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Consequences: Iodine deficiency can lead to rheumatoid arthritis lungs order naprosyn overnight congenital hypothyroidism and irreversible mental retardation arthritis in back at night generic naprosyn 250 mg on-line, making it the most common preventable cause of mental retardation [38 arthritis in fingers after pregnancy purchase naprosyn 250mg with visa, 39] arthritis in back exercises purchase naprosyn 500 mg online. There is also concern that mild and subclinical iodine deficiency can lead to neuropsychomotor deficits. Iodine supplementation in the first and second trimesters of pregnancy decreased the prevalence of moderate and severe neurological abnormalities and increased developmental test scores through 7 years, compared with supplementation later in pregnancy or treatment after birth. Currently, studies are required to determine the iodine intake and status of pregnant women in Australia. Children: Systematic review [46] of trials of iodine in children found iodine supplementation (especially iodised oil) is an effective means of decreasing goitre rates and improving iodine status in children. Indications of positive effects on physical and mental development and mortality were also reported. Newborn infants: the immediate neonatal requirements for iodine are high as a result of the postnatal thyroid hormone surge and the small calculated intra-thyroidal reserve pool of thyroid hormone. The recommended enteral intake of iodine for is at least 15 ?g/kg/day for term infants and 30 ?g/kg/day for preterm infants. In turn, the iodine content of breast milk is dependent on the iodine status of the lactating woman and reduced by maternal smoking [49]. Preterm infants: Only one randomised trial has examined the effect of iodine supplementation in preterm infants. Infants (n=121) were randomised to standard (68 ?g/l) versus increased (272 ?g/l) iodine in preterm formula. There was no effect on thyroid hormone levels and no effect on growth or neonatal morbidity. Iodine excess: Infants exposed to excess iodine are at risk of iodine overload resulting in transient hypothyroidism. The long term effects of iodine excess and transient neonatal hypothyroidism are unknown. Incidence and risk factors: the incidence of transient hypothyroidism related to iodine overload depends upon the cumulative exposure to iodine of the newborn infant, with one Australian study reporting an incidence of 25% in an iodine using perinatal centre, compared to none in a control centre not using iodine containing antiseptics or contast agents. Risk factors for neonatal iodine overload include: Maternal exposure to iodine povidone-iodine use for skin disinfectant during caesarean section or vaginal delivery [43] and amiodorone treatment of maternal, fetal arrhythmia or neonatal [51, 52]. Postnatal exposure to iodine during: routine umbilical cord care and skin disinfection prior to procedures,[5, 53] and injection of iodinated contrast material for radiographic visualization of central venous lines. Consequences: There are no published reports on the effect of transient hypothyroidism due to iodine overload on neonatal morbidity, mortality and subsequent neurodevelopment. Interventions: There are no data from controlled trials to determine whether thyroid hormone treatment of infants with transient hypothyroidism affect neurodevelopmental outcome. The incidence of neurodevelopmental disability did not differ between infants with and without transient hypothyroidism. Infants with transient hypothyroidism were treated with thyroid hormone replacement. In neonatal units using povidone-iodine, trials of chlorhexidine versus povidone-iodine are required. In developed countries, there is no evidence that use of an antiseptic (including povidone-iodine) for cord care is better than keeping the cord clean and dry without antisepsis use [57]. Radiology contrast agents: There are reports [6, 7] of transient hypothyroidism in response to iodinated contrast agents, although not all are consistent. All agents have iodine but at differing concentrations liberating differing quantities of free iodine. In view of concerns regarding the potential for iodine overload, the use of radio-opaque contrast materials should be limited to central line placements which are inadequately visualized by plain x-ray and ultrasound. Plain x-ray has been reported to be imprecise in determining central line tip position in neonates [59-61]. Transient hypothyroxinemia of prematurity In preterm infants, levels of T4 and fT4 in the first day vary directly with gestation. Incidence and risk factors: There is no consistent definition of transient hypothyroxinemia in newborn infants. Studies have reported: Incidence of infants with severely depressed T4 values (below 4 