Measurement Of Thyroid Function Research Articles

Persistent Pleural Effusions in Primary Systemic Amyloidosis: Etiology and Prognosis

Restrictive cardiomyopathy frequently complicates primary systemic amyloidosis (AL), yet only a small number of these patients develop large pleural effusions refractory to diuretic therapy and thoracentesis. We hypothesized that disruption of pleural function by amyloid deposits underlies persistent pleural effusions (PPEs) in patients with AL disease. We performed a retrospective study of AL patients with and without PPEs who had been referred to Boston University between 1994 and 2001. The presence of PPEs was defined by a failure to resolve the condition with thoracentesis and aggressive diuresis. AL cardiomyopathy patients without pleural effusions constituted the control (cardiac) group. Indexes of plasma cell dyscrasia, nephrotic syndrome, thyroid function, and echocardiographic measures of left and right ventricle performance were compared between groups. When available, closed needle biopsies and autopsy specimens of parietal pleura were examined for amyloid deposits. Among 636 patients with AL, 35 PPE patients underwent a median of three thoracenteses each. No statistical differences were found between the PPE and cardiac groups in echocardiographic measures of septal thickness, left ventricular systolic function, or diastolic compliance. Right ventricular (RV) hypokinesis occurred more often in PPE patients; however, nearly half of this group had normal RV systolic function. Renal function, plasma protein levels, and thyroid function were the same between groups. Nephrotic range proteinuria (ie, > 3 g/d) was more prevalent in the cardiac group than in the PPE group (44% vs 26%, respectively; p = 0.057). All pleural biopsies in the PPE group (six biopsies) revealed amyloid deposits. Autopsy samples of parietal pleura were negative for disease in two cardiac patients. Eighteen patients had chest tubes placed, and 11 underwent pleurodesis. PPE signaled limited survival among patients who were ineligible for treatment. Untreated PPE patients lived a median 1.8 months vs 6 months for untreated cardiac patients (p = 0.031). Survival after intensive chemotherapy and autologous stem cell transplantation was comparable in the PPE and cardiac groups (21.8 vs 15.6 months, respectively; p = 0.405). In AL patients with cardiac amyloid, neither echocardiographic measures of ventricular function nor the degree of nephrosis distinguished those patients with PPEs. We conclude that pleural amyloid infiltration plays a central role in the creation and persistence of pleural effusions among patients with AL.

Thyroid function in children with newly diagnosed type 1 diabetes mellitus.

Evaluation of thyroid hormone indices was performed in 138 children with newly diagnosed type 1 diabetes, with their siblings serving as controls. The DKA group consisted of 76 children who had diabetic ketoacidosis (DKA) at initial diagnosis. The non-DKA group consisted of 62 children and the control group of 35. The thyroid function tests of the patients were measured within 3 days of the initial diagnosis of diabetes and at least one follow-up test one month to two years after adequate treatment of diabetes. The DKA group had significantly lower levels of T3, T4, free T4 and FTI than did the other two groups (p < 0.0001, p < 0.0001, p < 0.0001, and p < 0.0001, respectively). T3 concentration was lower in non-DKA subjects than in controls (p = 0.0003), but the two groups did not significantly differ in terms of T4, free T4, and FTI. The TSH level did not differ among the three groups. We conclude that DKA changes thyroid function measurements. In the absence of true thyroid disease, abnormal thyroid function tests are reversible after institution of good diabetic control. We suggest that thyroid function tests should be restricted to those patients suspected of having thyroid disorders at the initial diagnosis of type 1 diabetes.

Posttraumatic stress disorder: do electrical startle responses and thyroid function usefully supplement self-report? A study of Vietnam War veterans.

