PRL,TSH, and thyroid hormones in benign breast diseases

Summary The dynamic secretion of prolactin and TSH as well as the thyroid function were studied in patients with benign breast disease. The study included 13 patients with mastodynia, 15 patients with isolated galactorrhea, 6 patients with breast hypertrophy and 5 patients with fibroadenomata. Eleven healthy women served as controls. Prolactin and TSH were determined before and after TRH stimulation, using 0.2 mg TRH i.v. In addition thyroxine (T₄), trijodthyronine (T₃) and thyroxin-binding-globulin (TBG) were estimated.The following results were obtained: Basal prolactin levels were slightly but not significantly elevated in all patients studied. Maximal prolactin response to TRH was significantly greater as compared to the controls. TSH, T₄, T₃, and TBG-levels in the controls were within the normal range, while mastodynia and galactorrhea patients exhibited hormone patterns as known from endemic goiter (increased T₃- and relatively low T₄-levels). Mean TSH-responses reached the upper limit of the normal range. Mean TBG-levels in mastodynia patients exceeded the levels of the controls. In patients with breast hypertrophy thyroid hormone status indicated borderline hypothyroidism (borderline T₄- and normal T₃-levels, mean TSH-response slightly elevated to TRH). TSH secretion and thyroid function in patients with fibroadenomata did not differ from the controls.The presented data indicate an increased sensitivity of the lactotrophs representing possibly an important factor in the development of these benign breast diseases. The thyroid function tests in these patients revealed patterns known from endemic goiter and borderline hypothyroidism respectively.     

Prospective Observation of 5-Year Clinical Course of Subclinical Hypothyroidism in Korean Population

Subclinical hypothyroidism (SCH) is a common clinical condition, whereas it''s natural course has not been identified distinctly. We evaluated the natural history of 169 SCH patients over 5-yr and the prognostic factors including thyroid autoantibodies and thyroid ultrasonographic (USG) findings related to develop overt hypothyroidism. After 5 yr, 47.3% of patients showed normalization of TSH, while 36.7% of patients remained persistence of high level of TSH, and overt hypothyroidism developed in 11.2% of patients. There were painless thyroiditis (2.9%) and hyperthyroidism (1.7%) during 5 yr follow-up. The thyroid nodule was seen in 48.6% of patients. Most of patients had 1 to 2 nodules whereas only 3% of patients with thyroid nodule had more than 6 nodules. Overt hypothyroidism patients had more heterogenous echogenecity in USG compared to patients with normalization or persistent SCH (76.5% vs 50.0% vs 35.0%, P = 0.048) and higher prevalence positive anti-thyroid peroxidase (anti-TPO Ab) and anti-thyroglobulin antibody (anti-Tg Ab) and titer of anti-TPO Ab than other two groups. The cut off values for prediction of overt hypothyroidism were TSH > 7.45 µIU/mL, free T₄ < 1.09 ng/dL and Anti-TPO Ab > 560 IU/mL. SCH has various courses and initial TSH, free T₄, presence of thyroid autoantibody, titer of thyroid autoantibody; and thyroid USG findings can serve as a prognostic factor for progression of overt hypothyroidism. These parameters suggest consideration to initiate thyroid hormone treatment in SCH.     

Die Rolle des TSH für Psychische VerÄnderungen und BefindlichkeitsverÄnderungen bei Schilddrüsenfunktionsstörungen

