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PubMed2005

Management of Graves' disease during pregnancy: the key role of fetal thyroid gland monitoring.

BACKGROUND: Fetuses from mothers with Graves' disease may experience hypothyroidism or hyperthyroidism due to transplacental transfer of antithyroid drugs (ATD) or anti-TSH receptor antibodies, respectively. Little is known about the fetal consequences. Early diagnosis is essential to successful management. We investigated a new approach to the fetal diagnosis of thyroid dysfunction and validated the usefulness of fetal thyroid ultrasonograms. METHODS: Seventy-two mothers with past or present Graves' disease and their fetuses were monitored monthly from 22 wk gestation. Fetal thyroid size and Doppler signals, and fetal bone maturation were determined on ultrasonograms, and thyroid function was evaluated at birth. Thyroid function and ATD dosage were monitored in the mothers. RESULTS: The 31 fetuses whose mothers were anti-TSH receptor antibody negative and took no ATDs during late pregnancy had normal test results. Of the 41 other fetuses, 30 had normal test results at 32 wk, 29 were euthyroid at birth, and one had moderate hypothyroidism on cord blood tests. In the remaining 11 fetuses, goiter was visualized by ultrasonography at 32 wk, and fetal thyroid dysfunction was diagnosed and treated; there was one death, in a late referral, and 10 good outcomes with normal or slightly altered thyroid function at birth. The sensitivity and specificity of fetal thyroid ultrasound at 32 wk for the diagnosis of clinically relevant fetal thyroid dysfunction were 92 and 100%, respectively. CONCLUSION: In pregnant women with past or current Graves' disease, ultrasonography of the fetal thyroid gland by an experienced ultrasonographer is an excellent diagnostic tool. This tool in conjunction with close teamwork among internists, endocrinologists, obstetricians, echographists, and pediatricians can ensure normal fetal thyroid function.

Adult↗
PubMed1996

Thyroid autoimmune disorders in patients with chronic hepatitis C before and during interferon-alpha therapy.

BACKGROUND AND AIMS: Hepatitis C virus is involved in the induction of autoimmunity and interferon can also induce hepatic and non-hepatic autoimmune reactions. This study assessed the prevalence of thyroid autoantibodies and autoimmune thyroid disorders in patients with chronic hepatitis C before and during interferon therapy. PATIENTS AND METHODS: We studied prospectively 207 patients positive for anti-HCV and viral RNA. One hundred and forty-four of them received a therapeutic trial of one year with interferon-alpha. Free thyroxine, TSH and autoantibodies to thyroglobulin and thyroid microsomes were systematically tested at entry and at weeks 12 and 24 in both untreated and treated patients. RESULTS: Sixteen of the 207 patients (7.7%) had thyroid dysfunction, including positive antithyroid antibodies in 14 (6.7%) and hypothyroidism in 10 (4.8%) prior to interferon therapy. In addition, during pretreatment evaluation one patient developed clinical hyperthyroidism after transient subclinical hypothyroidism and another had subclinical hyperthyroidism. Prevalences of positive antithyroid antibodies and hypothyroidism were significantly higher in women (14.7 and 10.5%, respectively, vs 0% in men, P < 0.01) and were directly associated with increasing age (P < 0.01). The incidence of thyroid dysfunction was also significantly higher in patients with other autoantibodies such as anti-nuclear (ANA) (P < 0.01). A trial with interferon was initiated in 144 patients and 8 of 142 (5.6%) without previous thyroid abnormalities developed thyroid dysfunction, including positive antithyroid antibodies in 7 (4.9%) and hypothyroidism in 4 (2.8%) with a prevalence again significantly higher in women (12.7 and 8.3%, respectively, vs 1% in men, P < 0.01) and also directly related to increasing age (P < 0.01). An association was found between the development of thyroid dysfunction during interferon therapy and the presence of other autoantibodies, including ANA, anti-DNA and anti-Sjögren's antibodies (P < 0.01), as well as with the induction of autoimmune hepatitis and Sjögren's syndrome (P < 0.01 and < 0.05 respectively). Thyroid abnormalities were reversed in all patients when interferon therapy was discontinued. CONCLUSIONS: No significant association was found between chronic hepatitis C and the presence of thyroid autoimmunity in female patients. On the contrary, interferon therapy induced antithyroid autoantibodies and thyroid dysfunction de novo in patients with chronic hepatitis C without pre-existing thyroid abnormalities. Thyroid dysfunction secondary to interferon was reversible after discontinuation of therapy.

