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Type O red cells should be used for patients who have isoagglutinins against donor red blood cell antigens until the donor blood group type is fully established in the recipient breast cancer 7 cm ortho tri-cyclen 50 mg visa. In this situation breast cancer medication generic 50mg ortho tri-cyclen visa, liver biopsy should be performed to determine the dominant pathologic process women's health center of jackson wy order 50mg ortho tri-cyclen fast delivery. For patients already on entecavir and not appropriately responding pregnancy 0-12 weeks best ortho tri-cyclen 50 mg, consider alternative antiviral therapy. The aim of antiviral treatment is to suppress viral replication completely, thereby minimizing the risk of viral mutation. Patients should be treated for 12 months or 6 months after discontinuation of systemic immunosuppressive treatment, whichever is longer. The frequency of cirrhosis and end-stage liver disease caused by Hepatitis C in 40-year survivors of hematopoietic cell transplant is about 33%. The presence of hepatitis C viremia, even in high titer, is insufficient to make the 82 distinction between these two disorders. If the liver biopsy suggests both processes, immunosuppressive therapy should be administered, since ongoing lymphocytic attack leading to loss of interlobular bile ducts may result in severe and progressive cholestasis. Fulminant immune-rebound hepatitis C has been reported only rarely after withdrawal of immunosuppression. For patients with cirrhosis, endoscopic surveillance for esophageal varices is recommended. The mobilization of iron after transplant largely depends on the iron burden, especially cardiac iron. Extreme tissue iron overload (> 15 mg/g dry weight) has been associated with extensive organ toxicity in the post-transplant survivors of thalassemia, in whom organs at risk include the heart, liver, pancreas and pituitary gland, resulting in dysrhythmias and cardiac failure, portal fibrosis and cirrhosis, insulin-dependent diabetes mellitus and other endocrine insufficiencies. Iron overload increases the susceptibility to mucormycosis, aspergillosis, and infections caused by Listeria monocytogenes, non-cholera Vibrio species, Yersinia enterocolitica and Yersinia pseudotubera, among others [2, 4]. In patients with chronic hepatitis C, iron overload may accelerate the development of cirrhosis. Liver or marrow iron content correlates poorly with number of transfused red blood cell units. Marrow and liver iron contents have been determined by spectrophotometry among 10 consecutive autopsied patients who were transplanted for hematological malignancy. Marrow iron content can also be measured by morphometry based on digital photomicrographs of a Prussian blue-stained marrow biopsy. Because of correlation between morphometric and spectrophotometric 85 analyses of marrow iron content (r = 0. Earlier work also demonstrated a close relationship between biochemical concentration and histologic grading of marrow iron [12] although histological grading is subject to variation between and within observers [13]. Phlebotomies were well-tolerated by 14/16 patients, and they reached the target ferritin below 500ng/mL after a median of 16. Ferritin levels decreased significantly in 49/55 (80%) of patients after a median of 9 phlebotomies in another study [16]. Transient elastography: this is the preferred method if assessment of liver fibrosis and cirrhosis is a concern, particularly in thrombocytopenic patients for whom a liver biopsy poses significant risk of bleeding. Liver biopsy: Given the risks of the procedure, risk of sampling variability, and indolent course of hepatic siderosis, measurement of hepatic iron by spectrophotometry of liver biopsy should be an exception to be discussed case-by- case. Toxicity: Ocular and auditory abnormalities, sensorimotor neurotoxicity, renal insufficiency, pulmonary toxicity, and failure of linear growth. In general, assessment of body iron stores should also follow when deferoxamine toxicity occurs. Dosing: 20 to 40 mg/kg/day, administered 5-7 days per week by continuous overnight infusion, typically