Summary The characteristic psychic and somatic features found in patients with overt hyper- or hypothyroidism are usually attributed to elevated or diminished levels, respectively, of thyroid hormones. This concept does not sufficiently explain our previous investigations in which the same symptoms, albeit attenuated, were also seen in patients suffering from so-called latent disturbances of thyroid function. This state of disorder, however, exhibits normal concentrations of peripheral thyroid hormones. Only the response of thyroid-stimulating hormone (TSH) to thyrotropin-releasing hormone (TRH) stimulation is in accordance with the behaviour of the overt thyroid dysfunction and enables its differentiation from the euthyroid state. In this context, we investigated the question as to whether pathologic signs in thyroid disorders are correlated to alterations of peripheral thyroid hormones or to changes in the hypothalamus pituitary axis. Therefore, we investigated two groups of ten patients each who suffered from latent hyper- or hypothyroidism, respectively, and ten euthyroid controls. All were matched from sex and age. Endocrine function was estimated by TRH testing, TT3, TT4 and thyroxine binding globuline (TBG). Psychologic testing was performed by questionnaires concerning subjective somatic symptoms, emotional disturbances, psychomotoric performance, cognitive impairment and personality. Patients with latent hyperthyroidism were more subject to somatic symptoms and affective complaints than were those who had latent hypothyroidism. As compared with controls, there were significant differences in exhaustion and pain in the limbs and heart. In terms of affective complaints, patients were more depressive, anxious, touchy and irritable; their personalities showed a higher degree of emotional lability, excitement and irritability. Many symptoms described in overt thyroid dysfunction could be found in latent metabolic disturbances. Therefore, we conclude that the alterations of health in thyroid disorders are more likely to be caused by hypothalamic pituitary impairment than by changes in peripheral hormone levels. The stronger symptoms occurring in overt thyroid dysfunction as compared with latent metabolic disturbances may reflect the degree of hypothalamic pituitary dysfunction.

Diese Arbeit wurde erstellt im Rahmen des Sonderforschungsbereichs 258 der UniversitÄt Heidelberg, gefördert von der DFG     

Impact of hypothyroidism on the development of non-alcoholic fatty liver disease: A 4-year retrospective cohort study

Background/Aims

Hypothyroidism is reported to contribute to the development of nonalcoholic fatty liver disease (NAFLD). We compared the risk of the development of NAFLD among three groups with different thyroid hormonal statuses (control, subclinical hypothyroidism, and overt hypothyroidism) in a 4-year retrospective cohort of Korean subjects.

Methods

Apparently healthy Korean subjects without NAFLD and aged 20-65 years were recruited (n=18,544) at health checkups performed in 2008. Annual health checkups were applied to the cohort for 4 consecutive years until December 2012. Based on their initial serum-free thyroxine (fT4) and thyroid-stimulating hormone (TSH) levels, they were classified into control, subclinical hypothyroidism (TSH >4.2 mIU/L, normal fT4), and overt hypothyroidism (TSH >4.2 mIU/L, fT4 <0.97 ng/dL) groups. NAFLD was diagnosed on the basis of ultrasonography findings.

Results

NAFLD developed in 2,348 of the 18,544 subjects, representing an overall incidence of 12.7%: 12.8%, 11.0%, 12.7% in the control, subclinical hypothyroidism, and overt hypothyroidism groups, respectively. The incidence of NAFLD did not differ significantly with the baseline thyroid hormonal status, even after multivariate adjustment (subclinical hypothyroidism group: hazard ratio [HR]=0.965, 95% confidence interval [CI]=0.814-1.143, P=0.67; overt hypothyroidism group: HR=1.255, 95% CI=0.830-1.899, P=0.28).

Conclusions

Our results suggest that the subclinical and overt types of hypothyroidism are not related to an increased incidence of NAFLD.     

Substantially elevated TSH,not traditional clinical subclinical thyroid disorder groupings,are associated with smaller LDL-P mean size: ELSA-Brasil