To investigate the usefulness of electrical startle responses and thyroid function as supplements to self-report measures of posttraumatic stress disorder (PTSD). Invitations were sent to all New Zealand Vietnam War veterans known to be living in North Canterbury; 50 responded and the 35 living in or near Christchurch were included. Self-report measures of PTSD (the Davidson Trauma Scale (DTS) and the Symptom Check List (SCL-90-R) ), an eye blink electrical startle response and thyroid function were measured. The DTS was re-administered one to two weeks later to assess short-term test-retest reliability. Six months later the DTS and the electrical startle response were measured again. The veterans reported a wide range of PTSD severity, with 15/35 reporting prior diagnosis of PTSD. The DTS showed high short-term test-retest reliability (r = 0.93) and a moderate correlation after 6 months (r = 0.73). It also showed sensitivity to change; in one to two weeks the scores increased by nearly half a standard deviation, possibly because of an imminent "homecoming" march. The DTS and a PTSD scale from the SCL-90-R were highly correlated (r = 0.89). The total triiodothyronine (T3) to free thyroxine (T4) ratio measure of thyroid function correlated poorly with self-report (r < or = 0.27). The electrical startle response also correlated poorly with self-report (r < or = 0.26), showed low internal consistency between left and right sides (r = 0.43), and correlated 0.39 over six months. It was disliked by the veterans and had increased slightly at 6 month follow-up, perhaps because of sensitization. The DTS was reliable and correlated highly with the SCL-90-R PTSD scale. Neither thyroid function nor eye blink electrical startle correlated with each other or with self-report, and reliability was not good for electrical startle. These two measures do not appear to add anything useful to the assessment of PTSD.

Iodine sufficiency and measurements of thyroid function in maternal hypothyroidism.

To test the hypothesis that thyroglobulin (Tg) and free T4 (FT4) concentrations more than 2SD from the control mean are not increased in pregnancy in an iodine replete area in the absence of elevated TSH concentrations. The second hypothesis to be tested was that if such abnormalities in FT4 and Tg in the absence of elevated TSH concentrations were to exist they would not be associated with lowered IQs in the progeny. Cross-sectional study in New England comparing TSH, Tg, antibodies to Tg and FT4 in volunteer nonpregnant women 20-40 years old with those in hypothyroid mothers and matched euthyroid control mothers. The results are contrasted with those from similar studies reported from iodine deficient areas. Sera obtained at 17 weeks gestation and stored at -20 degrees C for 8 years were retrieved and analysed from 62 mothers with subclinical hypothyroidism and 124 matched euthyroid mothers. The diagnosis of hypothyroidism was made by finding a TSH concentration > 97.7 percentiile for 25 000 consecutive pregnant women. Sera were also analysed from 53 healthy nonpregnant volunteer women aged 20-40 years. TSH, Tg and Tg antibodies were measured in the sera of the nonpregnant volunteers, and Tg and Tg antibodies in the sera of the pregnant women who had previously been analysed for TSH and FT4. The incidence of FT4 concentrations below the 2.3 percentile of nonpregnant laboratory controls was compared for the euthyroid and hypothyroid mothers and the laboratory normal controls. Thirty-one per cent of the 62 hypothyroid mothers had FT4 concentrations below the 2.3 percentile compared with only one (0.8%) of the euthyroid mothers. Mean Tg concentrations did not differ between the nonpregnant controls and the euthyroid pregnant women, 14 +/- 10 vs. 16 +/- 10 micro g/l. Tg concentration in the hypothyroid mothers was 44 +/- 61, significantly greater than for either of the euthyroid control groups, P < 0.005. Positive antibodies to Tg were found in 9% and 10% of the control groups and 57% of the hypothyroid mothers, P < 0.0005. When TSH is included as an independent variable in multiple linear and logistic regressions, FT4 and Tg no longer correlate significantly with IQs. The incidences of FT4 concentrations more than 2SD below the control mean and of Tg > 2SD above the control mean are significantly increased in hypothyroid mothers in iodlne-sufficient New England. However, in the absence of elevated TSH concentrations, the incidences of such abnormalities in FT4 and TG are negligible. Indeed, concentrations for FT4, Tg and Tg antibodies for nonpregnant and pregnant controls in our iodine-replete area do not differ significantly from each other or from previously reported normative concentrations with the methods used. Thus, pregnancy in New England neither increases Tg nor lowers FT4 concentrations.