Adult↗
PubMed1989

Routine thyroid function tests as a case-finding tool.

A comprehensive, multiphasic blood panel was used as a case-finding tool for 738 patients. The thyroid function tests T4 (total thyroxine), rT3U (resin T3 uptake), and FTI (free thyroxine index) were included in this panel. Among the 711 patients found to be clinically euthyroid without known thyroid disorder, 54 had at least one abnormal parameter. Of these patients, four new diagnoses of thyroid dysfunction were made. All four cases had an abnormal T4 and FTI. Two patients had a slightly elevated FTI and normal T4, and have remained clinically euthyroid. All other patients had a normal FTI, and no thyroid dysfunction was noted. This gives FTI in this study a sensitivity of 1.0 and specificity of 0.993, which is camparable to what others have found (1). The prevalence of unsuspected thyroid dysfunction was 0.56 per cent, again comparable to other studies (1-3). It would seem the high sensitivity/specificity of FTI offsets the relatively low prevalence of unsuspected thyroid dysfunction. Since FTI is a sensitive predictor of thyroid dysfunction, consideration should be given to the inclusion of thyroid function studies in existing multiphasic case-finding panels.

Family Practice↗
PubMed1988

Sensitive thyroid-stimulating hormone assays: clinical applications and limitations.

Sensitive TSH assays have important applications in various conditions, including the diagnosis of hypothyroidism and hyperthyroidism, monitoring thyroid hormone therapy and treated thyrotoxic patients, and evaluating thyroid dysfunction in nonthyroidal illnesses and pregnancy. Interpretation of the TSH value should be made with a clear understanding of its limitations. TSH may be inappropriately secreted by pituitary tumors and by pituitary dysfunction due to thyroxine resistance. At present, it is uncertain whether clinically euthyroid patients with autonomously functioning thyroid nodules, or with multinodular goiters, or patients taking thyroid hormone who have suppressed TSH values, are actually euthyroid at a cellular level. Other factors that affect TSH levels are the biologic variation in its secretion, the presence of heterophilic antibodies in a patient's serum, and various drugs. But perhaps the most important factor affecting the TSH assay is severe nonthyroidal illness in hospitalized patients. The new ultrasensitive TSH assay does not yet replace other thyroid function tests, but it is clearly emerging as an important means of screening patients for thyroid dysfunction, especially ambulatory patients without other serious illnesses. It can usually separate patients with thyroid dysfunction from euthyroid individuals. Good clinical assessment is always necessary, and other thyroid function tests are often needed. The sensitivity of these new TSH assays in the diagnosis of thyrotoxicosis and hypothyroidism is excellent; the specificity is not as good. Nonetheless, at present this test can be used in the initial diagnosis of thyroid dysfunction as outlined in Figure 2.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1996

Multiple changes in thyroid function in patients with chronic active HCV hepatitis treated with recombinant interferon-alpha.

