise, total thyroidectomy may be required for patients with multinodular goitre because of goitre size and or compressive symptoms if unilateral, lobectomy may suffice.
A physical examination and laboratory screening (e.g., complete blood count, liver function, serum testosterone level, serum vitamin B12, thyroid function) may be performed to exclude potential systemic causes of depressive symptomatology. Testosterone deficiency associated with depressive symptomatology (e.g., anhedo-nia, fatigue, and sexual dysfunction) has been described in males with PD and may possibly be managed with testosterone replacement therapy (120). Likewise, symptoms of hypothyroidism (e.g., anxiety, difficulty with concentration, dysphoria, fatigue, irritability, and motor retardation) resemble depressive symptomatology and are treatable with thyroid replacement. It is also important to ensure that patients are on optimal doses of antiparkinson drugs to minimize motor fluctuations that may contribute to mood fluctuations.
Disease affecting the thyroid gland can present as enlargement (called goitre) that may be diffuse or nodular or as a consequence of hormonal imbalance rarely there may be pain. Hypothyroidism is characterised by lethargy, mental slowness or depression, intolerance of cold or weight gain
Two animal models of GHRH deficiency have been described. In one, administration of monosodium glutamate (MSG) to mice causes a selective loss of arcuate nuclei neurons (14,15). MSG-exposed rodents have impaired growth, obesity, hypogonadism, and hypothyroidism (16). The other animal model of GHRH deficiency is the Gsh-1 homeobox gene knockout mouse (17). Homeobox genes encode a family of DNA binding proteins, and the Gsh-1 gene encodes a product necessary for GHRH gene transcription and translation. Gsh-1 knockout mice have extreme postnatal dwarfism, sexual infantilism, leukopenia, significant perinatal mortality, a shortened life span, and biochemical evidence of GHRH deficiency. Their anterior pituitary glands are one-third normal size and possess decreased numbers of somatotrophs and lactotrophs.
Cretinism (see Chapter 11 ) occurs when there is a deficiency in fetal thyroid hormone (T3 and T4) or thyroid agenesis. It results in growth retardation, skeletal abnormalities, mental retardation, and neurologic disorders. Cretinism is rare except in areas where there is a lack of iodine in the water and soil.
The diagnosis of MDD involves a constellation of symptoms in addition to depressed mood. After taking a careful history, including asking the patient about his or her sleeping patterns, appetite, sex drive, and mood, the doctor will give the patient a physical examination to rule out other possible causes of the symptoms. Certain other disorders may resemble MDD, including cognitive dysfunction caused by the direct effects of a substance (drug of abuse, medication, or toxic chemical) various medical conditions (i.e., an underactive thyroid gland strokes or early stages of dementia), or other mental disorders. Such stressful life events as normal bereavement may also produce behaviors similar to those associated with MDD while a bereaved person may appear to have many of the characteristics of MDD, the disorder would not be diagnosed unless the symptoms continued for more than two months or were extreme in some way. As part of the diagnostic interview, the doctor may give the patient a...
The hormonal effects of radiation are similar to those associated with surgery, being a localized treatment that can damage organs and glands with systemic implications. Radiation of the thyroid, classically in mantle radiation for Hodgkin's disease and also for other cancers such as non-Hodgkin's lymphoma or head and neck cancer, commonly induces hypothyroidism.45 It is dose-dependent, increasing with doses above 25 Gy, and usually occurs within 2-3 years.46 Much less frequently, cranial irradiation to doses above 50 Gy can affect the hypothalamus and pituitary leading to central hypothyroidism.46,47 The National Comprehensive Cancer Network (NCCN) guidelines (www.nccn.org) recommend at least annual TSH monitoring for hypothyroidism in patients who have undergone neck irradiation. Thyroid cancer can also develop in a radiated thyroid, and so there should be a low threshold to biopsy thyroid nodules in such patients.48
All patients require a full medical history and physical examination. Treatable causes (such as brain tumour, subdural haematoma, normal pressure hydrocephalus, infections, hypothyroidism, or vitamin B12 deficiency) may be revealed by investigations such as blood count and ESR, urea and electrolytes, liver function tests, thyroid function tests, B12 and folate, calcium and phosphate, serological tests for syphilis, HIV antibody testing (with informed consent), chest radiography, EEG, and brain scan.