for 8-12 hours. Dose should not exceed 50 mg/kg/day Infusion rate should not exceed 15 mg/kg/hour to avoid hypotension. Therapeutic index: Most of the toxicity caused by deferoxamine occurs when the dose exceeds 50 mg/kg/day or when the iron burden is not high. Therapeutic index is calculated by: (number of days per week X daily dose in mg/kg) / (7 X serum ferritin in ng/mL) [22]. Dose modification: 5-10mg/kg/day increments every 3-6 months if necessary depending on serum ferritin trends. Dose reduction: 50% for starting dose if creatinine clearance 40-60mL/min or moderate (Child-Pugh B) hepatic impairment. If the serum creatinine level increases more than 33% over the course of two consecutive visits, the dose should be reduced by 10mg/kg. For pediatric patients, the dose should be reduced by 10mg/kg 91 if the serum creatinine is greater than the upper limit of normal on 2 consecutive visits. Administration: Exjade should be taken once daily on an empty stomach (at least 30 min prior to eating). Tablets should be completely dispersed by stirring in water, orange juice, or apple juice until there is a fine suspension. After swallowing, any residue should be resuspended in a small volume of liquid and swallowed. Jadenu is available in 90mg, 180mg, and 360mg tablets or granules (Jadenu Sprinkles). If the serum creatinine level increases more than 33% over the course of two consecutive visits, the dose should be reduced by 7mg/kg. For pediatric patients, the dose should be reduced by 7mg/kg if the serum creatinine is greater than the upper limit of normal on 2 consecutive visits. Administration: Jadenu should be taken once daily preferably at the same time of the day, on an empty stomach or with a light meal (contains less than 7% fat content and approximately 250 calories). Commercial crushers with serrated surfaces should be avoided for crushing a single 90 mg tablet. The dose should be immediately and completely consumed and not stored for future use. In combination therapy, deferoxamine should be prescribed as above, preferably 7 days a week; if patient is admitted, it may be placed as a 24-hour infusion. Deferiprone is an oral medication for iron chelation, available in 500mg tablets and 100mg/mL oral solution. Contraindications: severe hepatic impairment, creatinine clearance below 2 15ml/min/1. Dose reduction: not recommended for mild or moderate liver impairment, or 2 creatinine clearance above 15ml/min/1. Administration: take first dose in the morning, second dose at midday, third dose in the evening, with meal. Allow at least 4-hour intervals between deferiprone and medications or supplements containing polyvalent cations. Prior to starting treatment: obtain complete blood count with neutrophil count, serum transaminases, and zinc levels. Autologous patients should continue supplementation for one year if dietary intake does not meet daily requirements. Iron supplementation should not be used routinely in any patient unless iron deficiency is clearly documented. Calcium and Vitamin D daily intake requirements Adequate calcium and vitamin D intake are necessary in order to decrease the risk of bone complications after transplant. Women with ovarian failure and patients who require long-term treatment with corticosteroids have a high risk of osteoporosis, and pediatric patients can have poor bone development after chemotherapy and radiation. Patients who cannot consume adequate calcium or vitamin D from foods should receive supplements to meet their daily requirements. Supplemental calcium should be given in divided doses, preferably as calcium citrate. Some "natural" calcium supplements do not contain enough bioavailable calcium to prevent osteopenia. Daily requirements ++ Age (years) Elemental Ca Vitamin D 1 - 5 800 mg 400 International Units 6 - 8 1200 mg 400 International Units 9 - 18 1500 mg 400 - 800 International Units >18 1500 mg 800 International Units B. All patients receiving these immunosuppressive drugs require magnesium supplementation and monitoring serum magnesium levels monthly, or more often as indicated. Oral magnesium with protein (133 mg/tablet) is better tolerated than magnesium oxide.