OBJECTIVE: Recombinant human interferon-alpha (r-IFN-alpha) is often successfully used in the treatment of patients with chronic viral hepatitis B and C. Thyroid dysfunction has been reported to occur with variable frequency during r-IFN-alpha therapy especially in patients with preexisting thyroid autoimmunity. We have prospectively evaluated the effect of r-IFN-alpha on various aspects of thyroid function in patients with HCV chronic hepatitis. DESIGN: Thirty-two patients with HCV chronic active hepatitis were studied prospectively before and during r-IFN-alpha therapy. Serum TSH, FT4, FT3, and thyroid receptor (TSR) and thyroid peroxidase (TPO) antibodies, and the iodide-perchlorate discharge test (I-C10(4)) to detect subtle defects in the thyroid organification of iodide were carried out during the study. Thyroid radioactive iodine uptakes (RAIU) were obtained in patients who developed thyrotoxicosis. RESULTS: All patients were clinically and biochemically euthyroid prior to r-IFN-alpha therapy with negative I-C10(4) discharge tests. Four patients became thyrotoxic, 3 secondary to destructive or inflammatory thyroiditis with a low thyroid RAIU, and 1 patient developed hypothyroidism. The I-C10(4) discharge test became positive in 7 of the 32 patients studied prospectively; 5 of these patients did not develop other evidence of thyroid dysfunction and did not have positive TPO antibodies. In these 5 patients the test became negative after r-IFN-alpha was discontinued. Appropriate therapy of the patients with thyrotoxicosis (methylprednisolone for 3 patients with destructive thyroiditis and methimazole for 1 patient with hyperthyroidism) or with hypothyroidism (L-thyroxine) was successful. CONCLUSIONS: Thyroid dysfunction, especially destructive or silent thyroiditis resulting in thyrotoxicosis, is not infrequently observed in patients receiving r-IFN-alpha therapy for chronic active hepatitis. Although underlying autoimmune thyroid disease appears to predispose patients to develop thyroid dysfunction, other patients become thyrotoxic or hypothyroid in the absence of baseline positive TPO-Ab. Subtle defects in the thyroidal organification of iodine as determined by the I-C10(4) discharge test, in the absence of autoimmune thyroid disease, was observed in 5 patients who remained euthyroid, suggesting that r-IFN-alpha directly reduces the intrathyroidal organification of iodine.

Adult↗
PubMed1996

The role of complement in the pathogenesis of postpartum thyroiditis: ultrasound echogenicity and the degree of complement-induced thyroid damage.

Postpartum thyroiditis (PPT) is a transient autoimmune thyroiditis occurring during the postpartum year that is characterized by circulating antithyroid antibodies, abnormal thyroid ultrasound echotexture, and episodes of hyperthyroidism, hypothyroidism, or both. In this study we examined the relationship between lymphocytic thyroiditis, as indicated by echotexture changes, and complement-activating thyroid autoantibodies. Thyroid ultrasound echotexture, thyroid function, and bioactive (complement-activating) thyroid peroxidase (TPO) antibodies have been measured in a group of 63 TPO antibody-positive women during the postpartum year. When the maximum bioactive TPO antibody activity recorded was compared with echogenicity and thyroid status, there was a correlation between hypoechogenicity, elevated antibody activity, and abnormal thyroid status (r = 0.72, p < 0.001). However, 7 cases showed severe ultrasound changes in the absence of any thyroid dysfunction (3 of these cases showed normal bioactive antibody activity), while 4 (all hyperthyroid PPT) showed thyroid dysfunction in the absence of any ultrasound changes. Within the euthyroid ultrasound normal group, bioactive TPO antibody activity remained low throughout the postpartum year. Antibody activity in the hypoechogenic euthyroid women was significantly elevated (p < 0.001) compared with the echo normal group, but was indistinguishable from the activity curve obtained in women whose PPT included a hypothyroid phase. The determination of echotexture by thyroid ultrasonography gives a useful, noninvasive measure of the degree of thyroiditis in these women. However, as a significant number of cases with severe changes in echotexture remained euthyroid, we conclude that the development of thyroid dysfunction is not an inevitable consequence of lymphocytic thyroiditis during the postpartum and suggests that other factors must also be involved in progression to overt thyroid dysfunction.

Autoantibodies↗
PubMed1999

[Postpartum autoimmune thyroid syndrome].

