High prevalence of thyroid ultrasonographic abnormalities in primary aldosteronism

The study was performed to evaluate the prevalence of thyroid abnormalities detected by ultrasonography and, in particular, of multinodular nontoxic goiter in primary aldosteronism. We analyzed 80 consecutive of patients with primary hyperaldosteronism (40 with unilateral adenoma and 40 with idiopathic hyperaldosteronism) and 80 normotensive healthy controls, comparable for age, sex, iodine intake, and geographical area. Blood pressure, thyroid palpation, thyroid function, and ultrasonography were evaluated. The prevalence of ultrasonographic thyroid abnormalities was 60% in primary aldosteronism and 27% in controls (p<0.0001). There was a statistically significant difference in prevalence of these abnormalities in unilateral adenoma and idiopathic hyperaldosteronism with respect to controls (p<0.05 and p<0.0001, respectively). The prevalence of multinodular nontoxic goiter in idiopathic hyperaldosteronism was higher than in controls (p<0.001) and, in particular, in female patients. From these data it seems to be worth considering the existence of primary hyperaldosteronism in patients with multinodular goiter and hypertension.     

Association of melasma with thyroid autoimmunity and other thyroidal abnormalities and their relationship to the origin of the melasma

Melasma is localized hyperpigmentation over the forehead, upper lips, cheeks, and chin. In this study, evidence suggesting an association between autoimmune thyroid disorders and melasma and the relationship of thyroid disorders to the origin of melasma is presented. A total of 108 nonpregnant women, aged 20-56 yr, were divided into 2 groups for the purpose of this study: 1) melasma, 84 patients; 2) control group, 24 patients from the Dermatology Clinic matched for age and sex. Microsomal thyroid autoantibodies (MCHA) were sought in all subjects. TRH-TSH tests were performed in patients with melasma and in those women with goiter and/or positive MCHA tests from the control group. Studies were completed with serum T4, T3, and antithyroglobulin antibody (TGHA) measurements in all patients with thyroid abnormalities. In patients with melasma, the frequency of thyroid disorders (58.3%) was 4 times greater than in the control group. The MCHA-negative patients had 1) simple goiter (13.1%), 2) Plummer's disease (2.4%), and 3) TSH hyperresponse to TRH in nongoitrous patients (10.7%). Patients with positive MCHA tests (32.1%) were divided into 2 subgroups. One comprised those women with an apparently normal thyroid gland and thyroid function (n = 7), while the other included all patients with goiter and/or subclinical hypothyroidism (n = 20). Regarding the origin of the melasma, it was found that 70% of women who developed melasma during pregnancy or while using oral contraceptives had thyroid abnormalities compared to 39.4% of patients with idiopathic melasma. Subjects from the control group had a 12.5% incidence of thyroid abnormalities, and only 8.3% had positive MCHA. Estrogen, progesterone, or both could be the triggering factor in the development of melasma in women who have a particular predisposition toward both melasma and thyroid autoimmunity. Patients with idiopathic melasma had a lower frequency of thyroid abnormalities, suggesting that there may be different genetic patterns linked to autoimmune thyroid disease. We conclude that there is a true association between thyroid autoimmunity and melasma, mostly in women whose melasma develops during pregnancy or after ingestion of oral contraceptive drugs.     

Thyroid-stimulating hormone levels in idiopathic euthyroid goiter.

Utilizing a double antibody radioimmunoassay for human TSH we compared distribution of serum TSH in 167 normal individuals and 51 patients with idiopathic euthyroid goiter. In addition to being clinically euthyroid both groups had normal total thyroxine, and free thyroid index. Forty-two percent of the goiter group had high TSH and the general distribution of TSH values in the goiterous patients was significantly higher than normal (P less than 0.001). Anlysis of subgroups of the normal and goiter populations indicated that the high TSH could not be attributed to age, sex, use of birth control pills or differences between diffuse and multinodular goiter. TSH levels were significantly higher in patients with goiter less than 1 yr compared to goiter greater than 1 yr (P less than 0.025). In patients with goiter greater than 1 yr the TSH levels remained significantly higher than normal (P less than 0.025). These results support the hypothesis that TSH plays a role in the genesis of idiopathic goiter. The elevation may be present only early in the course of goiter development but is also present in a significant number of patients with long standing goiter.     