BackgroundLDL appears to drive atherogenesis in overt hypothyroidism, but in subclinical dysfunction, its role is not completely elucidated.ObjectiveThe aim of this study was to evaluate subfractions of LDL in subclinical (SC) thyroid disorders.MethodsIndividuals were divided into three groups by baseline thyroid function (SC hypothyroidism, euthyroidism, and SC hyperthyroidism). LDL particle (LDL-P) subfractions were analyzed by Nuclear Magnetic Resonance (NMR) spectroscopy. The association between LDL-P subfractions and thyroid groups and quintiles was evaluated by linear regression models.ResultsWe evaluated 3304 participants (54.1% women, 51.2% white, mean age 50.6 ± 8.7 years). In the univariate analysis, small LDL particle concentrations (SLDL-P) were not different between SC hypo- and hyperthyroidism compared to euthyroid individuals (p = 0.485 and p = 0.314, respectively). Large LDL-P (LDL-P) levels also did not differ in SC hyperthyroidism and SC hypothyroidism compared to euthyroidism (p = 0.698 and 0.788 respectively). Intermediate LDL-P levels were not different across the groups. These numbers did not materially change in multivariate analysis. However, we also analyzed LDL subfractions according to quintiles of TSH. We showed that in the higher TSH quintile LDL subfractions presented a significantly smaller mean size of LDL subfractions compared to the first quintile.ConclusionsSC thyroid disorders are not associated with significant changes in LDL-P subfractions measured by NMR spectroscopy. However, it seems that the LDL mean size decreases as TSH levels increase, which may represent a more atherogenic lipid profile.     

Episodic variations of prolactin, thyroid-stimulating hormone, luteinizing hormone, melatonin and cortisol in infertile women with subclinical hypothyroidism

Preliminary data have suggested that female infertility due to corpus luteum insufficiency may be caused by subclinical hypothyroidism [exaggerated thyroid-stimulating hormone (TSH) response to thyrotrophin- releasing hormone (TRH) stimulation]. L-Thyroxine supplementation has been recommended to achieve pregnancies in subclinical hypothyroid women. This controlled study was carried out in order to investigate the biochemical diagnosis of subclinical hypothyroidism as a possible infertility factor. Five infertile patients (aged 25-36 years) with subclinical hypothyroidism (n = 4, stimulated TSH >20 microU/ml) or primary hypothyroidism (n = 1) and five healthy controls (aged 22-39 years) with normal thyroid function (stimulated TSH <15 microU/ml), regular cycles and no history of infertility were studied in the early follicular phase. In the pre-study evaluation, eight of 23 volunteers (34.8%) had to be excluded because of subclinical hypothyroidism with stimulated TSH values (TSHs) >15 microU/ml. Cycle function of patients and controls was compared by the method of LH pulse pattern analysis. Therefore blood samples were drawn every 10 min during a 24 h period. Sleep was recorded from midnight to 7 a.m. Repetition of the TRH tests at the end of the 24 h blood sampling period confirmed the difference in stimulated TSH values of the two study groups. Pulse analysis for luteinizing hormone (LH), TSH and prolactin showed no differences between patients and controls for pulse frequency, amplitude, height, length, area under curve (AUC) and the 24 h mean. Even the hypothyroid patient had a normal LH pulse pattern. Additional measurement of melatonin in pooled sera every 30 min gave the well-documented diurnal profiles during day and night for both groups. Patients had significantly higher melatonin values at seven time points during the night. Peaks for LH, TSH, prolactin and cortisol were correlated with the sleep stages wake, rapid eye movement, 1 + 2 and 3 + 4. We concluded that corpus luteum insufficiency in female infertility cannot be explained by subclinical hypothyroidism and thus should not be treated with L-thyroxine for fertility reasons.      

Thyroid hemiagenesis and elevated thyrotropin levels in a child with Williams syndrome.

A girl with Williams syndrome (WS) presented with elevated thyrotropin (TSH) levels (7.0 microU/ml), normal free thyroid hormone concentrations, and absent antithyroid autoantibodies. Thyroid ultrasonography and scintigraphy showed hemiagenesis of the left lobe and no evidence of ectopic tissue. TSH response to thyrotropin-releasing hormone (TRH) injection (200 microg/mq, i.v.) was exaggerated and prolonged, suggesting subclinical hypothyroidism. The biological activity of circulating TSH was slightly below the normal range [TSH bioactivity (B) to immunoreactivity (I) ratio (TSH B/I) = 0.4, normal: 0.6-2.2]. These abnormalities are similar to those seen in patients with hypothalamic hypothyroidism. Thyroid function is not a recognized manifestation of WS and is not routinely investigated. However, abnormalities of the hypothalamic-pituitary-thyroid (HPT) axis and thyroid dysgenesis have been found in other WS cases. Genes mapping at 7q11.23, contiguous to the chromosomal region deleted in most WS patients, may be involved in the development of the thyroid gland, contributing to the complex phenotype of WS.     