Unrecognized thyroid dysfunction in patients with cancer.

Abnormal thyroid function can cause subtle medical symptoms in "healthy" individuals. Because cancer can cause similar symptoms, physicians may fail to suspect and test for thyroid abnormalities. We measured thyroid function in 158 patients with various types of cancers being followed at a comprehensive cancer center and found that 16% of them had a thyroid abnormality, which had not been diagnosed and treated in any of them. We conclude that thyroid dysfunction is usually unrecognized in cancer patients and may possibly contribute to their morbidity.

Endocrine measurements in survivors and non-survivors from critical illness

To compare measurements of thyroid and adrenal function between survivors and non-survivors in critical illness. Prospective, observational study at the medical/surgical intensive care unit (ICU) at Royal Infirmary of Edinburgh, Scotland. 163 patients admitted to the intensive care unit over a 4-month period. We took blood samples within 1 h of ICU admission, and at 08:00 hours on the subsequent 2 days of ICU admission. We measured serum total (TT(4)) and free (fT(4)) thyroxine, total (TT(3)) and free (fT(3)) tri-iodothyronine, thyrotropin (TSH) and plasma cortisol concentrations. TT(3) and TT(4) concentrations were significantly less in non-survivors than in survivors on admission and on day 1 but not on day 2. Cortisol concentrations were higher in non-survivors on admission and on day 1 but not on day 2. TSH, fT(3) and fT(4) concentrations did not differ significantly between survivors and non-survivors at any time. Only TT(4) and cortisol were independent predictors of outcome. Prediction of outcome from the admission sample values was not better than using APACHE II scoring. Thyroid hormone and cortisol concentrations differ between survivors and non-survivors on admission to intensive care, but the values overlap. These differences do not allow accurate prediction of outcome from critical illness.

Goitrogenic and estrogenic activity of soy isoflavones.

Soy is known to produce estrogenic isoflavones. Here, we briefly review the evidence for binding of isoflavones to the estrogen receptor, in vivo estrogenicity and developmental toxicity, and estrogen developmental carcinogenesis in rats. Genistein, the major soy isoflavone, also has a frank estrogenic effect in women. We then focus on evidence from animal and human studies suggesting a link between soy consumption and goiter, an activity independent of estrogenicity. Iodine deficiency greatly increases soy antithyroid effects, whereas iodine supplementation is protective. Thus, soy effects on the thyroid involve the critical relationship between iodine status and thyroid function. In rats consuming genistein-fortified diets, genistein was measured in the thyroid at levels that produced dose-dependent and significant inactivation of rat and human thyroid peroxidase (TPO) in vitro. Furthermore, rat TPO activity was dose-dependently reduced by up to 80%. Although these effects are clear and reproducible, other measures of thyroid function in vivo (serum levels of triiodothyronine, thyroxine, and thyroid-stimulating hormone; thyroid weight; and thyroid histopathology) were all normal. Additional factors appear necessary for soy to cause overt thyroid toxicity. These clearly include iodine deficiency but may also include additional soy components, other defects of hormone synthesis, or additional goitrogenic dietary factors. Although safety testing of natural products, including soy products, is not required, the possibility that widely consumed soy products may cause harm in the human population via either or both estrogenic and goitrogenic activities is of concern. Rigorous, high-quality experimental and human research into soy toxicity is the best way to address these concerns. Similar studies in wildlife populations are also appropriate.

Thyroid function in mice with compound heterozygous and homozygous disruptions of SRC-1 and TIF-2 coactivators: evidence for haploinsufficiency.