Surgical treatment of a patient with idiopathic portal hypertension and hepatic encephalopathy.

Idiopathic portal hypertension is clinically characterized by splenomegaly and portal hypertension. Hepatic encephalopathy is rare in cases with idiopathic portal hypertension. In a 59-year-old man with recurrent hepatic encephalopathy for one year, a large splenorenal shunt was detected in the computed tomography and angiography, and liver biopsy revealed a portal fibrosis consistent with idiopathic portal hypertension. Devascularization of the upper stomach, splenectomy and closure of the splenorenal shunt were done. The patient has had no experience of encephalopathy since the operation even without drug treatment. Surgery should be considered for treatment of chronic hepatic encephalopathy in patients with idiopathic portal hypertension and portosystemic shunts.     

Effects of Esophageal Transection Combined with Splenectomy on Portal Hemodynamics

Portal hemodynamics were studied in 69 patients with cirrhosis and 29 patients with idiopathic portal hypertension to investigate the effects of an operative procedure for varices that consists of transabdominal esophageal mucosal transection, paraesophagogastric devascularization, pyloroplasty, and splenectomy. Portal venous flow measured by the pulsed Doppler flowmeter in 14 patients with cirrhosis and nine patients with idiopathic portal hypertension, who underwent operation 2-5 yr earlier, was significantly reduced compared with that in unoperated 49 patients with cirrhosis and 17 patients with idiopathic portal hypertension who had esophageal varices (410 +/- 158 versus 660 +/- 263 ml/min in cirrhosis; 443 +/- 185 versus 912 +/- 189 ml/min in idiopathic portal hypertension). In nine patients (six cirrhosis, three idiopathic portal hypertension), portal venous flow and portal vein pressure were measured before and after operation. In patients with cirrhosis, portal vein pressure did not change significantly postoperatively even though portal venous flow was reduced. In contrast, portal vein pressure decreased in two patients with idiopathic portal hypertension in whom portal venous flow was reduced. Portal vein pressure was elevated in one patient with idiopathic portal hypertension in whom portal venous flow was increased postoperatively as a result of resection of a large gastro- and splenorenal shunt conducted additionally.     

Portal and pulmonary hypertension in a patient with MCTD]

A 42-year-old woman with mixed connective tissue disease (MCTD) died due to the rupture of esophageal varices. The autopsy revealed fresh thrombi in the main trunk of the portal vein. Microscopic examination disclosed wide-spread periportal fibrosis and stenosis of peripheral portal veins without remodeling of hepatic lobular architecture, which was compatible to idiopathic portal hypertension (IPH). Anti-phospholipid antibody was negative. Accordingly it is likely that portal vein thrombosis developed secondary to IPH. In the literature 6 (37.5%) of 16 collagen vascular disease patients with IPH died, and three of them were due to rupture of esophageal varices. Therefore IPH should be considered to be one of the most important complications affecting its grave prognosis in patients with collagen vascular disease. The patient also had had pulmonary hypertension (PH) when the diagnosis of portal hypertension was made. In the literature we found 5 collagen vascular disease patients with both PH and IPH like this case. The most outstanding common clinical feature among these 6 patients was Raynaud's phenomenon associated with positive anti-RNP antibody. Moreover 5 of 6 cases including this case simultaneously developed both PH and IPH. The clinical course of these patients suggests there may be a common pathogenetic factor for these two lesions. A possible candidate involved in the pathogenesis of PH and IPH may be endothelin, one of the vasoactive substances, since its receptor is said to be expressed abundantly in pulmonary and portal vasculatures. However, further investigation is necessary to elucidate the mechanism of PH and IPH in collagen vascular diseases.     