Spontaneous and stimulated GH secretion is markedly attenuated in clinical and biochemical hypothyroidism in humans this abnormality corrects during thyroid hormone replacement (7,57,58). Thyroid hormone deficiency is associated with reduced hypothalamic GHRH production, leading to GH deficiency and down-regulation of GHRH receptor numbers on pituitary somatotropes (7,59). Thyroid hormone facilitates binding of GHRH to its receptor. GH secretion is reduced in hypothyroid subjects following pyridostigmine and arginine administration (60), substances known to decrease somatostatin tone (61,62). GH synthesis, rather than secretion, appears to be impaired in hypothyroidism (59).
Primary and Secondary Primary causes of frailty would be age-related mechanisms (e.g., changes in gene expression, oxidative DNA damage, telomere shortening) and secondary causes would be diseases (e.g., congestive heart failure, depression, hypothyroidism, malignancy) (Fried et al., 2004 Walston, 2004).
Fine needle aspiration cytology (FNAC) using 25-22-G needles has become the first-order investigation in many cancers due to its speed, cost-effectiveness, proficiency and convenience for both clinician and patient. It can not only provide specific inflammatory (e.g. Hashimoto's thyroiditis) and malignant diagnoses (e.g. thyroid papillary carcinoma) but can sort patients into various management groups viz, inflammatory
Hashimoto's disease (autoimmune thyroiditis) Hashimoto's disease, which is an autoimmune thyroiditis, is the commonest cause of bilateral non-thyrotoxic goitre in Australia. Features are patients may be hypothyroid or euthyroid Hashimoto's disease may present as postpartum hypothyroidism. The hypothyroidism may resolve in 6-12 months or may be permanent. 3
FIGURE 5-37 Model of TSHR with the TSH site and the TSHRAb epitopes defined in a three-dimensional array. Determinants for blocking TSHRAbs (TSBAb) and stimulating TSHRAbs (TSAb) are approximated to compose the TSHR site. The former are implicated in the expression of disease by patients with idiopathic myxedema and hypothyroidism the latter are implicated in patients with Graves' disease and hyperthyroidism. They are presumed to comprise the high-affinity TSH-binding antagonist site and the agonist site for TSH, respectively, on the basis of the competitive antagonism or agonism of TSH with monoclonal inhibiting and stimulating receptor antibodies. The loop between residues 303 and 392 is X-marked and separated from the remainder of the external domain since residues within it can be deleted with no loss in receptor function. This loop includes residues 352-366, which comprise the immunogenic peptide used to produce a specific antibody to the receptor. The immunogenic peptide is...
Hypothyroidism Thyroid hormone plays a critical role in regulating metabolism. In hypothyroidism, the basal metabolic rate is decreased due to a lack of thyroid hormone, resulting in bradycardia, cold intolerance, alopecia, and weight gain. Neurologic symptoms are relatively common in hypothyroidism and include paresthesias in up to 80 of patients as well as ataxia, coma, headache, seizure, cerebellar signs, and psychosis (132,133). Cranial nerve involvement has also been reported, with the vestibulocochlear nerve most commonly affected in 15 to 31 of patients with hypothyroidism (132). Involvement of the facial nerve is considered rare. Its mechanism is thought to be a compressive phenomenon. In hypothyroidism, myxedematous infiltration and swelling of the soft tissue are hypothesized to have a compressive effect on the facial nerve through the tight confines of the fallopian canal. Anecdotal reports of facial nerve decompression in hypothyroidism have been described (134), but...