Steroid receptor coactivator (SRC)-1 and transcriptional intermediary factor (TIF)-2 are homologous nuclear receptor coactivators. We have investigated their possible redundancy as thyroid hormone (TH) coactivators by measuring thyroid function in compound SRC-1 and TIF-2 knock out (KO) mice. Whereas SRC-1 KO (SRC-1(-/-)) mice are resistant to TH and SRC-1(+/-) are not, we now demonstrate that TIF-2 KO (TIF-2(-/-)) mice have normal thyroid function. Yet double heterozygous, SRC-1(+/-)/TIF-2(+/-) mice manifested resistance to TH of a similar degree as that in mice completely deficient in SRC-1. KO of both SRC-1 and TIF-2 resulted in marked increases of serum TH and thyrotropin concentrations. This work demonstrates gene dosage effect in nuclear coactivators manifesting as haploinsufficiency and functional redundancy of SRC-1 and TIF-2.

Apparent Increase in Type I 5’-Deiodinase Activity Induced by Antiepileptic Medication in Mentally Retarded Subjects

Background/Objectives: Thyroid function measurements in 3 mentally retarded patients treated with antiepileptic drugs (phenytoin or carbamazepine) showed normal thyroid-stimulating hormone (TSH) responses in spite of markedly low levels of total thyroxine (T₄), triiodothyronine (T₃), and free thyroxine (FT₄) concentrations; free triiodothyronine (FT₃), as well as mean thyroxine-binding globulin (TBG) concentrations were normal. The objective of the present investigations was to determine if antiepileptic medication in these patients contributed to the disparate TSH and thyroid hormone (TH) levels. Methods: Thyroid tests and other laboratory parameters were measured by conventional techniques. Results: Circulating TH changes noted in retarded patients were similar to those observed in control subjects receiving carbamazepine alone. Reverse T₃ (rT₃) levels in all patients were either undetectable or below the normal range. Conclusions: As type I 5′-deiodinase has a higher affinity for rT₃ than T₄, an increased activity of this enzyme would enhance rT₃ deiodination and reduce serum rT₃ concentration whereas enhanced T₄ deiodination would aid in normalizing intracellular FT₃ concentration. The finding of normal serum FT₃ concentration was consistent with normal TSH response and clinical euthyroidism in both retarded and control subjects. While phenytoin-induced increase in type I 5′-deiodinase has been previously noted, the present studies demonstrate a similar effect of carbamazepine on 5′-deiodinase.

A spontaneously arising mutation in connexin32 with repeated passage of FRTL-5 cells coincides with increased growth rate and reduced thyroxine release.