Heterogeneous hepatic enhancement on CT angiography in idiopathic portal hypertension

BACKGROUND: Idiopathic portal hypertension is an uncommon condition characterized by presinusoidal portal perfusion disturbance without known causes. METHODS: In the present study, portal and arterial perfusion dynamics were evaluated in two cases with idiopathic portal hypertension using computed tomography during arterial portography and hepatic arteriography. Ten cases with liver cirrhosis were also studied as a reference. RESULTS: In cases with idiopathic portal hypertension, portal perfusion was conspicuously heterogeneous and decreased especially at the periphery of the liver where arterial perfusion was reciprocally increased. When the spatial heterogeneity of an enhancement of the liver was quantified using a densitometric analysis of computed tomography during hepatic arteriography images, the densities at the periphery were higher and varied more than those of the inner areas in cases with idiopathic portal hypertension. In contrast, the densities did not vary between the periphery and the inner areas at the cases with liver cirrhosis. CONCLUSIONS: The heterogeneous increase of arterial perfusion in periphery of the liver may be an important feature of idiopathic portal hypertension.     

A case of idiopathic hypoparathyroidism complicated with chronic thyroiditis]

It has been suggested that autoimmunity and genetic factors may play a specific role in the development of idiopathic hypoparathyroidism. We reported a case of idiopathic hypoparathyroidism complicated with chronic thyroiditis. The patient, a woman 40 years old, visited our clinic because of tetany of both hands and dizziness. She was of short stature with a round face. She also had a goiter, hypocalcemia, hyperphosphatemia and decreased parathyroidal function, but renal function was normal. Her TSH level was slightly high with a positive microsome test (x 1600), and the levels of thyroid hormones tended to be low. Based on Ellsworth-Howard test findings, a diagnosis of idiopathic hypoparathyroidism was made, with the complication of chronic thyroiditis confirmed by the thyroidal biopsy. Administration of l alpha-OH-D3 normalized the level of serum calcium. No special treatment was given for the chronic thyroiditis in order to observe its natural course. Her TSH returned to normal, and the level of thyroid hormones was increased to normal ranges. Tests were positive for anti-adrenal antibody and anti-gastric antibody. The complication of chronic thyroiditis, an autoimmune disease, and a positive finding for every antibody suggested the possible involvement of autoimmunity in the mechanism of development of idiopathic hypoparathyroidism. The administration of 1 alpha-OH-D3 resulted in an increase in the serum calcium level and also normalization of levels of TSH and thyroid hormones. Thus, it is likely that the elevation of the calcium ion or immunoregulation by active vitamin D may have induced the increase in thyroid hormone secretion.     

Hepatopulmonary syndrome in noncirrhotic portal hypertensive patients

Hepatopulmonary syndrome has yet not been sufficiently assessed in noncirrhotic portal hypertension. The prevalence of hepatopulmonary syndrome was determined in 31 consecutive patients with noncirrhotic portal hypertension (19 idiopathic portal hypertension, 7 portal vein thrombosis, 5 congenital hepatic fibrosis) and 46 patients with liver cirrhosis. Contrast echocardiography was carried out in all patients. Macroaggregated albumin lung perfusion scans were performed in patients with positive contrast echocardiogram. Hepatopulmonary syndrome was detected in 5 (10.8%) cirrhotic and 3 (9.7%) noncirrhotic portal hypertensive patients (2 idiopathic portal hypertension, 1 portal vein thrombosis). All patients with hepatopulmonary syndrome had an increased shunt fraction (13–62%) and a decreased diffusion capacity of carbon monoxide (40–79%), and 7 of them were hypoxemic (P_aO₂, 31.6–69.8 mm Hg). These findings show that hepatopulmonary syndrome may occur in both liver cirrhosis and noncirrhotic portal hypertension and that portal hypertension is the predominant etiopathogenic factor related to hepatopulmonary syndrome.     