Thyroid dysfunction frequently (around 5%) occurs after delivery through immune rebound mechanism. More than half of the patients suffer from postpartum thyroiditis. Initially, patients have a thyrotoxic phase, later passing through euthyroidism to hypothyroidism and, finally, return to euthyroidism. After delivery, other forms of autoimmune thyroid dysfunction also occur, including Graves' disease, transient hypothyroidism without preceding destructive thyrotoxicosis, and persistent hypothyroidism. To include all these conditions, the term postpartum autoimmune thyroid syndrome is often used. To predict who will develop postpartum thyroid dysfunction, the measurement of anti-thyroid microsomal antibody (MCAb) during pregnancy is useful because 62% of subjects with positive MCAb show thyroid dysfunction after delivery.

Autoimmune Diseases↗
PubMed1999

Autoimmunity resulting from cytokine treatment predicts long-term survival in patients with metastatic renal cell cancer.

PURPOSE: In patients undergoing cytokine therapy, systemically applied interleukin-2 (IL-2) and/or interferon-alpha (IFN-alpha) have been reported to induce thyroid dysfunction as well as thyroid autoantibodies. We analyzed the correlation of thyroid autoimmunity with HLA phenotype, various other autoimmune parameters, and patient survival. PATIENTS AND METHODS: For this purpose, antithyroglobulin autoantibodies, antimicrosomal thyroid autoantibodies, thyroglobulin receptor autoantibodies, thyroid dysfunction, and multiple clinical parameters were determined in 329 unselected patients with metastatic renal cell cancer before and after systemic IL-2 and IFN-alpha2 therapy. For statistical analysis, we used both univariate and multivariate Cox proportional hazards models and the two-tailed Fisher's exact test. RESULTS: Antithyroglobulin autoantibodies and antimicrosomal thyroid autoantibodies were detected in 60 patients (18%); positive autoantibody titers of various other autoimmune parameters were statistically unrelated. The presence of thyroid autoantibodies was correlated with prolonged survival (P<.0001). There was a statistically significant difference in frequencies of HLA-Cw7 expression between thyroid autoantibody-positive and -negative patients (P< or =.05), and the Cw7 expression was associated with prolonged overall survival (P = .009). CONCLUSION: The evaluation of thyroid autoantibodies during cytokine therapy could be a useful prognostic marker for patients with renal cell carcinoma who benefit from cytokine treatment. IL-2- and IFN-alpha2-induced tumor control and prolonged survival may require breaking of immunologic tolerance against self-antigens.

Adult↗
PubMed1975

Thyroid disease in pregnancy.

It is frequently difficult to establish a diagnosis of hyperthyroidism in association with pregnancy. Signs and symptoms suggestive of hyperthyroidism may occur in normal pregnancy. Moreover, tests to rule out hyperthyroidism under these conditions are not readily available. Mild hyperthyroidism is not a hazard to an otherwise normal pregnancy and does not require therapy on the basis of this presumption. Hyperthyroidism of a clinically significant degree is safely treatable by medical means without hazard to the fetus. Hyperthyroidism is an uncommon cause for the failure of pregnancy to proceed to term. Treatment with thyroid based on a presumption of this diagnosis is justified, but such patients should be studied carefully after delivery to establish the true state of thyroid function for the future. Other conditions of thyroid dysfunction, including thyroiditis, thyroid carcinoma, nontoxic goiter, and ovarian struma rarely interfere with an otherwise normal pregnancy.

Antithyroid Agents↗
PubMed1998

Thyroid and celiac disease: clinical, serological, and echographic study.