In this study we examine changes in the cellular properties of FRTL-5 cells as a function of passage number, with particular emphasis on gap junction expression, karyotype, morphology, growth rate and thyroxine (T(4)) release. Early passage FRTL-5 follicular cells transfer dye through gap junctions from injected cell(s) to third-order neighboring cells and beyond within their respective follicles and have immuno-detectable connexin32 (Cx32) type gap junctional plaques in their lateral contacting plasma membranes. By contrast, FRTL-5 cells established as monolayers, or as follicles from cultures passed more than 15 times, did not transfer microinjected Lucifer Yellow dye to contiguous neighboring cells and did not express any immuno-detectable rat thyroid specific connexins (Cx43, Cx32 or Cx26). Western blots confirmed that total, membrane and cytosolic Cx32 protein was present only in early pass follicular cultures. To better understand the passage-dependent loss of Cx32 expression, RT-PCR primers were made to the most unique sequences of the rat Cx32 molecule, the cytoplasmic and carboxyl-terminal regions. These primers were used to screen FRTL-5 RNA from cultures of various passage numbers. The results revealed that later passage cultures had a single base deletion in the middle of the Cx32 cytoplasmic loop region at nucleotide position 378. This base deletion was in the middle position of the codon for amino acid 116, which is normally a CAC (histidine) but read with the frame shift was a CCC (proline). The four amino acids that followed this deletion were also altered with the fourth one becoming UAA, the ochre translation stop codon. This premature stopping of translation resulted in a truncation of 60% of the protein, which included the remaining cytoplasmic loop, third and fourth transmembrane regions and the carboxyl-terminus. The later passage cultures did not produce a carboxyl-terminal RT-PCR product, indicating that the mRNA was also truncated. These regions of the Cx32 molecule contain the sequences and epitopes to which probes and antibodies are directed, and as such alterations of these regions with repeated passage explains reports by others that FRTL-5 cells do not express Cx32, and implies that cultures used for these assessments were passed more than 15 times. To determine if genetic or epigenetic abnormalities existed in FRTL-5 cells we performed chromosome spreads from various passage cultures. FRTL-5 cells have been reported to be diploid and more recently non-diploid; however, we found them to be fully tetraploid. This tetraploidy appears to be unstable in that later passes are tetraploid plus two or three extra chromosomes. There were no obvious translocations, breaks or large-scale interstitial deletions of any chromosomes in the FRTL-5 cultures tested. As FRTL-5 cells were repeatedly passed their morphology changed. Monolayer areas spread from beneath the follicles, and the follicles became flattened in appearance. These physical changes were coincident with dramatically increased growth rates. Early cultures (passed 3-12 times) divided on average every 49+/-1 h, whereas later passes (passes 20-25) divided every 28+/-3 h. To correlate these changes with a measure of thyroid function we assayed T(4) output. Early passage follicular cultures incubated for 6 h with sodium iodide, released on average 5.27+/- 0.33 ng/ml of T(4)/100 follicles. Later passes, or early passes treated with heptanol to down-regulate Cx32, released an average of 3.84+/-0.50 ng/ml of T(4)/100 follicles. There was a 27% difference in T(4) release between early follicular cultures, that were coupled by Cx32, and late or down-regulated early follicular cultures, that were uncoupled (P<0.0001). Collectively, the physical changes documented in this study were coincident with the loss of functional Cx32. This implies a relationship between the loss of intercellular communication and changes in morphogenic appearance, growth rate and reduced thyroid function and supports the previously postulated, tumor-suppressor role for Cx32. FRTL-5 cultures from low passage numbers are an excellent model of primary thyroid cells. However, many reports in the literature ascribe features to FRTL-5 cells that are mutually inconsistent. These differences may be resolved in the future by addressing the passage number and the conditional differences of the cultures being studied.

Pretreatment prevalence of hypothyroidism in patients with head and neck carcinoma.

Hypothyroidism in the normal population age > 60 years is encountered in the range of 0.5-5% clinically, and 5-20% have subclinical hypofunction. Hypothyroidism is recognized as a common complication of treatment in patients with head and neck carcinoma (HNC) and is reported in up to 75% of patients who receive combined treatment. Surprisingly, base-line pretreatment measurements of thyroid function in large series of patients have not been reported. Serum thyroid-stimulating hormone, free T4, and total T3 levels were recorded in 110 patients with nonthyroid HNC prior to treatment in a prospective, controlled study. The mean patient age (+/- standard deviation) was 65 years +/- 13.8 years, and 82% of patients had squamous cell carcinoma. A diagnosis of hypothyroidism already was established in 4.5% of patients, and subclinical hypothyroidism was discovered in an additional 6.4% of patients. Sixteen patients had other equivocal anomalies in thyroid function and were referred for further endocrine evaluation. No patients with formerly unrecognized clinical hypothyroidism were found. Hypothyroidism in patients with head and neck carcinoma in Israel corresponds with the reported incidence in the general population. Hypothyroidism after treatment for head and neck carcinoma stems from the effects of treatment. The need for pretreatment evaluation of thyroid function should be considered.

Comparison of thyroid function in pregnant and non-pregnant Asian and western Caucasian women

Background: Gestational thyrotoxicosis may be more prevalent in Asian women. Methods: We have measured thyroid function, ferritin and bone specific alkaline phosphatase (BALP) as peripheral markers of thyroid function and hCG in Asian and western Caucasian women in non-pregnant and early pregnancy. Results: TSH was lower in Asian women in non-pregnancy but not during normal pregnancy and this may reflect increased sensitivity of the thyroid gland to thyroid stimulation in the Asian population. No ethnic difference was found in FT3, FT4 or hCG but ferritin was lower and BALP higher in Asian women whether pregnant or not and this may be a reflection of iron balance and vitamin D status. Conclusions: We found during normal pregnancy that dynamic patterns of change for thyroid hormones and hCG are not different in Asian and western Caucasian women. We have developed gestation related reference intervals, which are a pre-requisite to the study of ethnic differences in gestation thyrotoxicosis in pregnancy.