Idiopathic portal hypertension.

Idiopathic portal hypertension is reported in five cases including one case of chronic arsenical intake and one case of chronic industrial vinyl chloride exposure. In all five cases the patients presented with gastrointestinal bleeding as the chief complaint. Physical examination was within normal limits except for splenomegaly in all. Results of liver function tests were normal, except for the relative clearance of sulfobromophtalein. A surgical liver biopsy specimen was obtained in all cases and showed moderate degrees of portal fibrosis, but no cirrhosis. Combined umbilicoportal, hepatic vein and superior mesenteric artery catheterization was performed in all cases. Hepatoportographies showed distortion of the intrahepatic portal venous system and cut-off of small portal venules. Porto-hepatic gradients ranged from 14.0 to 20.5 mm Hg. The portal hypertension was both sinusoidal and presinusoidal in nature but mainly presinusoidal. Hepatic extraction of indocyanine green and of albumin microaggregates was normal, thereby suggesting normal functional portal blood supply to the liver. The patients with arsenical or vinyl chloride exposure could not be differentiated from the other three patients with idiopathic portal hypertension. These results suggest that idiopathic portal hypertension may be related to domestic or industrial exposure to other hepatotoxins.     

Clinical study of eighty-six cases of idiopathic portal hypertension and comparison with cirrhosis with splenomegaly

The clinical features of 86 cases of idiopathic portal hypertension, the equivalent of hepatoportal sclerosis in the United States and of noncirrhotic portal fibrosis in India, are presented. This disease is characterized by overt splenomegaly with pancytopenia, portal hypertension, and relatively mild abnormalities in liver function tests. Although differential diagnosis from liver cirrhosis is not always easy, liver histology, laparoscopy, portography, hepatic venography, and measurement of wedged hepatic vein pressure are useful in diagnosis. Prognosis is relatively benign if variceal bleeding is controlled or prevented, and the disease does not progress to cirrhosis. The etiology is still undetermined, but the liver pathology characterized by occlusive changes of the intrahepatic portal radicles, portal and periportal fibrosis, and irregularly distributed parenchymal atrophies suggests some sort of portal venopathy that causes decreased portal perfusion of peripheral liver parenchyma. These patients with idiopathic portal hypertension were compared with 63 cases of cirrhosis with splenomegaly and 80 cases of cirrhosis without splenomegaly. There was some similarity in hematologic findings between idiopathic portal hypertension and cirrhosis with splenomegaly, but the basic disease process seemed distinctly different. The cause of marked splenomegaly does not seem to be simply congestion, and remains an enigma.     

Role of hepatic vein catheterisation and transient elastography in the diagnosis of idiopathic portal hypertension

Background

Idiopathic portal hypertension is a rare cause of portal hypertension, frequently misdiagnosed as cryptogenic cirrhosis. This study evaluates specific findings at hepatic vein catheterisation or liver stiffness in idiopathic portal hypertension.

Methods

39 cases of idiopathic portal hypertension patients were retrospectively reviewed. Hepatic vein catheterisation and liver stiffness measurements were compared to matched patients with cirrhosis and portal hypertension, and non-cirrhotic portal vein thrombosis, included as controls.

Results

Hepatic vein-to-vein communications were found in 49% idiopathic portal hypertension patients precluding adequate hepatic venous pressure gradient measurements in 12. In the remaining 27 patients, mean hepatic venous pressure gradient (HVPG) was 7.1 ± 3.1 mmHg. Only 5 patients had HVPG ≥ 10 mmHg. HVPG was markedly lower than in cirrhosis (17 ± 3 mmHg, p < 0.001). Mean liver stiffness in idiopathic portal hypertension was 8.4 ± 3.3 kPa; significantly higher than in non-cirrhotic portal vein thrombosis (6.4 ± 2.2 kPa, p = 0.009), but lower than in cirrhosis (40.9 ± 20.5 kPa, p = 0.005). Only 2 idiopathic portal hypertension patients had liver stiffness >13.6 kPa.