OBJECTIVE: We sought to reevaluate the prevalence of thyroid dysfunction and thyroid autoimmunity in 47 patients with celiac disease; 91 healthy subjects were studied as controls. Both patients and controls were from Sardinia, Italy. METHODS: Diagnosis of celiac disease was made on the basis of clinical history, presence of positive antigliadin IgA (AGA-A) and IgG (AGA-G) antibodies, antireticulin antibodies (ARA), antiendomysium antibodies (EMA), and was confirmed by jejunal biopsy. HLA class II typing for DQB1 and DQA1 alleles was performed in 36/47 celiac patients. Thyroid was evaluated by palpation and echography; serum free thyroid hormones (FT4, FT3), thyrotropic hormone (TSH), and antithyroid peroxidase autoantibodies (anti-TPO) were assayed by radioimmunoassays. RESULTS: The prevalence of anti-TPO was higher in celiac patients (29.7%) than in healthy controls (9.6%) (p < 0.001) and thyroid echography frequently displayed (42.5%) a hypoechogenic pattern. Five anti-TPO-positive celiac patients were hypothyroid (two overt, three subclinical). A higher but not significantly different prevalence of anti-TPO (3/7 = 42.8%) was found in celiac patients displaying the DQB1*0502 genotype, when compared with the remaining patients (8/29 = 27.6%). CONCLUSIONS: An elevated prevalence of clinical and subclinical autoimmune thyroid autoimmunity was found in Sardinian celiac patients, especially in those displaying the DQB1*0502 genotype; this finding could be related to a particular genetic background of the Sardinian population.

Adult↗
PubMed1990

Effects of interferon-gamma therapy on thyroid function, T-lymphocyte subpopulations and induction of autoantibodies.

Treatment with human leucocyte interferon (IFN alpha) has been associated with the development of thyroid autoimmunity and hypothyroidism, but it is not certain whether this phenomenon was a result of contamination with IFN gamma, which induced HLA class II antigen expression on T-lymphocytes. We prospectively studied 11 subjects (5 females and 6 males; mean age, 26.8 yr; range, 18-36) with chronic active hepatitis B who were randomized to receive recombinant human IFN gamma (rhIFN gamma; 10(6) U/m2.day, im, 3 times/week) for 16 weeks. Goiter was not present, and no patient had a history or family history of autoimmune diseases. Serial thyroid functions, including serum T4, T3, free thyroid hormone index, free T4 and TSH before, during, and on subsequent follow-up for a period of 1 yr were all normal. Eight patients had adequate serial samples for study of serological and lymphocyte subpopulations. None of the patients treated with rhIFN gamma developed thyroglobulin or thyroid microsomal antibodies. However, four patients developed antinuclear and smooth muscle autoantibodies during or after rhIFN gamma treatment. Treatment with rhIFN gamma resulted in a significant increase in circulating T-lymphocytes and HLA-DR-positive T-cells (P less than 0.05), with equal proportions of circulating CD4+ and CD8+ T-cells becoming DR positive. The percentage of HLA-DR-positive T-cells remained elevated after discontinuation of rhIFN gamma. Also, rhIFN gamma treatment led to a decrease in the number of circulating granulocytes and interleukin-2 receptor-positive cells. In conclusion, we did not observe any thyroid dysfunction or thyroid autoimmunity in our patients treated with the studied dose of rhIFN gamma, but induction of other autoantibodies was observed.

Adolescent↗
PubMed2004

[Amiodarone and the thyroid].

Amiodarone is an iodine-rich drug widely used for the management of cardiac arrhythmias. During long-term amiodarone therapy drug toxicity may occur and a substantial proportion of amiodarone-treated patients develop either hypothyroidism or thyrotoxicosis. Several mechanisms are involved in amiodarone-induced thyroid dysfunction: defective thyroid auto-regulatory mechanism in presence of excessive iodine offer, immunological factors and cytotoxicity. Approximately 50% of patients taking amiodarone present abnormal thyroid function. Therefore, for adequate clinical follow up of these patients, it is critical a careful monitoring of thyroid hormones and TSH, before and during treatment.

Amiodarone↗
PubMed2006

[Thyroid hormone and the cardiovascular system].