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Iodine excess In normal individuals women's health issues australia effective 50 mg ortho tri-cyclen, the acute and chronic excess of iodinerarely leads to profound clinical thyroid dysfunction women's health clinic st louis generic 50mg ortho tri-cyclen otc, because of the rapid activation of several autoregulatory mechanisms menstruation night sweats cheap ortho tri-cyclen 50mg on line. However menstrual fluid order ortho tri-cyclen 50mg otc, in some individuals, such as newborns, the escape from the inhibitory effect of large doses of iodine is not achieved and clinical (symptomatic hypothyroidism) or subclinical hypothyroidism (asymptomatic hypothyroidism or altered serum thyroid parameters) the most frequently identified sources of excess iodine leading to problems in neonates result from the use of iodine-containing disinfectants (10,000 microg of iodine/mL) and from radiograph contrast media (250-370 mg of iodine/mL) given for radiological examination. The total concentration of iodine in plasma comprises the iodine in circulating T4 and T3, plus the circulating iodide and any iodine contained in contrast media, or other contaminating compounds. Urinary iodine concentrations above 16 microg/dL, 20 microg g/dL, and 25 microg g/dL may impair thyroid function in neonates. Some iodinated contrast agents, such as ipodate and iopanoic acid, are well- known inhibitors of all known iodothyronine deiodinases. The role of thyroid hormones on human central nervous system during fetal and postnatal life the close involvement between human brain development and thyroid hormones is widely accepted (Morreale de Escobar G et al. The effects of T3 on the central nervous system are mediated by the regulation of the expression of genes that synthesize proteins implicated in cerebral neurogenesis, neuronal migration and differentiation, axonal outgrowth, dendritic ontogeny, and synaptogenesis. They are also necessary for cerebellar neurogenesis (predominantly during early postnatal life), gliogenesis (predominantly during late fetal life to 6 months postnatally), and myelogenesis (during the second trimester of gestation to 2 years of postnatal life). Low T4 levels during neonatal life, especially if persistent, could be a negative factor contributing to the neurodevelopmental problems of very preterm infants. Indeed, retrospective studies have shown a relationship between hypothyroxinemia and developmental delay and an increased risk of disabling cerebral palsy (De Vries et al. Alterations of the thyroid function during the neonatal period risk factors There are many more associations of postnatal factors with transient alterations of thyroid function than had previously been considered in newborn infants. A oblique preventative 196 A New Look at Hypothyroidism approach may be necessary through reduction in the incidence or severity of individual illness(es). Similarly, alternatives to those drugs that interfere with the hypothalamic- pituitary-thyroid axis should be evaluated (e. The adaptive response of the thyroid axis at the interruption of the placental circulation is insufficient. Causal factors of transient alterations of thyroid function in the preterm newborn. If it develops soon after birth, it is called hypothyroidism acquired in the newborn period. Hypothyroidism in the newborn may be caused by: a missing or poorly developed thyroid gland, a pituitary gland that does not stimulate the thyroid gland or thyroid hormones that are poorly formed or do not work. The most common cause of hypothyroidism in the newborn is complete absence or underdevelopment of the thyroid gland. Endemic cretinism is caused by iodine deficiency, and is occasionally exacerbated by naturally occurring goitrogens. Dysgenesis of the thyroid gland, including agenesis (ie, complete absence of thyroid gland) and ectopy (lingual or sublingual thyroid gland) may be a cause. The incidence of congenital hypothyroidism, as detected through newborn screening, is approximately 1 out of every 3,000 births, but the incidence is different depending on the country, sex, race, ethnicity, gestational age. Less commonly, the thyroid gland is present but does not produce normal amounts of thyroid hormones. Some Hypothyroidism and Thyroid Function Alterations During the Neonatal Period 197 infants identified as having primary congenital hypothyroidism may have transient disease and not permanent congenital hypothyroidism. Family history should be carefully reviewed for information about similarly affected infants or family members with unexplained mental retardation. Neonatal screening for congenital hypothyroidism in premature infants is not as well established as in term newborns regarding age and number of samples. Congenital hypothyroidism