Significance of latent hyperthyroidism

Summary In euthyroidism the circadian rhythm and pulsatility of TSH is well known. With regard to hyperthyroidism only very preliminary data were described. In this tudy we investigated the secretion pattern of the pituitary-thyroid axis hormones during 24 h in latent and overt hyperthyroidism and in euthyroidism with regard to common and different properties. Blood was obtained for 24 h at 10-min intervals. In euthyroidism we found intraindividually three overlapping patterns of TSH, which are different in amplitude and frequency and can be found interindividually, too. These patterns are equal to the circadian rhythm, pulsatile secretion and lastly to the methodic rustle. The circadian rhythm in latent hyperthyroidism is distinctly suppressed and in overt hyperthyroidism totally. Whereas in latent hyperthyroidism pulsatile secretion is extant, in overt hyperthyroidism the TSH pulses are absent. To record the patients' TSH circadian rhythm with only three blood samples, we defined the TSH-Triplex. In young as well as in elderly healthy volunteers it demonstrated significantly higher TSH levels at midnight (at 24:00 h) than it did at 4 p.m. and 8 a.m. The present study shows a significantly different TSH pattern in latent hyperthyroidism compared to euthyroidism. It should be discussed whether latent hyperthyroidism could be defined as hyperthyroidism stage I. On the other hand, latent hyperthyroidism could be an illness with its own cause, different from hyperthyroidism. Our data suggest that the laboratory findings of latent hyperthyroidism in each age are non-physiological. However, the cause for this disorder is unclear until now; hence further investigations are necessary.Abbreviations TT4 total thyroxine - TT3 total triiodothyronine - TSH thyroid stimulating hormone - TBG thyroxin binding globin - mean - SD standard deviation - TRH thyrotropin releasing hormone - MR methodic rustle Supported by Deutsche Forschungsgemeinschaft (SFB 258)     

Thyroid hemiagenesis and elevated thyrotropin levels in a child with Williams syndrome

A girl with Williams syndrome (WS) presented with elevated thyrotropin (TSH) levels (7.0 μU/ml), normal free thyroid hormone concentrations, and absent antithyroid autoantibodies. Thyroid ultrasonography and scintigraphy showed hemiagenesis of the left lobe and no evidence of ectopic tissue. TSH response to thyrotropin-releasing hormone (TRH) injection (200 μg/mq, i.v.) was exaggerated and prolonged, suggesting subclinical hypothyroidism. The biological activity of circulating TSH was slightly below the normal range [TSH bioactivity (B) to immunoreactivity (I) ratio (TSH B/I) = 0.4, normal: 0.6–2.2]. These abnormalities are similar to those seen in patients with hypothalamic hypothyroidism. Thyroid function is not a recognized manifestation of WS and is not routinely investigated. However, abnormalities of the hypothalamic-pituitary-thyroid (HPT) axis and thyroid dysgenesis have been found in other WS cases. Genes mapping at 7q11.23, contiguous to the chromosomal region deleted in most WS patients, may be involved in the development of the thyroid gland, contributing to the complex phenotype of WS. Am. J. Med. Genet. 85:491–494, 1999. © 1999 Wiley-Liss, Inc.     