mg/dL) ranged from 40% at 23 weeks gestation to 10. Consequences: Infants who are extremely premature and sick are more likely to have transient hypothyroxinemia. Whether transient hypothyroxinemia is causative of adverse neonatal outcomes or is merely associated with illness severity is unclear. Associations with transient hypothyroxinemia reported in observational studies include: Intraventricular haemorrhage, [73, 79] Chronic lung disease, [71] Death, [71, 73, 80] and Neurodevelopmental disability: Three cohort studies [8-12] have documented an association between low thyroid hormone levels (T3 or T4) in the first weeks after birth and abnormal neurodevelopmental outcome. All three cohorts documented a measure of abnormal mental development in children who had low neonatal thyroid hormone levels. The associations in the cohorts persisted despite correction for potential confounders including gestation, measures of fetal growth (either birth weight or presence of growth restriction) and, in some studies, many factors relating to severity of illness in preterm infants and independent risk factors for abnormal neurodevelopmental outcome. The following reviews the evidence from systematic reviews of thyroid hormones in preterm infants: Prophylactic postnatal thyroid hormones for prevention of morbidity and mortality in preterm infants: systematic review [13] found 4 trials enrolling 318 infants. All studies commenced treatment in the first 48 hours, with doses of T4 ranging from 8 to 20 ?g/kg/day. No significant difference was found in neonatal morbidity, mortality or neurodevelopmental outcome up to 10 years in infants who received thyroid hormones compared to control. A subgroup analysis from one trial [81] of infants born <27 weeks gestation reporting a benefit from thyroid hormones should be viewed with caution given imbalances after randomisation and the fact the analysis was not prespecified. No significant difference was reported any neonatal morbidity up to 36 weeks corrected age and no difference in growth in weight, head circumference or length. Postnatal thyroid hormones for respiratory distress syndrome in preterm infants: systematic review [14] found 2 studies that enrolled preterm infants with respiratory distress, with one study comparing treatment with L-thyroxine 50 ?g/dose at 1 and 24 hours to no treatment, and the other L triiodothyronine 50 ?g/day in two divided doses for two days or no treatment. Neither study reported any significant benefits in neonatal morbidity or mortality from use of thyroid hormones. Infants of mothers with Hashimotos thyroiditis Infants of mothers with Hashimotos thyroiditis are at low risk of transient hypothyroidism from thyroid blocking antibodies (incidence estimated at 1:180000), and rarely of thyrotoxicosis from coexistent thyroid stimulating antibodies. Incidence and risk factors: the reported prevalence of Graves disease in pregnant women is approximately 0. A further 3% of babies of mothers with Graves disease have biochemical thyrotoxicosis in the absence of symptoms. Effects on pregnancy: Although data are sparse, pregnancies affected by maternal hyperthyroidism may be at increased risk of: Miscarriage [84] Stillbirth [85] Intrauterine growth restriction [86] Preterm labor and other pregnancy complications including pregnancy induced hypertension and thyroid crisis [86] Fetal effects: the fetus may develop goitre, tachycardia, hydrops associated with heart failure, growth retardation, craniosynostosis, increased foetal motility and accelerated bone maturation. Neonatal effects: In the neonate, overt symptoms and signs usually occur in the first few days of life and may last for 36 months, proportional to the clearance of maternal IgG [87]. However, overt thyrotoxicosis has been reported to occur as late as 45 days [87], delayed by the presence of transplacentally transferred maternal antithyroid drugs or blocking antibodies. Affected neonates may have irritability, restlessness, goitre, excessive weight loss, failure to regain birth weight, diarrhoea, sweating, flushing and eye signs including peri-orbital edema, lid retraction and proptosis [86, 88-90]. Initial sinus tachycardia can progress to tachyarrhythmia and congestive cardiac failure [91]. Advanced bone age, craniosynostosis, and microcephaly may be evident in both the fetus and newborn. The developmental outcome for infants of mothers with treated hyperthyroidism is generally within the normal range and similar to a matched control group [96]. Prevention: Infants of mothers with Graves disease during pregnancy who are appropriately managed with antithyroid medication will usually have infants who are asymptomatic, although they are still at risk of biochemical hyperthyroidism (T4 >35 pmol/L). Contact the on call Endocrinologist at either Sydney Childrens