is more common in infants with birthweights less than 2,000 g or more than 4,500 g. Thyroglobulin defect (ie, inability to form or degrade thyroglobulin), Deiodinase defect. Thyroid hormone resistance (ie, thyroid hormone receptor abnormalities) may also be a cause. If present with these 198 A New Look at Hypothyroidism deficiencies, hypothyroidism is usually milder and is not associated with the significant neurologic morbidity observed in primary hypothyroidism. Later, the newborn may become sluggish (lethargic) and have a poor appetite, low muscle tone, constipation, a hoarse cry, and a bulging of the abdominal contents at the bellybutton (an umbilical hernia). The morbidity from congenital hypothyroidism can be reduced to a minimum by early diagnosis and treatment. Untreated infants will have delayed development, intellectual disability, and short stature. Because early treatment can prevent intellectual disability, all newborns should receive a screening blood test in the hospital early after birth to evaluate thyroid function. Many newborns with hypothyroidism require thyroid hormone given by mouth for their entire life. Treatment is directed by a doctor who specializes in treating children with problems of the endocrine system (a pediatric endocrinologist). Somteimes, the levels of the active hormones will be within the laboratory reference ranges. In maternal autoimmune disease, transplacental passage of antibodies cause transient or permanent hypothyroidism. A very high intake of iodine can produce a blockage in the synthesis of thyroid hormones. Although iodide is a substrate for thyroid hormones, high levels reduce iodide organification in the thyroid gland, decreasing hormone production. The antiarrhythmic agent amiodarone can cause hyper- or hypothyroidism due to its high iodine content. Iodine in contrast agents or skin disinfectants can cause hypothyroidism or hyperthyrotropinemia in premature neonates (Lopez ?Sastre et all. Occasionally, it appears as result of an excess of iodine or deficiency and is more frequent in preterm infants. Generally the disorder does not require treatment, but it must be monitored in order to exclude primary hypothyroidism. Low T4 levels in preterm infants are associated with persistent neurodevelopmental deficits in cognitive and motor function. Thyroid hormone substitution trials to date are underpowered and show inconsistent results; the question remains that if low T4 levels simply an epiphenomenon or not. The aetiology of transient hypothyroxinaemia is multifactorial and the components amenable to correction form the basis of the therapeutic strategy: rectification of iodine deficiency in parenteral nutrition; a reduction of non-thyroidal illnesses and attenuation of their severity; and substitution of drugs that interfere with the hypothalamic-pituitary- thyroid axis. Thyroxine substitution therapy should only be done in the context of clinical trials and only in those infants who are severely hypothyroxinaemic. Approximately 20,000 births each year in the United States are of < 28 weeks gestation and 70% of them (~14,000) now survive. Approximately 12% of survivors (nearly 1,700 children) will have disabling cerebral palsy. However, unlike many other risk factors uncovered in population-based clinical research, this association is supported by a solid body of laboratory and clinical evidence, including the well-known adverse effects on the brain of thyroid and iodine deficiency. Since previous work could not prove the need to treat due to sample size and concern that excessive treatment is itself a risk, outright intervention is not advocated at this time. The state of low concentrations of T3, often observed in newborns, 200 A New Look at Hypothyroidism would be a reflection of fetal status. As in other ages, levels of T3 may fall in the presence of concomitant diseases and undernutrition. In some newborn infants hypoxemia, acidosis, hypocalcemia and infection, postnatal malnutrition have been found to be associated to low T3 levels by inhibiting the peripheral conversion of T4 to T3, leading to prolong (1-2 months at a time) the low values observed in adaptation to extrauterine life. Low serum total T3 is the most common abnormality in infants with neonatal illness, observed in about 70% of hospitalized patients. Serum total T3 levels can range from undetectable to normal in critically ill patients, with the mean total T3 level being approximately 40% of normal. It is believed that low serum T3 is a result of decreased production of T4, rather than increased degradation or increased disposal of T3. Unlike T4, which is produced solely in the thyroid, about 80% of circulating T3 is produced by extrathyroidal conversion of T4 to T3 by 50- monoiodinases present in organs such as the liver and kidney.