Thyroid function tests

About 80% of thyroid disease consists of thyroid-specific autoimmune diseases, Hashimoto's disease and Grave's disease. To diagnose thyroid diseases, testings for (1) thyroid function and (2) pathogenetic autoantibodies are indispensable. To assess thyroid function, serum hormone concentrations, such as TSH, FT4 and FT3 are measured. Among these hormones, serum TSH concentrations are the most reliable and informative regarding thyroid function, correcting indicating a hyperthyroid, euthyroid or hypothyroid state. Therefore, TSH measurement appears to be the first choice in selecting the hormone determination. Reference intervals for normal healthy subjects of TSH are around 0.4-5.0 microU/ml. The second choice for thyroid function assessment are FT4 which supersedes total T4(TT4). TT4 is affected by changes in serum thyroid hormone binding proteins(TBG, TTR, Albumin). For example, euthyroid pregnant women whose serum TBG are physiologically higher than those of non-pregnant women show augmentation of TT4. However, FT4 depicts within reference intervals, although measurement of FT4 alone is unable to detect any abnormality of thyroid hormone binding proteins. According to its plasma concentration and binding affinity, FT3 measurement deserves no more significance than T3. Another important test for thyroid diseases is to detect serum autoantibodies against thyroid tissues, such as TgAb, TPOAb. Much more important is TSH receptor antibody which differentiates Graves' disease from Hashimoto's thyroiditis. In patients who show hyperthyroidism and some very uncommon hypothyroidism, TSH receptor antibodies should be measured. Three indicators are available as routine tests; TRAb measured by radioreceptor assay; TSAb determined by bioassay using cultured porcine thyroid cells. Usually, TRAb activity clinically correlates well with TSAb. TSBAb was initially discovered in patients with severe hypothyroidism with atrophic thyroid gland. TSBAb blocks thyroid stimulating activity of TSH and consequently causes severe hypothyroidism. TRAb and TSAb are very useful to diagnose and follow patients with Grave's disease.     

Thyroid function in multidrug-resistant tuberculosis patients with or without human immunodeficiency virus (HIV) infection before commencement of MDR-TB drug regimen

BackgroundMycobacterium tuberculosis and human immunodeficiency virus (HIV) are known to cause abnormal thyroid function. There is little information on whether HIV infection aggravates alteration of thyroid function in patients with MDR-TB.ObjectivesThis study was carried out to determine if HIV co-infection alters serum levels of thyroid hormones (T3, T4) and thyroid stimulating hormone (TSH) in patients with MDR-TB patients and to find out the frequency of subclinical thyroid dysfunction before the commencement of MDR-TB therapy.MethodsThis observational and cross-sectional study involved all the newly admitted patients in MDR-TB Referral Centre, University College Hospital, Ibadan, Nigeria between July 2010 and December 2014. Serum levels of thyroid stimulating hormone (TSH), free thyroxine (fT4) and free triiodothyronine (fT3) were determined using ELISA.ResultsEnrolled were 115 patients with MDR-TB, out of which 22 (19.13%) had MDR-TB/HIV co-infection. Sick euthyroid syndrome (SES), subclinical hypothyroidism and subclinical hyperthyroidism were observed in 5 (4.35%), 9 (7.83%) and 2 (1.74%) patients respectively. The median level of TSH was insignificantly higher while the median levels of T3 and T4 were insignificantly lower in patients with MDR-TB/HIV co-infection compared with patients with MDRT-TB only.ConclusionIt could be concluded from this study that patients with MDR-TB/HIV co-infection have a similar thyroid function as patients having MDR-TB without HIV infection before commencement of MDR-TB drug regimen. Also, there is a possibility of subclinical thyroid dysfunction in patients with MDR-TB/HIV co-infection even, before the commencement of MDR-TB therapy.     