Hospital (93821111) or Childrens Hospital Westmead (98450000) 2. The treatment of thyrotoxicosis is supported by case reports in the literature and is consistent with the treatment of hyperthyroidism in other populations of patients. Iodide solution, which suppresses thyroid hormone synthesis and has a prompt effect in inhibiting the release of thyroid hormones, may be used in conjunction with case reports in the literature of their use. Beta-Blockers are effective in controlling symptoms caused by adrenergic stimulation, in particular, cardiovascular symptoms associated with tachycardia or tachyarrhythmia. Potential side effects include hypoglycaemia, bradycardia, and hypotension, so babies require close monitoring. Specific treatment for cardiac failure may be required, for example Digoxin and Diuretics. Severely thyrotoxic babies may be treated with prednisolone [98] which suppresses deiodination of T4 to T3 and compensates for hypercatabolism of endogenous glucocorticoids induced by T3 and T4. Other general measures: Sedatives may also be helpful in managing irritability and restlessness. Assess fluid balance infants may have increased fluid requirements secondary to increased transepidermal water losses associated with hyperthermia and losses associated with diarrhoea.
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Autosome Chromosomes that do not contain genes for sex differentiation; in humans arthritis pain under knee cap discount naprosyn 500 mg otc, chromosome pairs 1 ?22 arthritis in the back of the head order 500 mg naprosyn visa. Azurophilic granules the predilection of some granules (primary granules) within myelocytic leukocytes for the aniline component of a Romanowsky type stain arthritis in my feet and toes purchase genuine naprosyn on line. These granules appear bluish purple or bluish black when observed microscopically on a stained blood smear rheumatoid arthritis neck purchase naprosyn 250 mg with amex. Basophilic normoblast A nucleated precursor of the erythrocyte that is derived from a pronormoblast. The nuclear chromatin is coarser than the pronormoblast, and nucleoli are usually absent. Basophilic stippling Erythrocyte inclusions composed of precipitated ribonucleoprotein and mitochondrial remnant. Observed on Romanowsky stained blood smears as diffuse or punctate bluish black granules in toxic states such as drug (lead) exposure. Formed from highly organized, differentiated cells that do not spread or invade surrounding tissue. Bilineage leukemia A leukemia that has two separate populations of leukemic cells, one of which phenotypes as lymphoid and the other as myeloid. Biphenotypic leukemia An acute leukemia that has myeloid and lymphoid markers on the same population of neoplastic cells. Birefringent Characteristic of a substance to change the direction of light rays that are directed at the substance; can be used to identify crystals. As the H+ concentration in tissues increases, the affinity of hemoglobin for oxygen is decreased, permitting unloading of oxygen. Bone marrow trephine Removal of a small piece of the bone marrow biopsy core that contains marrow, fat, and trabeula. Examination of the trephine biopsy is useful in observing the bone marrow architecture and cellularity and allows interpretation of the spatial relationships of bone, fat, and marrow cellularity. Butt cell Circulating neoplastic lymphocyte with a deep indentation (cleft) of the nuclear membrane. Cabot ring Reddish-violet erythrocyte inclusion resembling the figure 8 on Romanowsky stained blood smears that can be found in some cases of severe anemia. Carboxyhemoglobin Compound formed when hemoglobin is exposed to carbon monoxide; it is incapable of oxygen transport. It is produced by the choroid plexus cells, absorbed by the arachnoid pia and circulates in the subarachnoid space. It is characterized by leukocytosis, <30% blasts, and a predominance of mature lymphoid cells. In the chronic phase, there are less than 30% blasts in the bone marrow or peripheral blood, whereas in the blast crisis phase there are more than 30% blasts. An absolute monocytosis (>1 X 109/L) is present and immature erythrocytes and granulocytes may also be present. The bone marrow is hypercellular with proliferation of abnormal myelocytes, promonocytes, and monoblasts, and there are <20% blasts. Spherocytes are not readily found, differentiating these anemias from hereditary spherocytosis. Chylous A body effusion that has a milky, opaque appearance due to the presence of lymph fluid and chylomicrons. Circulating leukocyte the population of neutrophils actively circulating pool within the peripheral blood stream. Can be detected by the identification of only one of the immunoglobulin light chains (kappa or lambda) on B cells or the presence of a population of cells with a