Conclusions

Patients with idiopathic portal hypertension frequently have hepatic vein-to-vein communications and, despite unequivocal signs of portal hypertension, HVPG and liver stiffness values much lower than the cut-off for clinical significant portal hypertension in cirrhosis. These findings oblige to formally rule-out idiopathic portal hypertension in the presence of signs of portal hypertension.     

Portal hemodynamics in primary biliary cirrhosis as evaluated by per-rectal portal scintigraphy with Tc-99m pertechnetate

BACKGROUND/AIMS: Portal circulation can be evaluated in a relatively noninvasive manner by per-rectal portal scintigraphy. We used this method to evaluate portal hemodynamics in patients with primary biliary cirrhosis and idiopathic portal hypertension. We did the procedures simultaneously in some patients to examine the relation between portal circulation and hepatic functional reserve in these diseases. METHODOLOGY: Per-rectal portal scintigraphy with Tc-99m pertechnetate was done in 17 healthy subjects, 154 patients with chronic hepatitis, 447 patients with cirrhosis, 40 patients with primary biliary cirrhosis, and 20 patients with idiopathic portal hypertension. Eighty-three patients (14 with hepatitis, 48 with cirrhosis, 16 with primary biliary cirrhosis, and 5 with idiopathic portal hypertension) also underwent scintigraphy with Tc-99m galactosyl human serum albumin with 2 weeks. A solution containing Tc-99m pertechnetate was instilled into the rectum, and serial scintigrams were taken while radioactivity curves for the liver and heart were recorded sequentially. The per-rectal portal shunt index was calculated from the curves. A receptor index was calculated by dividing the radioactivity of the liver region of interest by that of the liver-plus-heart region of interest 15 min after the injection of Tc-99m galactosyl human serum albumin. The index of blood clearance was calculated by dividing the radioactivity of the heart region of interest at 15 min by that of the heart region of interest at 3 min. RESULTS: The shunt index was higher for more severe disorders, increasing in the order of chronic hepatitis, cirrhosis without varices, and cirrhosis with varices. The shunt indices in patients with primary biliary cirrhosis and idiopathic portal hypertension were higher than that in patients with chronic hepatitis. In terms of receptor index, the standard residuals were more than 0 in 10 of 16 patients with primary biliary cirrhosis and 4 of 5 patients with idiopathic portal hypertension. In terms of index of blood clearance, the standard residuals were more than 0 in 10 of 16 patients with primary biliary cirrhosis and 4 of 5 patients with idiopathic portal hypertension CONCLUSIONS: Abnormalities of portal hemodynamics in patients with primary biliary cirrhosis or idiopathic portal hypertension occur while hepatic functional reserve is still satisfactory as compared with patients who have chronic hepatitis or cirrhosis.     

定量检测人甲状腺过氧化物酶抗体化学发光酶免疫分析法的临床应用

目的 应用人甲状腺过氧化物酶抗体(hTPOAb)的化学发光酶免疫分析(CLEIA)试剂盒,检测正常人及各类甲状腺疾病患者,探讨该试剂盒在临床应用中的价值.方法 用该试剂盒共测定333例样品血清中的hTPOAb,包括正常人133名,各类甲状腺疾病患者200例,其中桥本甲状腺炎(HT) 94例,Graves病68例,结节性甲状腺肿19例,亚急性甲状腺炎10例,单纯性甲状腺肿9例.结果 确立本试剂盒hTPOAb阳性切限值为3.22 IU/ml,hTPOAb浓度以中位数表示,分别为HT5.48 IU/ml,阳性率为91.50％;Graves病1.88 IU/ml,阳性率为29.40％;结节性甲状腺肿1.83 IU/ml,阳性率为10.50％,亚急性甲状腺炎2.54 IU/ml,阳性率为20.00％;单纯性甲状腺肿2.21 IU/ml,阳性率为0.HT患者血清hTPOAb阳性率高于其他患者(x2=67.22,60.13,35.49,49.89,P均＜0.01).结论 该定量检测hTPOAb的CLEIA试剂盒在HT中有很高的阳性率,可作为HT有效的诊断手段.     