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The moderate form of thyroid orbitopathy is characterized by the edema of the eyelids women's health clinic greeley co discount ortho tri-cyclen 50mg overnight delivery, chemosis womens health kaley cuoco buy cheap ortho tri-cyclen 50 mg on line, swollen caruncle menstrual bleeding 8 days generic ortho tri-cyclen 50 mg without prescription, proptosis menstrual vs estrous discount ortho tri-cyclen 50mg without a prescription. In severe orbitopathy, the patients may have double vision because of impaired eye movements, corneal defects or even a pressure on optical nerv associated with a decrease in visual acuity. Namely, low intrathyroidal iodine content presents an additional risk for deleterious effects of iodine. Prevalence of thyroid autonomy is higher in iodine-deficient or previously-iodine-deficient areas. It seems, that in iodine-deficient areas, hyperplasia of the thyroid gland occurs already in youth. In hyperplastic glands, the rate of mutations is increased, resulting in thyroid autonomy or in dedifferentiated cold thyroid nodules. Often it takes many years, before hyperthyroidism aggravates from subclinical to overt. It has been reported that hyperthyroidism develops when the product between the weight of autonomous tissue, the efficiency per gram of tissue, and iodide supply goes above a treshold. Hence it follows that an increase in iodine intake represents a risk factor for aggravation of hyperthyroidism in these patients. Iodine excess often deteriorates subclinical or overt hyperthyroidism to the severe stage. Low intrathyroidal iodine concentration, as observed in patients with toxic adenomas when compared with healthy thyroids, presents an additional risk for deleterious effects of iodine load. Hyperthyroidism Patients with thyroid autonomy may be euthyroid, subclinical or overt hyperthyroid. In the hyperthyroidism due to thyroid autonomy, the patients are often oligosymptomatic. They may have an enlarged thyroid gland, palpitations, arrythmias, restlessness or weight loss. Because hyperthyroidism develops slowly, the patients get used to the increasingly higher levels of thyroid hormones, probably by down-regulation of thyroid receptors. In that type of hyperthyroidism, the laboratory tests usually show mild hyperthyroidism but rarely severely increased thyroid hormones. This is probably due to the low iodine content in the thyroid cells in autonomous tissue, while cells in the healthy thyroid gland secrete more fT4 than fT3. However, even in subjects with healthy thyroid gland, hyperthyroidism may developed after iodine load. How much iodine is too much for the development of iodine-induced hyperthyroidism? This depends on the previous iodine supply, on the source and amount of iodine intake and on previous thyroid pathology. Autoregulation is a mechanism that enables a normal thyroid function in spite of iodine excess. Autoregulation decreases the intrathyroidal iodine content after an initial increase following the iodine load. The main sources of iodine excess are amiodarone, contrast media in radiology, topical antiseptics and iodine containing vitamins. Among them, the most important are amiodarone - because of its high iodine content, radiology contrast agents - because of their broad usage, the same holds true for iodine containing vitamins. The most important iodine source is amiodarone, a fat-soluble agent with a prolonged half-life of 100 days. One 200 milligram tablet contains 75 milligrams of iodide, about 10% is deiodized daily. Water soluble contrast media contain around 400 milligrams of iodide per mL, but only a small amount as a free iodide, which is rapidly cleared from the plasma through kidneys. During recent years, multivitamins which, beside other vitamins, usually also contain 100 to 200 micrograms of iodine, have become increasingly popular in different age groups, especially in older people and in pregnant women. This way, they can increase the iodine intake above recommended or even above safe values. Besides large amounts of iodine, amiodarone influences the thyroid status also by inhibition of deiodinase D1, which decreases serum