common phenotype. Clot Extravascular coagulation, whether occurring in vitro or in blood shed into the tissues or body cavities. Clot retraction the cohesion of a fibrin clot that requires adequate, functionally normal platelets. Retraction of the clot occurs over a period of time and results in the expression of serum and a firm mass of cells and fibrin. Coagulation factors Soluble inert plasma proteins that interact to form fibrin after an injury. Cobalamin A cobalt-containing complex that is common to all subgroups of the vitamin B12 group. Cold agglutinin disease Condition associated with the presence of cold reacting autoantibodies (IgM) directed against erythrocyte surface antigens. Colony forming unit A visible aggregation (seen in vitro) of cells that developed from a single stem cell. Colony stimulating factorCytokine that stimulates the growth of immature leukocytes in the bone marrow. Committed/progenitor Parent or ancestor cells that differentiate into cells one cell line. Common coagulation One of the three interacting pathways in the pathway coagulation cascade. The common pathway includes three rate-limiting steps: (1) activation of factor X by the intrinsic and extrinsic pathways, (2) conversion of prothrombin to thrombin by activated factor X, and (3) cleavage of fibrinogen to fibrin. Compensated hemolytic A disorder in which the erythrocyte life span is disease decreased but the bone marrow is able to increase erythropoiesis enough to compensate for the decreased erythrocyte life span; anemia does not develop. Complement Any of the eleven serum proteins that when sequentially activated causes lysis of the cell membrane. Congenital Heinz body Inherited disorder characterized by anemia due hemolytic anemia to decreased erythrocyte lifespan. Erythrocyte hemolysis results from the precipitation of hemoglobin in the form of heinz bodies, which damages the cell membrane and causes cell rigidity. Contact group A group of coagulation factors in the intrinsic pathway that is involved with the initial activation of the coagulation system and requires contact with a negatively charged surface for activity. Continuous flow analysisAn automated method of analyzing blood cells that allows measurement of cellular characteristics as the individual cells flow singly through a laser beam. Contour gating Subclassification of cell populations based on two characteristics such as size (x-axis) and nuclear density (y-axis) and the frequency (z axis) of that characterized cell type. A line is drawn along the valley between two peaks to separate two cell populations. Coverglass smear Blood smear prepared by placing a drop of blood in the center of one coverglass, then placing a second coverglass on top of the blood at a 45? angle to the first coverglass. Cryopreservation the maintaining of the viability of cells by storing at very low temperatures. Cyanosis Develops as a result of excess deoxygenated hemoglobin in the blood, resulting in a bluish color of the skin and mucous membranes. Cytochemistry Chemical staining procedures used to identify various constituents (enzymes and proteins) within white blood cells. Useful in differentiating blasts in acute leukemia, especially when morphologic differentiation on romanowsky stained smears is impossible. Cytokine Protein produced by many cell types that modulates the function of other cell types; cytokines include interleukins, colony stimulating factors, and interferons. This occurs because the primary hemostatic plug is not adequately stabilized by the formation of fibrin. Dohle bodies An oval aggregate of rough endoplasmic reticulum that stains light gray blue (with Romanowsky stain) found within the cytoplasm of neutophils and eosinophils. It is associated with severe bacterial infection, pregnancy, burns, cancer, aplastic anemia, and toxic states. The antibody reacts with erythrocytes in capillaries at temperatures below 15?C and fixes complement to the cell membrane. Upon warming, the terminal complement components on erythrocytes are activated, causing cell hemolysis. Downey cell An outdated term used to describe morphologic variations of the reactive lymphocyte. Drug-induced hemolytic Hemolytic anemia precipitated by ingestion of anemia certain drugs. Dutcher bodies Intranuclear membrane bound inclusion bodies found in plasma cells. Dysfibrinogenemia A hereditary condition in which there is a structural alteration in the fibrinogen molecule. Dyshematopoiesis Abnormal formation and/or development of blood cells within the bone marrow. Dyspoiesis Abnormal development of blood cells frequently characterized by asynchrony in nuclear to cytoplasmic maturation and/or abnormal granule development.