The TRH stimulation test in endemic goitre in Greece

Summary The serum T₄=T₄(D), T₃ in vitro uptake=RT₃U and TSH were measured before and 30 min after the injection of 200 µg of TRH in 30 subjects from an iodine deficient area of Central Greece. These persons were divided in two groups of 16 goitrous and 14 nongoitrous patients and the results from each group compared to each other and also with the same parameters obtained from 14 controls subjects, all nongoitrous and from a nonendemic area. It has been found that in this area with a mild iodine deficiency serum T₄ is the only hormone decreased whereas RT₃U and TSH both before and 30 min after TRH injection are normal. There existed however a negative correlation between serum T₄ and TSH in the goitrous group. Why the nongoitrous iodine deficient persons achieve the same compensation without thyroid gland enlargement remains unresolved but it may be stated from the present results that goitre development should be regarded as a maladaptation rather than a compensatory process.This work was supported by the Hellenic Ministry of Social Services.     

Thyrotoxic crisis in Graves' disease: Indication for immediate surgery

Summary Thyrotoxic crisis (thyroid storm) is a rare complication of hyperthyroidism. It can be observed not only in thyroid autonomy with latent hyperfunction after exposure to iodine, but also in Graves' disease with overt hyperfunction. Adequate management of thyrotoxic crisis is still controversial. We report about four patients (four women, mean age 75 years) with Graves' disease who developed thyrotoxic crisis during therapy with antithyroid drugs so that surgical intervention became necessary. The patients had been admitted to the hospital for nonspecific symptoms such as headache, cachexy, and psychosis. Thyroid hormone levels had reached twice the normal range prior to surgery. All patients showed severe neurological deficits leading to coma. In three cases euthyroidism was achieved within two days after surgery. The neurological symptoms disappeared after an average of four days. The postoperative course did not show severe complications and all patients recovered completely.Especially in the elderly a monosymptomatic or nonspecific course of thyroid storm with neurological symptoms may represent a severe and life-threatening situation. In these cases surgery can become necessary even if euthyroidism has not been achieved preoperatively.Abbreviations dl deciliter - FT3 free triiodthyronine - FT4 free thyroxine - Hg mercury - l liter - MAK microsomal antibodies - mg milligram - ml milliliter - mU milliunit - ng nanogram - T3 triiodthyronine - T4 thyroxine - TAK thyroglobulin antibodies - TBG thyroxine-binding globulin - TRAK TSH-receptor antibodies - TRH thyrotropin-releasing hormone - TSH thyroid-stimulating hormone - TT3 total triiodthyronine - TT4 total thyroxine - g microgram     

The measurement of the serum sex-hormone binding globulin in various thyroid diseases

Synthesis of "sex-hormone binding globulin" (SHBG) is influenced by thyroid hormones and its concentration in the serum of female subjects may be a marker of thyroid hormone effect at the peripheral tissue (liver) level. Compared to the levels found in euthyroid females (n = 46), the mean (+/- S.D.) serum SHBG concentration was found elevated in overt hyperthyroidism (Graves' disease: n = 56; 141.6 +/- 37.6 vs. 48.3 +/- 16.2; toxic nodular goiter: n = 16; 119.9 +/- 50.7 vs. 48.3 +/- 16.2 nmol/l; P less than 0.001). In contrast, it was decreased in manifest hypothyroidism (n = 25; 24.9 +/- 14.8 vs. 48.3 +/- 16.2; P less than 0.001). In the group of preclinical hyperthyroidism (n = 43), despite suppressed TSH secretion, the serum value of SHBG was normal (47.4 +/- 16.8), while its serum level approached the lower border of the normal range in subclinical hypothyroidism (n = 10; 33.6 +/- 6.1 vs 48.3 +/- 16.2 nmol/l; P less than 0.01). Data indicate that the pituitary responds more sensitively than the liver to a slight change of the serum thyroid hormone level. During thyroid hormone replacement for hypothyroidism, measurement of serum SHBG may provide help to assess the response of the target organ to the given therapy. In patients with generalized resistance to thyroid hormone, the serum SHBG level is within the normal range (51.3 +/- 9.8 nmol/l), thus, its determination supports the diagnosis of this disease.     