concentrations of fT3, by inhibiting transcription of T3 receptor and by a cytotoxic action on thyroid follicular cells. The latter effect can lead to abnormal thyroid function even in normal, healthy thyroid glands and not only in individuals 22 Gaberscek S. Hyperthyroidism with preexisting thyroid disease, who are usually more susceptible to deleterious effects of amiodarone. The incidence of thyroid function abnormalities under the influence of amiodarone lies between 14 and 18%. In areas with adequate iodine intake, amiodarone provokes hypothyroidism more often than hyperthyroidism. This is due to the large amount of iodine, the higher incidence of thyroid autoimmunity and due to a sort of resistance of thyroids, probably caused by the changed autoregulatory mechanism. In iodine-deficient areas, hyperthyroidism is more frequent than hypothyroidism because of higher incidence of autonomy in goiters. The patients with iodine-induced hyperthyroidism are often older, suffering also from other diseases, especially cardiovascular. Iodine-induced hyperthyroidism is a very serious condition to treat and it often takes several months to restore the normal thyroid function. This is due to a faster synthesis of T4 in the thyroid gland due to a very high iodine supply. At the initial stage of the development of iodine-induced hyperthyroidism, we can observe increased fT4 level and only slightly increased fT3 level, which later follows fT4 level more adequatly, when hyperthyroidism begins to increase deiodase D1 activity. Thyroiditis causes follicular disruption and release of thyroid hormones, stored in the thyroid cells, into the blood, resulting in hyperthyoidism. Patients suffer from fever, severe pain that extends to the ear, and they may have symptoms of hyperthyroidism. This is probably due to the predominant release of fT4 from the intrathyroid stores. Hyperthyroidism is often mild and transient, followed by euthyroidism and hypothyroidism, which can be transient or permanent in 30%. Some patients have only several symptoms, while others develop a whole spectrum of symptoms. Most frequent clinical manifestations of hyperthyroidism are nervousness, fatigue, weakness, heat intolerance, tremor, hyperactivity, palpitations, weight loss, rarely weight gain, hyperactivity, tachycardia or atrial fibrillation, systolic hypertension, warm and moist skin. In continuation, clinically most relevant symptoms and signs of hyperthyroidism will be listed. Thyroid hormones decrease the systemic vascular resistance and the diastolic blood pressure, and increase the cardiac output, the nitric oxide, the systolic blood pressure, the heart rate, the cardiac contractility, the cardiac mass and the blood volume. Patients may have anemia due to ineffective erytropoiesis, iron deficiency, vitamin B12 deficiency and folate deficiency. They have difficulty arising from a sitting or supine position and raising arms over the head. The degree of muscular weakness is more connected with the duration of hyperthyroidism than with the biochemical severity. Meta analysis showed a 41% increase in all-cause mortality in case of subclinical hyperthyroidism, the risk seems to be dependent on the age at diagnosis, with a significant increase beginning at the age of 60 years, especially in men (6). These data indicate that even a very mild hyperthyroidism should be treated, even in asymptomatic older patients. Besides clinical data, diagnostics of hyperthyroidism include also laboratoy findings, ultrasound of the thyroid gland, and if necessary, also scintigraphy of the thyroid gland. For the determination of thyroid status, free thyroid hormones should be measured. Approximately 1% of patients has a normal fT4 and an increased fT3 level (tri-iodothyronine toxicocis). If one only relied on the determined fT4 levels, these patients would be misdiagnosed. If pituitary is more affected by mutation than the periphery, the patients have symptoms and signs of hyperthyroidism. The patients with iodine-induced hyperthyroidism have significantly higher fT4 than fT3 values. Colour flow Doppler sonography seems not to be useful for the distinction between cold and hot nodules.