It is important to utilise a type of fail-safe mechanism to avoid missing the diagnosis of these disorders. Some practitioners refer to consultations that make their 'head spin' in confusion and bewilderment, with patients presenting with a 'shopping list' of problems. It is in these patients that a checklist is useful. Consider the apparently neurotic patient who presents with headache, lethargy, tiredness, constipation, anorexia, indigestion, shortness of breath on exertion, pruritus, flatulence, sore tongue and backache. In such a patient we must consider a diagnosis that links all these symptoms, especially if the physical examination is inconclusive this includes iron deficiency anaemia, depression, diabetes mellitus, hypothyroidism and drug abuse. hypothyroidism
There is variation in the size of the tongue among individuals, and no normal measurements have been established. Most pediatricians, however, have established their own norms for children. Detection of a large tongue or macroglossia is important, particularly in the neonatal and infantile periods, to allow early diagnosis of certain conditions such as congenital hypothyroidism. An illusion of a large tongue may be seen in a disorder
Hormones other than PTH and calcitonin have major effects on bone growth. One such hormone is pituitary growth hormone (GH, somatotropin). This hormone stimulates growth in general and, especially, growth of epiphyseal cartilage and bone. Oversecretion in childhood leads to gigantism, an abnormal increase in the length of bones absence or hypose-cretion of somatotropin in childhood leads to failure of growth of the long bones, resulting in pituitary dwarfism. Absence or severe hyposecretion of thyroid hormone during development and infancy leads to failure of bone growth and dwarfism, a condition known as congenital hypothyroidism. Oversecretion of somatotropin in an adult leads to acromegaly, an abnormal thickening and selective overgrowth of hands, feet, mandible, nose, and intramembranous bones of the skull.
There is suggestive evidence of a preventive role for iodine in breast cancer. As far back as 1896 research has suggested a link between iodine deficiency, thyroid disease and breast cancer (Smyth 2003). More recently, epidemiological data have demonstrated a correlation between increased incidence of breast cancer and a range of thyroid conditions, most notably hypothyroidism (Smyth 2003). In addition, the observed low rates of breast cancer in Japan are speculated to be partly due to a high dietary iodine intake, further suggesting a protective effect. Besides the diminished antioxidant effect, studies with animal models show that iodine deficiency results in changes in the mammary gland that makes it more sensitive to the effects of oestradiol (Strum 1979). Oestradiol stimulates cell division, which eventually results in cyst formation, and dietary supplementation with iodine can improve these alterations.
In patients refractory to first-line hormonal therapy with castration or estrogens, aminog-lutethimide with hydrocortisone produces a symptomatic and biochemical response up to 48 of the time, with responding patients often experiencing clinical improvement for some months and occasionally up to 3-4 years.159-162 Side effects include adrenal insufficiency (in the absence of corticosteroid-replacement therapy), skin rash, hypothyroidism, and less commonly thrombocy-topenia.159,163,164 Another troublesome side ef
Adults with DS show a variety of age-related changes in physical and functional capacities suggestive of premature or accelerated aging (Martin, 1978), including changes in skin tone, hypogonadism, increased frequency of cataracts, increased frequency of hearing loss, hypothyroidism, seizures,
Depression can be an integral part of the symptomatology of some medical conditions, including neurological disorders such as Parkinson's disease, dementia, multiple sclerosis, and anaemia endocrine disorders such as hypothyroidism virus infections such as influenza and deficiencies of vitamins such as B12 and folate.
This was a 74 year old female with several medical problems including adult onset diabetes mellitus, hypothyroidism treated with thyroxine, congestive hear failure and one transient cerebral ischemic attack without residual deficit. She was partially deaf and required a left hearing aid. Her body habitus and primary amenorrhea suggested Turner's syndrome, and a buccal smear performed several years before demonstrated 4 Barr bodies consistent with Turner's mosaicism. The patient was admitted to the hospital with signs and symptoms of CHF. She experienced somnolence, increasing dyspnea and pedal edema for several weeks. On admission, her vital signs were BP 100 86mm Hg, P 80, irregular RR 20, and T 37 C. Significant findings on her physical exam included webbed neck, jugular venous distension, bilateral carotid bruits and delayed upstroke of the carotid pulsations, fullness in the anterior neck wide-spaced nipples normal S1 and S2, S4, a III VI systolic ejection murmur at the aortic...