MEDICAL EMERGENCIES IN THE PATIENT WITH DIABETES DURING PREGNANCY

Although the outcome of pregnancies complicated by diabetes is now approaching the success seen in the normal healthy pregnant population, this improvement is only realized when careful attention is paid to the metabolic, hemodynamic, and vascular perturbations associated with the changes of pregnancy. The diabetic woman must not only pay attention to nutrition but also blunt moment-to-moment swings in blood glucose by taking frequent does of insulin. In addition, she must be under constant surveillance for a host of other complications of pregnancy, such as hypertension, retinopathy, infection, acidosis, thyroid dysfunction, nephropathy, and sudden death in utero. Any or all of these problems become medical emergencies if left untreated. Rigorous vigilance to sustain normoglycemia and normotension, examination of the retina, culture of urine, assays for ketosis, measurements of thyroid function, and monitoring of renal function and fetal status are paramount in the management of pregnancy complicated by diabetes.

Thyroid Disease: A Review for Primary Care

Manifestations of thyroid disease include hyperthyroidism and hypothyroidism. In the past, the diagnosis of thyroid disease has been perplexing due to the multisystemic effects of thyroid hormone and the lack of specificity in laboratory tests. New methods of measuring thyroid function have made screening and diagnosis of thyroid dysfunction both more accurate and cost-effective. Testing for thyroid stimulating hormone (TSH) is now a first-line diagnostic procedure and, in some cases, may be the only test indicated. The general pathophysiology of thyroid, the diagnosis and management of thyroid disease, and current screening recommendations are reviewed here.

Lithium monitoring before and after the distribution of clinical practice guidelines.

To determine whether distribution of clinical practice guidelines improves lithium monitoring and whether standards of monitoring differed between patients in psychiatric contact and those seen only in primary care. Standards of monitoring were assessed for patients on lithium in northeast Scotland throughout 1995 and/or throughout 1996. Guidelines were circulated in January 1996 to all local general practitioners and psychiatrists. Monitoring was compared between 1995 and 1996 and for patients with and without psychiatric contact. Both primary care and psychiatric records were scrutinized for 422 and 403 patients prescribed lithium throughout 1995 and 1996, respectively. While monitoring was poor on several parameters during both years, frequency of measurement of both thyroid and renal function improved in 1996. Standards of monitoring were better for patients in psychiatric care. Standards of lithium monitoring require further improvement. Locally agreed practice guidelines are helpful but patients on lithium should be in continuing contact with an experienced psychiatrist.

Identification of Two Novel Deletion Mutations within the Gsα Gene (GNAS1) in Albright Hereditary Osteodystrophy1

Albright hereditary osteodystrophy (AHO) is a genetic disorder characterized by short stature, skeletal defects, and obesity. Within AHO kindreds, some affected family members have only the somatic features of AHO [pseudopseudohypoparathyroidism (PPHP)], whereas others have these features in association with resistance to multiple hormones that stimulate adenylyl cyclase within their target tissues [pseudohypoparathyroidism type Ia (PHP Ia)]. Affected members of most AHO kindreds (both those with PPHP and those with PHP Ia) have a partial deficiency of Gs alpha, the alpha-subunit of the G protein that couples receptors to adenylyl cyclase stimulation, and in a number of cases heterozygous loss of function mutations within the Gs alpha gene (GNAS1) have been identified. Using PCR with the attachment of a high melting domain (GC-clamp) and temperature gradient gel electrophoresis, two novel heterozygous frameshift mutations within GNAS1 were found in two AHO kindreds. In one kindred all affected members (both PHP Ia and PPHP) had a heterozygous 2-bp deletion in exon 8, whereas in the second kindred a heterozygous 2-bp deletion in exon 4 was identified in all affected members examined. In both cases the frameshift encoded a premature termination codon several codons downstream of the deletion. In the latter kindred affected members were previously shown to have decreased levels of GNAS1 messenger ribonucleic acid expression. These results further underscore the genetic heterogeneity of AHO and provides further evidence that PHP Ia and PPHP are two clinical presentations of a common genetic defect. Serial measurements of thyroid function in members of kindred 1 indicate that TSH resistance progresses with age and becomes more evident after the first year of life.