Disorders of the thyroid gland in neonates and youth: latent hypothyroidism and hyperthyroidism

Etiology and clinical manifestation of subclinical hypothyroidism is different in neonates and in young. In the neonatal period babies present with jaundice and/or constipation due to thyroid hypoplasia, thyroid ectopia or transient hypothyroidism. The main reason for subclinical hypothyroidism in the youth is Hashimoto thyroiditis. Indication for thyroxin therapy in subclinical hypothyroidism is discussed controversial in the literature. For best growing and maturation in childhood thyroxin therapy should be given. Subclinical hyperthyroidism is rare in childhood. The main reasons are Graves' disease or Hashimoto thyroiditis (initial period). The therapy of subclinical hyperthyroidism is the same as in overt hyperthyroidism.     

Schilddrüsenhormone bei Frauen mit Leberzirrhose

Summary Basal thyroid hormone levels were measured in 68 women with liver cirrhosis (LC) of different etiology (alcoholicn=34, posthepatitic Bn=9, PBCn=5, cryptogeneticn=18, M. Wilsonn=2). In addition the rise of TSH after 400 µg TRH was measured in 23 women with LC and compared with the data obtained from 17 women of a control group. There was no difference of the median T4-concentrations (LC 8.0 µg/dl versus 7.2 µg/dl) but a significant correlation of T4 to the grade of decompensation of LC. In contrast of T4 there was a marked decrease of T3 in LC-patients (109 ng/dl versus 143 ng/dl) and a rise of reverse T3 (0.21 ng/ml versus 0.13 ng/ml). The decrease of T3 and rise of reverse T3 equally correlated to the severeness of LC. TBG concentrations fell according to the grade of decompensation of LC and T4/TBG-quotient exhibited no difference to the control data (0.51 both). Though basal thyroid hormones and TSH show euthyroidism the significant augmented TSH release after TRH (-TSH 7.0 versus 3.2 µU/ml) indicate a status of latent hypothyroidism. In alcoholic cirrhosis the degree of TSH release was much higher than in non alcoholic cirrhosis. Estradiol and estrone levels correlated significantly negatively to T4, T3, estrone negatively to TBG and positively to reverse T3 but not to TSH and TSH release. Otherwise TSH release correlated positively to estradiol. The thyroid status in women with liver cirrhosis does not differ from the thyroid hormone profile found in men with cirrhosis.

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Abkürzungen K Kontrollen - LZ Leberzirrhose - n Anzahl - PBC primär biliäre Zirrhose - RT3 reverse T3 (35-Trijodthyronin) - T3 Trijodthyronin - T4 Thyroxin - TBG thyroxinbindendes Globulin - TRH Thyreotropin - TSH Thyreotropin-Releasing-Hormon     

Répercussions biologiques de l'hypothyroïdie fruste

Subclinical hypothyroidism, defined by an isolated increased TSH level, is a frequently encountered condition the clinical outcomes of which are difficult to assess. It's therapeutic management is being discussed. It is essential that biological changes resulting from subclinical hypothyroidism should be known, because they contribute to the prognosis of this condition. Conversion to overt hypothyroidism is not systematic. It is however more likely to occur when the TSH concentration exceeds 10 mUI/l and in patients with thyroid autoimmunity. The impact of subclinical hypothyroidism, as a cardiovascular risk factor seems to be related to lipid abnormalities. An increase in total cholesterol and LDL-cholesterol, reversible with thyroxine treatment, is significant only when the TSH concentration exceeds 10 mUI/l. New biological risk factors — Lp(a), CRP, plasmatic homocysteine — are neither disturbed nor influenced by thyroxine treatment. Other biological abnormalities are less significant and do not contribute to the diagnosis or prognosis of subclinical hypothyroidism.     