Decreases in plasma sodium levels below 120 mM, which occurs following disruption of kidney electrolyte handling, results in the rapid development of brain oedema, which is the main cause of mortality. Disruption of electrolyte secretion reuptake in kidneys can be triggered by a variety of clinical factors, including endocrine pathology (e.g. hypothyroidism or overproduction of antidi-uretic hormone), heart failure, HIV infection etc.
Phenotypically, the weaver mouse exhibits profound ataxia resulting from a near total loss of granule cells in the cerebellum (76-78) tremor resulting from a 70 loss of dopamine in the dorsolateral striatum due to selective degeneration of dopamine neurons of the SNpc (79) male infertility due to degeneration of Sertoli and sper-matogenic cells (80) and seizures possibly due to hippocampal abnormalities and hypothyroidism (81,82).
Fatigue is one of the three most frequently disabling symptoms of MS (129) and may be considered abnormal in as many as 78 of patients (130,131). A particular feeling of enervation, severe enough to prevent a patient from carrying out duties and responsibilities or to interfere with work, family, or social life, occurs (132). This specific, but poorly understood, type of fatigue in MS must be distinguished from symptoms of depression, medication side effects, consequences of other medical conditions such as anemia, hypothyroidism, or simple physical tiredness. No definitive explanation for fatigue in MS has been established. One type of fatigue, so-called handicap fatigue, is characterized by the requirement for an increased effort to perform routine tasks. This may be a consequence of the fact that nerve conduction in demyelinated fibers is susceptible to exhaustion, rate-dependent block, and conduction block with increased temperature.
GH treatment of GH-deficient children has been associated with hypothyroidism thought to be related to increased SRIF tone and its inhibitory effect on thyroid-stimulating hormone (TSH) secretion. TRH stimulation testing of TSH secretion during formal assessment of the hypothalamic-pituitary GH axis frequently identifies subjects with hypothalamic or pituitary hypothyroidism prior to initiation of GH replacement therapy (B. Bercu, unpublished data). Thus, a direct effect of GH replacement and thyroid dysfunction is unlikely. Along with increases in SRIF, in vitro studies suggest GH inhibits GHRH release in a dose-dependent fashion (7) indicating GH autofeedback is under dual control of both hypothalamic peptides.
Nutrients and aging genes If genes that convey longevity could be discovered, then these will be relevant to aging. This possibility rests on the likelihood that (1) especially in extreme old age, these genes may reduce rates of aging, and (2) these genes may modify cellular and biochemical pathways involved in gene-nutrient determined mechanisms of aging and age-related disease. The best-known example of such a gene is the s4 allele of the apolipoprotein E gene that decreases markedly in frequency with advancing age, whereas the much rarer e2 allele becomes more frequent. These findings are attributed to increased mortality in Alzheimer's and cardiovascular diseases associated with the fi4 allele and the slight protection afforded by the s2 allele. The siblings and children of centenarians show reduced rates of age-related cardiovascular diseases, hypertension, diabetes, and stroke but not osteoporosis, cancers, and thyroid disease, suggesting that genetic effects are greater in the...