Radioprotection of salivary glands by S-2-(3-aminopropylamino)-ethylphosphorothioic (amifostine) obtained in a rabbit animal model

Background: Impairment of salivary gland function following high-dose radioiodine treatment (HDRIT) is a well-recognized side effect of the treatment. Because differentiated thyroid cancer has an excellent prognosis, reduction of long-term side-effects is mandatory. Therefore, the aim of this study was to investigate the radioprotective effect of amifostine in a rabbit animal model. Methods: Salivary gland scintigraphy was performed in a total of 16 New Zealand White rabbits. Uptake of 99mTc-pertechnetate was calculated in percentage of injected activity as a quantitative measure of both salivary gland and thyroid function. Reproducibility of salivary gland scintigraphy was evaluated in one rabbit without any intervention. Fifteen rabbits were studied prior to and up to 6 months after high-dose radioiodine treatment applying 2 GBq 131I. Ten animals received 200 mg/kg amifostine prior to high-dose radioiodine therapy, and 5 served as controls. Salivary glands were examined histopathologically. Results: Variation coefficient of parenchymal function was less than 3.8% in salivary glands. Prior to HDRIT, thyroid uptake was 0.417 ± 0.373% and 0.421 ± 0.241% in control and amifostine-treated rabbits, respectively. Four weeks after HDRIT, complete ablation of the thyroid was achieved in both groups. Prior to HDRIT, uptake of 99mTc-pertechnetate in salivary glands of five control rabbits was not significantly different from ten amifostine-treated rabbits. In control rabbits 6 months after HDRIT, parenchymal function was reduced significantly ( p < 0.0001) by 75.3 ± 5.3% and 53.6 ± 17.4% in parotid and submandibular glands, respectively. In contrast, in amifostine-treated rabbits, parenchymal function was reduced by 10.6 ± 3.4% and 6.5 ± 4.3% ( p > 0.05) in parotid and submandibular glands, respectively. Histopathologically, marked lipomatosis was observed in control animals but was negligible in amifostine-treated animals. Conclusion: Parenchymal damage in salivary glands induced by high-dose radioiodine treatment can be significantly reduced by amifostine in this rabbit animal model. This corresponds to data obtained in patients with differentiated thyroid cancer.

Perioperative nutrition

Perioperative nutrition

The Monitoring of Potential Long-Term Complications in Treated Adult Cancer Patients

A wide variety of long-term complications may be noted following conventional cancer treatment. These include overwhelming postsplenectomy sepsis syndrome, central and peripheral nervous system toxicity, cardiovascular complications, chronic liver damage, and secondary malignancy. Follow-up monitoring usually incorporates both physical examination and the result of radiological and laboratory investigations. Primary care physicians will often be responsible for the majority of the follow-up monitoring involving cured cancer patients and need to be aware of possible long-term therapy-related problems, especially those that present years after successful treatment of the original malignancy.

TREATMENT OF THYROID DISEASE IN PREGNANCY

With appropriate therapy, complications related to thyroid disease in pregnancy can be minimized. Although the diagnosis of thyroid endocrinopathy may be difficult in pregnancy, few therapies are contra-indicated. Because medications may cross the placenta, however, clinicians need always to be mindful of potential fetal effects and should work to use the minimal dose necessary to achieve maternal euthyroidism. Thyroid function tests, in particular free T4 and TSH, remain good measures of thyroid function and therapy in pregnancy.