Thyroid hormone has many effects on the heart and vascular system. Many of the clinical manifestations of hyperthyroidism are due to the ability of thyroid hormone to alter cardiovascular hemodynamics. The hemodynamic effects of hypothyroidism are opposite to those of hyperthyroidism, although the clinical manifestations are less obvious. This review will integrate what is known about the mechanisms of thyroid hormone action on the heart with recent observations from both experimental and clinical studies of hyperthyroidism and hypothyroidism. Thyroid hormone has both direct and indirect actions on the cardiovascular system. Patients with thyroid disease, especially those with hyperthyroidism, often have symptoms and signs indicating changes in cardiovascular hemodynamics. Indeed, symptoms and signs referable to the cardiovascular system may be the only manifestations of thyroid dysfunction, and thyroid function should therefore be assessed by the measurement of serum thyrotropin concentrations in all patients with cardiovascular disease. Some suggest that the administration of triiodothyronine may benefit some patients with cardiovascular disease.

Animals↗
PubMed1984

Controversies in thyroid function testing.

Thyroid function tests can be abnormal in certain patients in the absence of thyroid dysfunction. All thyroid function tests can be affected in these patients, including the free thyroxine assays and free thyroxine index. Familiarity with the conditions affecting thyroid function tests is necessary to avoid incorrect diagnosis and unnecessary testing.

Female↗
PubMed1993

Traumatic optic neuropathy complicated by thyroid eye disease.

BACKGROUND: Thyroid eye disease is the most common orbital disorder found in adults. Ocular changes may occur with or without systemic hyperthyroidism. Blunt orbital trauma can affect the eye in many ways and can confound and alter the natural course of thyroid eye disease. METHODS: A 76-year-old patient with a number of ophthalmic findings and associated symptoms which could have been related to previous blunt ocular trauma. Careful optometric evaluation, systemic laboratory testing, and review of the ocular and medical findings demonstrated the onset of thyroid dysfunction. RESULTS: Thyroid disease was diagnosed on the basis of the presence of enlarged extraocular muscles by CT scan and elevated tensions on attempted upgaze. The patient demonstrated an elevated T3 uptake and low TSH levels for which he was treated with propylthiouracil. The occurrence of thyroid disease and damage from blunt trauma confounded the diagnosis because forced duction testing and optic atrophy could well have been the result of previous blunt trauma. CONCLUSIONS: This case elucidates the many differential diagnoses and complications that result from the combination of previous blunt trauma and the occurrence of new thyroid disease with ophthalmic findings.

Aged↗
PubMed2006

Prevalence of thyroid autoimmunity in sporadic idiopathic hypoparathyroidism in comparison to type 1 diabetes and premature ovarian failure.

CONTEXT: Thyroid autoimmunity is the most common coexistent endocrinopathy in type 1 diabetes (T1D), Addison's disease, and premature ovarian failure (POF). Although the role of autoimmunity is being investigated in patients with sporadic idiopathic hypoparathyroidism (SIH), there is little information on coexistent thyroid autoimmunity. OBJECTIVE: Our objective was to assess the prevalence of thyroid peroxidase autoantibodies (TPOAb) and thyroid dysfunction in patients with SIH and its comparison with that in T1D, POF, and Hashimoto's thyroiditis (HT) and age- and sex-matched healthy controls (for SIH). DESIGN AND SETTING: We conducted a case control study in a tertiary care setting. PATIENTS AND METHODS: Subjects were consecutive patients with SIH (n = 87), T1D (n = 100), POF (n = 58), and HT (n = 47) and healthy controls (100 females and 64 males). Serum free T3, free T4, TSH, and TPOAb (normal < or = 34 IU/ml) were measured by electrochemiluminescence assay. Subjects with 1) serum TSH at least 5 microU/ml along with TPOAb more than 34 IU/ml; 2) TSH at least 10 microU/ml but normal TPOAb titers; or 3) Graves' disease were considered to have thyroid dysfunction. RESULTS: TPOAb positivity (> 34 IU/ml) in females was 14.6% in SIH, 24.1% in POF, and 42.1% in T1D compared with 76.6% in HT and 9% in healthy controls. The frequencies of TPOAb positivity and thyroid dysfunction in patients with SIH were comparable to those in control and POF groups, but significantly less than in T1D and HT groups. CONCLUSION: The frequencies of TPOAb and thyroid dysfunction were not significantly higher in patients with SIH than in healthy controls, unlike in patients with T1D and POF.