Rate of emptying is reduced in some diabetics, local pyloric lesions (pyloric ulcers, pyloric stenosis), and hypothyroidism. Gastric emptying rate is increased in hyperthyroidism and in the presence of duodenal ulcers Vigorous exercise reduces emptying rate Gastric emptying difficulties often encountered after gastric surgery
Severe iodine deficiency is uncommon in Western countries, such as Australia and New Zealand, but several local surveys have identified that mild to moderate deficiency is more prevalent than once thought. A research group at Monash Medical Centre in Melbourne screened 802 pregnant women and found that 48.4 of Caucasian women had urinary iodine excretion (UIE) concentrations below 50 fjg L compared to 38.4 of Vietnamese women and 40.8 of Indian Sri Lankan women (Hamrosi et al 2005). These figures are disturbing when the WHO defines healthy UIE levels as greater than 100 g L, mild deficiency is diagnosed at 51-100 g L and moderate to severe deficiency at
A study of non-pregnant adults in 1999 demonstrated iodine deficiency in 26.3 of 'healthy' subjects and 34.1 of diabetic subjects (Gunton et al 1999). Clinical note Why is iodine deficiency on the rise The emergence or re-emergence of iodine deficiency is not limited to Australia. One study found that the median UIE had declined by more than 50 in between 1971 and 1994 in the United States (Gunton et al 1999). Three reasons have been proposed to explain the emergence of iodine deficiency in developed countries. First, milk has traditionally been viewed as a good dietary source of iodine however, since the 1990s its iodine content has reduced significantly because iodine-containing sanitisers have been gradually replaced with chlorine-containing sanitisers. The significance of this change within the dairy industry was recently shown by Li et al (2006) who compared the iodine content of Australian milk products from 1975 and 2004. They identified mean iodine concentrations of 593.5 fig...
(vii) The physical and psychomotor development of three maternal UPD16 patients, aged 1.5, 3.2, and 4.5 years, was reported (Exeler et al., 1996). No catch-up growth in these cases with severe initial intrauterine retardation was observed, as postnatal length and weight acquisitions proceeded along the 3rd centile. One proband had congenital hypothyroidism, while a cardiac septal defect has been diagnosed in the two others. Psychomotor development was within normal limits in two and slightly retarded in one.
Toxins and metabolic abnormalities should be considered in all cases of dementia, but especially in the elderly, who have a higher prevalence of systemic illness and medication use. The list of toxic metabolic causes of dementia is extensive (see Table 8.2). Many of these conditions produce an acute confusional state more often than a dementia. Nonetheless, they are not infrequently identified in epidemiological studies of dementia. In 200 elderly patients with symptoms for three or more months, medications (9.5 ) and hypothyroidism (3 ) were the leading toxic metabolic causes of dementia (Larson, Reifler, Suni, Canfield, & Chinn, 1986). Features that favored a toxic metabolic cause were a higher number of prescription medications and a shorter duration and lesser severity of dementia. This chapter reviews the toxic metabolic dementias associated with alcoholism, thyroid disease, and
In addition to history, physical examination, review of systems, and laboratory testing to rule out other medical causes of symptoms such as sleep changes or amotivation are useful. This workup should be keyed to the patient's comorbid illnesses and other symptoms identified on review of systems. Common medical triggers for acute behavioral changes include medical conditions such as thyroid disease or urinary tract infections and medication changes side effects (Teri & Logsdon, 2000).
When following a patient with dementia, it is important to determine whether the clinical course is consistent with the diagnosed etiology. In many instances, a toxic or metabolic cause may be contributory, but not the sole cause of dementia. Thus, continued evaluation is necessary when a reversible etiology has been discovered. For example, if B12 deficiency or hypothyroidism is discovered, cognition should be reassessed following appropriate therapy. Continued progression warrants further evaluation for an alternate cause of dementia.
Serum SHBG levels are affected by several conditions. SHBG levels are inversely correlated with increased total body fat, subcutaneous and visceral adiposity (Couillard et al., 2000). Levels also vary inversely with hyperinsulinism in nondiabetic subjects. They seem to be an indicator of general adiposity rather than an index of altered insulin glucose homeostasis in morbidly obese subjects. Hyperinsulinism decreases SHBG synthesis by cultured hepatic cells. These observations have been interpreted to show that obesity causes insulin resistance and hyperinsulinism, and hyperinsulinism decreases SHBG levels. Hypothyroidism and the nephrotic syndrome also reduce SHBG levels. Estrogen, hyperthy-roidism, some anticonvulsants, a high phytoestrogen diet, hepatic cirrhosis, and aging increase SHBG levels (Anderson, l974 Kley et al., l975).
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