Presence of antideoxyribonucleic acid antibody in patients with hyperthyroidism of Graves' disease

In 16 untreated patients with hyperthyroidism due to Graves' disease, serum antidouble stranded DNA antibody, measured by RIA, was positive (greater than 20 U/ml) in 14. In methimazole-treated patients with T3-suppressible thyroid uptake, anti-DNA antibody was found in 9% (3 of 35). The frequency of positive tests in methimazole-treated patients with T3-nonsuppressible thyroid uptake and in surgically treated patients was 24% (5 of 21) and 57% (4 of 7), respectively. Among anti-DNA antibody-negative (less than 9 U/ml) and weakly positive (10-19 U/ml) patients, those with T3-suppressible thyroid uptake had lower anti-DNA antibody titers than those with T3-nonsuppressible thyroid uptake. Among 32 patients with Hashimoto's thyroiditis, anti-DNA antibody was positive in 7. None of the patients with simple goiter had positive or weakly positive anti-DNA antibody results. Although the quantity of antibodies did not correlate well in individual patients, the rates of positive TSH binding-inhibiting immunoglobulin and anti-DNA antibody tests were roughly comparable in these patient groups. None of these patients with thyroid disease associated with anti-DNA antibody had clinical or other serological evidence suggestive of systemic lupus erythematosus or related collagen vascular disorders. The finding of anti-DNA antibody provides a new aspect of immunological abnormality associated with hyperthyroidism of Graves' disease.     

Thoracic duct and hepatic lymph in idiopathic portal hypertension

Lymph dynamics in idiopathic portal hypertension has been studied in two phases. In the first phase thoracic duct lymph transport was studied in 11 patients with idiopathic portal hypertension by cannulating the duct. This revealed altered lymph transport in the form of a distended thoracic duct, raised pressure in the duct, and haemorrhagic lymph with an increased flow rate. The lymph flow rate was analysed in relation to various hepatic haemodynamic and biochemical parameters. In the second phase of the study hepatic lymphatics were studied by percutaneous hepatography in 16 patients with idiopathic portal hypertension. By this technique hepatic lymphatics were opacified in patients with idiopathic portal hypertension and cirrhosis with equal frequency. The significance of this finding in relation to the altered hepatic haemodynamics and thoracic duct lymph transport is discussed.     

Differences in Portal Hemodynamics in Cirrhosis and Idiopathic Portal Hypertension

A comparative study of portal hemodynamics was made in 79 cirrhotics (24 cirrhotics with a large spleen greater than or equal to 500 cm3 in volume, 55 cirrhotics with a spleen less than 500 cm3 in volume), 22 patients with idiopathic portal hypertension, and 63 healthy adults who served as the control for portal and splenic venous flows. Portal and splenic venous flows were significantly increased in the group order of the cirrhosis without splenomegaly group, the cirrhosis with splenomegaly group, and idiopathic portal hypertension group. Intrahepatic shunt index was significantly greater in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly group, and it was negligible in the idiopathic portal hypertension group. Portal vein pressure was significantly elevated in the cirrhosis with splenomegaly group than in the cirrhosis without splenomegaly and idiopathic portal hypertension groups. Postsinusoidal resistances were significantly greater in the two groups of cirrhosis than in the idiopathic portal hypertension group, whereas presinusoidal resistance was significantly greater in the idiopathic portal hypertension group than in the two groups with cirrhosis. It is concluded that these differences are inconsistent with the view that cirrhosis with splenomegaly comes from idiopathic portal hypertension.     