Adolescent↗
PubMed1995

Autoimmune thyroid disease in primary Sjögren's syndrome.

PURPOSE: To evaluate the prevalence of autoimmune thyroid disease and thyroid dysfunction in patients with primary Sjögren's syndrome. PATIENTS AND METHODS: Thyroid function of 33 patients with primary Sjögren's syndrome was clinically and biochemically evaluated. Thyroid hormones and autoantibodies against thyroid peroxidase, thyroglobulin, and thyroid hormones were measured. RESULTS: Autoimmune thyroid disease and thyroid dysfunction were found in 15 cases (45%): autoimmune thyroiditis in 8 (24%); autoimmune hyperthyroidism in 2 (6%); and reversible iodine-induced hypothyroidism in the remaining 5 (15%). One or more of the evaluated autoantibodies were detected in 8 euthyroid patients (24%). Overall, the prevalence of autoantibodies against thyroid peroxidase, thyroglobulin, thyroxine, and triiodothyronine was 45%, 18%, 42%, and 36%, respectively. CONCLUSIONS: The high prevalence of autoimmune thyroid disease and thyroid dysfunction found in primary Sjögren's syndrome, using sensitive immunologic and thyroid function tests, suggest that both diseases are more frequently associated than it was previously thought, and should be sought clinically and by laboratory tests in all patients with primary Sjögren's syndrome.

Adult↗
PubMed1997

Thyroid abnormalities in chronic viral hepatitis and their relationship to interferon alfa therapy.

The prevalence of antithyroid peroxidase antibodies (ATPO) and/or of thyroid dysfunction was studied in 422 patients with chronic viral hepatitis C, B, and D. Baseline results were compared with those during and 6 months after interferon alfa (IFN-alpha) therapy. The overall prevalence of ATPO among untreated patients was 14.1%, with no significant differences between chronic hepatitis C, B, or D, as well as between males and females. However, high ATPO titers (> or = 18 IU/mL) clustered significantly among females (8.7% vs. 3.4%; P = .022), especially those with chronic hepatitis C (11.2% vs. 3.6%; P = .036). Before treatment, 3.7% of the patients had thyroid dysfunction, mostly hypothyroidism (3.5%), the latter increasing to 14.3% among patients with ATPO titers > or = 18 IU/mL. IFN-alpha treatment significantly increased overall thyroid dysfunction (9.7%; P = .001) and hypothyroidism (7.8%; P = .01), particularly among patients with high baseline ATPO (38.5%; P = .0002). Six months after stopping IFN-alpha treatment, the prevalence of thyroid dysfunction was 8.0%, still significantly higher than at baseline. By multivariate analysis, the only predictor positively associated with pre- or on-treatment hypothyroidism was the baseline titer of the ATPO antibodies (relative risk [RR], 3.0 and 3.8 per each log titer increase, respectively). In conclusion, patients with chronic viral hepatitis on IFN-alpha treatment exhibit an almost threefold increase of baseline thyroid dysfunction, persisting long after the end of therapy. High ATPO titers, clustering among females, particularly those with hepatitis C, represent the only predictor of pre- and on-treatment hypothyroidism by multivariate analysis. Patients with chronic viral hepatitis, especially females, should be tested for ATPO and thyroid function and monitored during and posttreatment for free thyroxin (FT4) and thyroid-stimulating hormone (TSH) levels.

Adolescent↗