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There is neither an agreed quantitative definition menopause 2 week period buy cheap ortho tri-cyclen 50 mg on line, nor an agreed mode of measurement for the condition menstrual cramps order ortho tri-cyclen 50 mg free shipping. Transient hypothyroxinaemia is not routinely Hypothyroidism and Thyroid Function Alterations During the Neonatal Period 203 monitored yet it is thought to affect about 50% of preterm infants; it was thought to be without long-term sequelae but observational studies indicate that neurodevelopment may be compromised menopause yellow vaginal discharge buy discount ortho tri-cyclen 50mg. There are significant contributions from the withdrawal of maternal?placental thyroxine transfer menopause lubricant buy 50 mg ortho tri-cyclen otc, hypothalamic?pituitary?thyroid immaturity, developmental constraints on the synthesis and peripheral metabolism of iodothyronines and iodine deficiency. It is not possible to distinguish clinically, or from laboratory measurements, whether transient hypothyroxinaemia is an independent condition or simply a consequence of non-thyroidal illness and/or drug usage. An answer to this question is important because studies of thyroid hormone replacement have been instigated, with mixed results. Proposed protocol for monitoring neonatal thyroid function in special circumstances. Until the aetiology of transient hypothyroxinaemia is better understood it would seem prudent not to routinely supplement preterm infants with thyroid hormones. Iodine deficiency, non-thyroidal illness and drug usage are the most modifiable risk factors for transient hypothyroxinaemia and are the clear choices for attempts at reducing its incidence. Parenteral nutrition does not supply the preterm newborn with enough iodine to meet the recommendations. Neonates and expecially preterm infants are a very important population at risk of suffering the consequences of both iodine deficiency and excess, because of the impact of neonatal hypothyroxinemia on brain development. Arrange to inform the family of the results on the same day and make arrangements to start thyroxine if necessary. J Clin Endocrinol Metab 82:1704-1712, 1997 Ares S, Garcia P, Quero J, et al: Iodine intake and urinary excretion in premature infants born after less than 30 weeks of gestation. J Clin Pediatr Endocrinol 17(3):509, 2004 Ares S, Pastor I, Quero J, et al: Thyroid gland volume as measured by ultrasonography in preterm infants. Acta Pediatr 84:58-62, 1995 Ares S, Pastor I, Quero J, et al: Thyroidal complications, including overt hypothyroidism, related to the use of non-radiopaque silastic catheters for parentheral feeding of prematures, requiring injection of small amounts of an iodinated contrast medium. Acta Paediatr 84:579-578, 1995 Ares S, Quero J, Duran S, et al: Iodine content of infant formulas and iodine intake of premature babies. Arch Dis Child 71:184-191, 1994 Ares S, Quero J, Morreale de Escobar G, and the Spanish Preterm Thyroid Group: Iodine during the neonatal period: too little, too much? J Pediatr Endocrinol Metab 20:163- 166, 2007 (suppl 1) Ares S, Quero J, Morreale de Escobar G: Neonatal iodine deficiency: clinical aspects. Curr Pediatr Rev 4:194-197, 2008 Biswas S, Buffery J, Enoch H, et al: A longitudinal assessment of thyroid hormone concentrations in preterm infants younger than 30 weeks? gestation during the first 2 weeks of life and their relationship to outcome. J Pediatr 105:462-469, 1984 Delange F: Iodine deficiency as a cause of brain damage. Postgrad Med J 77:217-220, 2001 Delange F: Optimal iodine nutrition during pregnancy. Thyroid hormone supplementation for the prevention of morbidity and mortality in infants undergoing cardiac surgery. The im pact of cardiopulmonary bypass on selenium status, thyroid function, and oxidative defense in children. Phase 1 trial of 4 thyroid hormone regimens for transient hypothyroxinemia in neonates of <28 weeks? gestation. J Clin Invest 111(7):1073-1082, 2003 Hypothyroidism and Thyroid Function Alterations During the Neonatal Period 207 LeFranchi S. Reduction in levels of triiodothyronine following the first stage of the Norwood reconstruction for hypoplastic left heart syndrome. Arch Dis Child 67:944-947, 1992 Morreale de Escobar G, Ares S: the hypothyroxinemia of prematurity. J Clin Endocrinol Metab 83:713-715, 1998 Morreale de Escobar G, Escobar del Rey F: Thyroid physiology in utero and neonatally, in Rubery E, Smales E (eds): Iodine Prophylaxis Following Nuclear Accidents. Oxford: Pergamon Press, 1990, pp 3-32 Morreale de Escobar G, Kester M, Martinez de Mena R, et al: Iodothyronine metabolism in human fetal brain. Eur J Endocrinol 151:U25-U37, 2004 National Research Council, Food and Nutrition Board. Paneth, N: Does transient hypothyroxinemia cause abnormal neurodevelopment in premature infants? Psychoeducational outcome in children with early-treated congenital hypothyroidism. Long-term neuropsychological sequelae of early-treated congenital hypothyroidism: effects in adolescence. Vanhole C, Aerssens P, Naulaers G, et al: L-thyroxine treatment of preterm newborns: clinical and endocrine effects. Am J Med 47:101-124, 1969 Zimmermann M, Delange F: Iodine supplementation of pregnant women in Europe: a review and recommendation. Introduction Thyroid hormones stimulate oxidative metabolism in many tissues in the body, however, testis is not one of them. Therefore, in this sense, testis is not considered as a target organ for thyroid hormones. However, recent findings clearly show that thyroid hormones have important functions on the testis development during neonatal-prepubertal life. Testis is an exocrine organ because it produces sperm and it is also an endocrine organ, because it produces hormones. In this chapter, general organization of the adult mammalian testis is first described to understand the organization of the adult testis. Thereafter, the general organization of the mammalian testis at birth is described, followed by how the neonatal- prepubertal hypothyroidism affects the testis development during this period, Esbablishment of the Sertoli and Leydig cell numbers in the adult testis during the neonatal- prepubertal life, is critical to the general maintenance and reproductive functions of the adult mammalian male; thyroid hormones play a crucial role in these processes. The effects of hypothyroidism on neonatal-prepubertal testis are discussed in this chapter using the observations generated with rodent models, focusing on testicular testosterone secretory capacity and sperm production, which are an essential function to the male mammal. The hormone testosterone is essential for the mammalian male for maintenance and proper functioning of many organ systems of the body such as muscle, bone and skin, in addition to its requirement for the reproductive function. Leydig cells in the testis are the primary source of testosterone in the male mammal. There are two populations of Leydig cells in mammals studied to date; fetal and adult Leydig cell populations. Fetal Leydig cells are differentiated during the fetal life and are still present at birth. However, the adult population of Leydig cells differentiate postnatally from the mesenchymal stem cells in the testis to establish the adult population Leydig cells of the sexually mature testes; they are the main source of testosterone during adult life. Therefore, establishing the adult population of Leydig cells in the postnatal testis, which occurs during the neonatal-prepbertal life, is an essential process in the mammalian testis for the well being of the adult mammalian male. Research with several rodent species has shown that Leydig stem cell differentiation in the postnatal testis is arrested with hypothyroidism, but can be stimulated by supplementation with thyroid hormones. Transient neonatal hypothyroidism causes larger testis at 210 A New Look at Hypothyroidism adulthood, although the process of Leydig cell differentiation is arrested during the period of hypothyroidism. Differentiated Leydig cells in these animals after the hypothyroid period is withdrawn, are smaller in size but two-fold in number compared to the euthyroid animals. Therefore, the fertility and circulating testosterone levels in these transiently neonatal animals at adulthood are similar to euthyroid animals. Under hypothyroid conditions during the neonatal -prepubertal period, fetal Leydig cells continue to function normally with no change in their testicular testosterone secretory capacity, although the postnatal differentiation of adult population of Leydig cells are absent. However, prolonging the hypothyroid condition beyond the neonatal-prepubertal period fails to maintain the fetal population of Leydig cells; they undergo cell atrophy and loose their testosterone secretory capacity, in addition to the arrest in differentiation of adult population of Leydig cells. During the hypothyroid period, in the neonatal-prepubertal animals, Sertoli cells in the seminiferous tubules fail to mature, but continue to proliferate. When the hypothyroid status is withdrawn, these Sertoli cells mature and are now greater in number per testis compared to a euthyroid testis, because they were subjected to prolonged proliferative period because of hypothyroidism. Because of this reason, testes of transiently hypothyroid animals become larger in volume and weight at adulthood and produce greater numbers of sperm compared to the control animals. These studies have revealed the importance of thyroid hormone for postnatal testis development in the mammalian testis. Gudernatsch (1912) provided the first evidence for thyroid hormones and their task in cellular differentiation. It is established now that thyroxine (T4) and triiodothyronine (T3) are produced by the thyroid gland and triiodothyronine is at least five times more potent than thyroxin. The most characteristic effect of thyroid hormones is their ability to stimulate oxidative metabolism in tissues in the body.

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