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The serum concentrations of growth hormone arthritis pain keeps me awake at night purchase 500 mg naprosyn with mastercard, prolactin and T4 rheumatoid arthritis chest pain order 500 mg naprosyn amex, which were depressed during exposure zoloft arthritis pain buy 500 mg naprosyn, returned to arthritis in dogs wrist purchase naprosyn 250mg without prescription control levels at 40?50 days of age i. The dose?response characteristics of the effect on testes were evaluated in 90-day-old male rats given 0, 0. Both testis weight and daily sperm production were significantly increased at all concentrations. The testis weight reached a plateau and the daily sperm production a peak value at the 0. Overall, these data support the conclusion that neonatal hypothyroidism in rats allows a prolonged period of proliferation of Sertoli cells, which ultimately leads to increased numbers of Leydig cells, increased testis weights and increased daily sperm production in adults. In order to study the effects of propylthiouracil on prostate weight, the offspring of Sprague-Dawley rats maintained on 0. The ventral prostate weights were lower than those of controls up to 95 days of age but increased from day 95, and the glands were about 40% heavier at 180 days of age. The increase in weight was at least partially due to the presence of new ductal structures. The histological appearance of the prostate was normal at all ages, but a transient increase in amiloride-inhibitable plasminogen activator activity was seen in the ventral and dorso-lateral prostate at 42 days of age. Treatment with propylthiouracil also increased the acti vity of metalloprotease in the ventral prostate at 21?42 days of age. In contrast to effects seen in males, the follicle-stimulating hormone concentration was not reduced in propylthiouracil-treated females (Dijkstra et al. Groups of 70?114-day-old female Sprague-Dawley rats were exposed to propyl thiouracil in the diet (0. The serum T4 concen trations of the dams were depressed through 120 days of age, and their body weight was diminished by about 20%. Neuroanatomical effects in 90-day-old offspring of treated dams included thinning of the cerebellar cortex and fewer synapses in Purkinje cells. In behavioural assessments which included differential reinforcement of low rate learning, escape and avoidance tasks and motor activity and exploration, control rats learned the escape and avoidance tasks faster and were hyperactive (Schalock et al. The effects of propylthiouracil on heart and kidney development were studied in Sprague-Dawley rats by treating their dams by subcutaneous injection of 20 mg/kg bw from gestation day 17 to lactation day 5, and by direct injection of the pups on post natal days 1?5. Propylthiouracil significantly impaired body growth and heart and kidney weights (by 10?25%), although the weights had returned to control levels by 50 days of age. Coronary arterioles were examined in 12-, 28 and 80-day-old Sprague-Dawley rats of dams that had received 0. The body weights of the offspring were significantly depressed after day 20, while their heart rates were significantly depressed at 12 and 28 days of age. Long-term depression of the cardiac mass was also noted, in the presence of capillary proliferation and marked attenuation of arteriolar growth (Heron & Rakusan, 1996). Propylthiouracil significantly reduced the live litter size and pup weight at all ages and also significantly reduced the volume of the neocortex. Further analysis indi cated reduced numbers of glial cells in the neocortex only at day 48, while the numbers of neurons were not significantly reduced at any age (Behnam-Rassoli et al. The auditory response (brainstem-response audiometry) to frequencies of 4 and 16 kHz was evaluated in Sprague-Dawley rats 12, 16, 25 and 125 days of age that had been exposed to propylthiouracil during various 10-day periods of development. The hormone concentrations were not significantly reduced when exposure began at 28 or 120 days of age. Treatment with propyl thiouracil significantly increased the latency of wave 1 (representing the cochlear nerve compound action potential) of the brainstem response when given from 3 days before parturition through 6 days of age, but had no permanent effect when given for 10 days starting 10 days after birth (Hebert et al. The effects of propylthiouracil on growth, motor development and auditory function were evaluated in Long Evans rats (six to eight litters per group) exposed via the drinking-water to propylthiouracil at 0, 1, 5 or 25 mg/L from gestation day 18 to postnatal day 21. At 5 and 25 mg/L, the serum T4 concentration was sharply reduced on days 1, 7, 14 and 21 after birth, while that of T3 was reduced on days 7, 14 and 21 at 25 mg/L and on day 21 at 5 mg/L. Pups exposed to 25 mg/L had reduced body weights, delayed eye opening, delayed preweaning motor activity and