Splanchnic Hemodynamics in Idiopathic Portal Hypertension: Comparison with Chronic Persistent Hepatitis

A comparative study of splanchnic hemodynamics was made in 12 patients with idiopathic portal hypertension and in eight patients with chronic persistent hepatitis, but without portal hypertension, who served as the control. Venous pressures were measured by portal and hepatic vein catheterizations, blood flow by the pulsed Doppler flowmeter, and organ volume by computed tomography. Splenic artery blood flow was 788 +/- 242 ml/min in idiopathic portal hypertension and about four times that in chronic persistent hepatitis (215 +/- 42 ml/min), whereas there was no difference in superior mesenteric artery blood flow between the former and the latter (408 +/- 142 vs. 389 +/- 32 ml/min). Spleen volume in idiopathic portal hypertension was six times that in chronic persistent hepatitis, and splenic artery blood flow showed a significant linear correlation with spleen volume in idiopathic portal hypertension (r = 0.71, p less than 0.02). The sum of splenic artery blood flow and superior mesenteric artery blood flow in idiopathic portal hypertension was 1195 +/- 294 ml/min, twice that in chronic persistent hepatitis (603 +/- 109 ml/min). Portal vascular resistance and intrahepatic portal vascular resistance were three times and four times those in chronic persistent hepatitis, respectively. These results indicate that both increased intrahepatic portal vascular resistance and increased splenic artery blood flow may play roles in the development of portal hypertension in idiopathic portal hypertension.     

Natural course of autoimmune thyroiditis in Thai children

Forty-seven pediatric patients with autoimmune thyroiditis were followed for an average of 5.18+/-2.89 years. The diagnosis was based on a firm goiter and a positive test for antithyroid antibodies. Initially, 23 patients had euthyroidism, 11 overt hypothyroidism, 6 compensated hypothyroidism and 7 with low TSH. All patients had clinical euthyroidism, except two who had overt hypothyroidism. The thyroid function tests, the size of the thyroid gland and the thyroid antibodies were regularly evaluated. After the follow-up, 26 patients had untreated euthyroidism, 12 with overt hypothyroidism received eltroxin for maintenance of euthyroidism, while 4 had compensated hypothyroidism and 5 low TSH levels. All had clinical euthyroid. The thyroid size was reduced in 12 patients (26%) while 4 (9%) had normal-sized gland. The goiter size in 35 patients (74%) remained unchanged. The antithyroglobulin and antimicrosomal antibody titers fluctuated higher in patients with overt hypothyroidism. Eltroxin was given only to those having overt hypothyroidism with diminished goiter size in 8 patients (73%).     

Graves病药物治疗停药复发相关因素分析

目的 探讨甲状腺刺激性抗体(TSAb)水平和甲状腺体积等相关因素对Graves病患者抗甲状腺药物治疗停药后复发的预测价值.方法 71例Graves病患者经抗甲状腺药物正规治疗(2.8±1.4)年后停药,随访(22±6.0)个月.对停药后复发与未复发组的年龄、性别及停药时的TSAb活性、甲状腺体积和甲状腺功能指标等进行分析比较.应用表达重组人促甲状腺激素受体的人胚肾(HEK-hTSHR)细胞测定TSAb活性.结果 71例患者随访期间有11例(15.5%)复发,治疗停药时TSAb阳性患者复发率(42.9%,6/14)显著高于阴性患者(8.8%,5/57,X2=9.97,P<0.01).停药时甲状腺正常体积、Ⅰ度肿大、Ⅱ度肿大复发比率分别为6.25%、12.2%、35.7%.复发组患者停药时TSAb活性、阳性率以及甲状腺体积均显著高于未复发组(P<0.05或P<0.01).结论 Graves病患者抗甲状腺药物治疗终止时TSAb活性和甲状腺大小是Graves病停药后复发的有效预测因子.