亚临床甲状腺功能紊乱的发病率及病因分析

目的：探讨亚临床甲状腺功能紊乱的发病率及病因。方法：对12592例本地区的门诊及住院病例的甲状腺功能检测的七项指标进行筛查分析。结果：12592例检测者中有874例TSH在异常范围内,检出率为6．94％,其中TSH高于正常者397例,检出率为3．15％,TSH低于正常者477例,检出率为3．79％;874例处于亚临床甲状腺功能紊乱者多见于伴相关甲状腺疾病者,如甲亢治疗后、甲减甲状腺制剂替代治疗中及其他甲状腺病变（甲状腺结节、甲状腺炎）。除外上述因素在无明显疾病的143人中,亚临床甲减者109人（874人中12．47％）,亚临床甲亢者34人（874人中3．89％）。亚临床甲状腺功能紊乱与TGA、TMA多同步上升,升高者269例,发生率为30．78％,其中TSH高于正常者147例,占16．82％,TSH低于正常者122例,占13．96％;874例中≥60岁老年人有256例,检出率为29．29％。结论：临床应重视对亚临床甲状腺功能紊乱的检测,特别是老年人具有较高的发病率。     

Effects of growth hormone treatment on thyroid function in pediatric patients with Prader–Willi syndrome

It is unclear whether hypothyroidism is present in patients with Prader–Willi syndrome (PWS). This study aimed to clarify the state of the hypothalamic–pituitary–thyroid axis and the effects of growth hormone (GH) treatment on thyroid function in pediatric patients with PWS. We retrospectively evaluated thyroid function in 51 patients with PWS before GH treatment using a thyroid‐releasing hormone (TRH) stimulation test (29 males and 22 females; median age, 22 months). We also evaluated the effect of GH therapy on thyroid function by comparing serum free triiodothyronine (fT3), free thyroxine (fT4), and thyroid stimulating hormone (TSH) levels at baseline, 1 year, and 2 years after GH therapy. TSH, fT4, and fT3 levels were 2.28 μU/ml (interquartile range [IQR]; 1.19–3.61), 1.18 ng/dl (IQR; 1.02–1.24), and 4.02 pg/dl (IQR; 3.54–4.40) at baseline, respectively. In 49 of 51 patients, the TSH response to TRH administration showed a physiologically normal pattern; in two patients (4.0%), the pattern suggested hypothalamic hypothyroidism (delayed and prolonged TSH peak after TRH administration). TSH, fT4, and fT3 levels did not change significantly during 1 or 2 years after GH treatment. The TSH response to TRH showed a normal pattern in most patients, and thyroid function did not change significantly during the 2 years after initiating GH treatment.     

Thyroid autoimmunity and dysfunction associated with type I interferon therapy

Abstract. Type I interferons are currently used for the treatment of chronic viral hepatitis, multiple sclerosis and several hematological and solid tumors. Side effects are not uncommon, and include multiple alterations in thyroid function, some of which are unrelated to autoimmunity. Review of the literature revealed an overall mean prevalence of incident thyroid dysfunction of 6.2%, hypothyroidism occurring more frequently (3.9%) than hyperthyroidism (2.3%). Destructive thyroiditis characterized by early transient thyrotoxicosis followed by hypothyroidism has also been described. Thyroid dysfunction was mainly subclinical, and spontaneous resolution occurred in almost 60% of patients with or without withdrawal of interferon. Risk factors for developing thyroid abnormalities were female sex and the presence of pre-existing autoimmune thyroiditis. Whether prolonged interferon therapy will increase the likelihood of experiencing thyroid dysfunction, as well as the relationship between incident thyroid autoimmunity and the efficacy of interferon therapy, are still open questions. Although the most-likely explanation for thyroid disease occurring with type I interferon therapy remains an autoimmune reaction or immune system dysregulation, a direct inhibitory effect on thyrocytes may be presumed in patients who developed hypothyroidism without autoimmunity. However, the mechanisms of thyroid damage induced by type I interferons have not yet been clarified in detail. We recommend routine evaluation of serum thyroid-stimulating hormone during interferon therapy. A systematic thyroid assessment is useful only for those patients with pre-existing thyroiditis or incident dysfunction. Although discontinuation of interferon therapy is seldom required, it may be necessary in patients who develop Graves disease and overt hyperthyroidism.