persistent postweaning hyperactivity. Adult offspring that had been exposed to 5 or 25 mg/L showed auditory startle deficits at all frequencies tested (range, 1?40 kHz) (Goldey et al. Histologically, the ovaries of propylthiouracil-treated females showed decreased numbers of primordial, multi laminar and Graafian follicles as folliculogenesis occurred during days 14?28. In males, there was evidence of reduced numbers of seminiferous tubules, but the histo logical appearance was normal. The inhibition could be reversed by increasing amounts of glutathione (Yamada et al. Propylthiouracil significantly decreased cytochrome c reductase and aniline hydroxylase activity in male Wistar rat microsomes (Raheja et al. Propylthiouracil inhibited glutathione transferases in a concentration-dependent manner, a 10-mmol/L concentration causing 25% inhibition. The S-oxides of propyl thiouracil were even more potent inhibitors: the 2-sulfonate inhibited the enzyme activity by 80% (Kariya et al. The effects were suppressed by iodide and did not occur when protein synthesis was inhibited by cycloheximide (Leer et al. Chromosomal aberrations were not induced in a mouse mammary carcinoma-derived cell line or in cultured thyroid cells [not otherwise defined] derived from male Wistar rats given drinking-water containing propylthiouracil at 0. It did not induce somatic recombination in eye cells of Drosophila melanogaster when administered continuously in feed to larvae. The main effect of propylthiouracil in humans and rodents is inhibition of thyroid peroxidase, which results in decreased plasma concentrations of T3 and T4 and an Table 1. Squirrel monkeys are much less sensitive to the effect of propylthiouracil on thyroid peroxidase than rats. Another effect of propylthiouracil is inhibition of conversion of T4 to T3 by inhibiting type-1 deiodinase. Alteration of thyroid hormone production is the presumptive mechanism for thyroid tumour formation in rodents. The lack of adequate data on genotoxicity for propylthiouracil precludes a conclusion regarding the mechanism of carcinogenicity. In two small studies in mice, oral administration of propylthiouracil produced thyroid follicular-cell carcinomas and tumours of the anterior pituitary. In multiple studies with various strains of rats, propyl thiouracil produced thyroid follicular-cell adenomas and carcinomas. In single studies, propylthiouracil produced thyroid follicular-cell adenomas and carcinomas in hamsters and adenomas in guinea-pigs. The main effect of propylthiouracil in humans and rodents is interference with thyroid peroxidase-mediated iodination of thyroglobulin, which results in decreased plasma concentrations of triiodothyronine and thyroxine and increases in those of thyroid-stimulating hormone, with consequent thyroid follicular-cell proliferation and thyroid growth. This is a plausible mechanism of propylthiouracil-induced tumori genesis in the thyroid. Propylthiouracil is not considered to be a human teratogen, although a small percentage of infants whose mothers received the drug during pregnancy developed transient hypothyroidism. Follow-up of small numbers of offspring exposed prenatally did not suggest impairment of intellectual development. Experimental studies on the effects of propylthiouracil focused on the consequences of the induction of hypo thyroidism during the early postnatal period on the development and functioning of the brain and reproductive tract. Hyperactivity, auditory deficits and increased sperm production have been observed in rats. The latter outcome is the result of a prolonged period of proliferation of Sertoli cells, and subsequently Leydig cells, in the testes that allows additional spermatogonia in adulthood. It did not induce mutations in bacteria, and it was only marginally mutagenic in yeast. It did not induce chromosomal aberrations in thyroid cells of rats exposed in vivo via the drinking-water. There is sufficient evidence in experimental animals for the carcinogenicity of propylthiouracil. Overall evaluation Propylthiouracil is possibly carcinogenic to humans (Group 2B). Endocrinology, 113, 921?928 Council of Europe (1997) European Pharmacopoeia, 3rd Ed. Analyst, 124, 125?128 European Commission (1981) Council Directive of 31 July 1981 concerning the prohibition of certain substances having a hormonal action and of any substances having a thyrostatic action. Thyroid, 7, 647?652 Medical Products Agency (2000) Uppsala Medicines Control Agency (2000) London Medicines Evaluation Board Agency (2000) the Hague Melander, A. Part 2: Influence of drop-out rates and of continued alcohol consumption in a clinical trial. Thio uracil is not currently used as a thyrostatic drug in humans (Astwood & VanderLaan, 1945; Stanley & Astwood, 1949).
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