Changes in total lipid profiles assessed by analytical capillary isotachophoresis throughout the acute phase of myocardial infarction

Coronary artery stenosis is a major complication of Kawasaki disease (KD). Several interventional methods in treating coronary artery stenosis have been introduced. However, there are few reports on the management of in-stent restenosis after coronary stent implantation in children. Reported is a 10-year-old boy who underwent successful stent graft insertion for treating in-stent restenosis with neoaneurysm formation after stent implantation for severe coronary stenosis after KD. Twenty-eight months follow-up studies showed no significant restenosis and perfusion defect.     

Liver injury induced by levothyroxine in a patient with primary hypothyroidism

We report a patient with primary hypothyroidism, who developed hepatocellular injury due to levothyroxine, synthetic thyroxine. A 63-year-old male was admitted to our hospital due to elevation of liver enzymes. The patient was diagnosed as having hypothyroidism and had been treated with levothyroxine for almost two months until admission. Drug-induced liver injury induced due to levothyroxine was suspected and liver enzymes were rapidly decreased after discontinuation of levothyroxine and dried thyroid powder, also containing thyroxine. Synthetic triiodothyronine, the deiodinated form of levothyroxine was administered instead, and was well tolerated by the patient. The drug-induced lymphocyte stimulation test (DLST) using levothyroxine was negative. Since triiodothyronine which structurally resembles levothyroxine did not cause liver injury, and DLST using levothyroxine was negative, it is unlikely that levothyroxine itself was targeted by the immune system. Rather, we assume that the complex of levothyroxine as the hapten and liver-related macromolecules in the body as the carrier might have acquired antigenicity in this patient and subsequently resulted in liver injury.     

左旋甲状腺素治疗对亚临床甲状腺功能减退症患者血脂的影响

目的 通过对47例亚临床甲状腺功能减退症(简称亚临床甲减)合并高脂血症患者使用左旋甲状腺素钠片治疗,观察治疗前后血脂变化.方法 治疗前记录各病例促甲状腺素(TSH)、血总胆固醇、甘油三脂、低密度脂蛋白胆固醇检查结果,给予左旋甲状腺素钠片,以TSH调整在正常范围为合适剂量,平均50～75 μg/d,治疗三个月后复查TSH及血脂结果并进行统计分析.结果 治疗后血脂明显下降,与治疗前存在显著差异(P<0.01).结论 用左旋甲状腺素钠片治疗亚临床甲减对改善血脂有临床意义.     

The effect of levothyroxine on arterial stiffness and lipid profile in patients with subclinical hypothyroidism

BACKGROUND: The influence of treatment for subclinical hypothyroidism (SCH) on cardiovascular morbidity and mortality, arterial stiffness, and lipid profile has not been elucidated yet. The aim of this study was to evaluate the effect of levothyroxine on arterial stiffness, lipid profile, and inflammation. METHODS: The study included 30 patients with SCH. Patients were treated with levothyroxine and were assessed at baseline and at 1, 4, and 7 months. Blood samples were taken for lipid profile and highly sensitive C-reactive protein (hs-CRP). Arterial stiffness was evaluated by augmentation index (AIx). In conditions that cause arterial stiffness, the pulse wave traveling from the periphery to the heart reaches the heart during systole, resulting in augmentation of the central pressure. This increase, calculated as the AIx, is a good expression of central aortic pressure. RESULTS: After accomplishing euthyroidism, the AIx decreased from 17.2 +/- 8.3 to 14.3 +/- 6.5 (p < 0.01) and AIx percentage decreased from 36.2 +/- 11.5 to 33.2 +/- 9.1 (p = 0.03). Systolic blood pressure (SBP) decreased from 134.7 +/- 20 to 127.6 +/- 13.7 mmHg (p < 0.01). In those patients whose AIx decreased, low-density lipoprotein (LDL) levels decreased by 0.4 +/- 0.96 mmol/L compared to the patients whose AIx did not decrease and LDL increased by 0.62 +/- 1.48 mmol/L (p = 0.057). Total cholesterol decreased by 0.72 +/- 1.64 mmol/L in the patients whose AIx decreased and increased by 1 +/- 2.53 mg/dL in the patients whose AIx did not improve (p = 0.06). CONCLUSIONS: In patients with SCH, treatment with levothyroxine had a significant beneficial effect on arterial stiffness and SBP, and no effect on lipid profile or hs-CRP.     

Prevention of progressive renal failure by levothyroxine sodium in a diabetic patient with renal insufficiency and hypothyroidism.

The progressive renal failure of a 49-year-old female diabetic patient with renal insufficiency and hypothyroidism was successfully prevented by levothyroxine sodium treatment. Her renal function worsened in parallel with the exacerbation of hypothyroidism. Cessation of progressive renal failure was observed after administration of levothyroxine sodium (0.05 mg daily) for more than 24 months. Mean slopes of reciprocal serum creatinine levels for 12 months before and after the administration of levothyroxine sodium were -1.67 x 10(-3) and +8.68 x 10(-4), respectively. It was suggested that levothyroxine sodium was effective in the prevention of progressive renal failure in this patient.     

Effect of levothyroxine replacement on lipid profile and intima-media thickness in subclinical hypothyroidism: a double-blind, placebo- controlled study

Subclinical hypothyroidism (sHT) is associated with dyslipidemia and enhanced cardiovascular risk. We assessed carotid artery intima-media thickness (IMT, high-resolution ultrasonography) and lipoprotein profile in 45 sHT patients (aged 37 +/- 11 yr) at baseline and after 6 months of randomized, placebo-controlled L-T(4) replacement. In comparison with 32 age- and sex-matched controls, sHT patients had elevated total and low-density lipoprotein (LDL) cholesterol and ApoB levels (P = 0.002, P = 0.0007, and P = 0.01, respectively) and higher mean-IMT values (P < 0.0001). In stepwise regression analysis, mean-IMT was positively related (r(2) = 0.71, P < 0.0001) to age, TSH, and LDL cholesterol. L-T(4) replacement significantly reduced both total and LDL cholesterol (P < 0.0001 for both) and mean-IMT (by 11%, P < 0.0001). The decrement in IMT was directly related to the decrements of both total cholesterol and TSH (P = 0.02 and P = 0.0001, respectively). We conclude that early carotid artery wall alterations are present in sHT patients. Whether such IMT increase is related to an early atherosclerotic involvement of the arterial wall cannot be clearly decided on the basis of the present results. However, the fact that L-T(4) replacement therapy was able to improve both the atherogenic lipoprotein profile and intima-media thickening suggests that lipid infiltration of arterial wall may represent a major mechanism underlying IMT increase in subclinical hypothyroidism.     

Effect of levothyroxine replacement therapy on coagulation and fibrinolysis in severe hypothyroidism

OBJECTIVE: We previously demonstrated that patients suffering from moderate hypothyroidism were at increased risk of thrombosis contrasting with the bleeding tendency of those presenting severe hypothyroidism. The latter state is associated with hemostatic anomalies including von Willebrand type 1 disease and increased fibrinolytic capacity. With the exception of von Willebrand type 1 disease, reversibility of hemostatic changes is not established after levothyroxine replacement therapy. Therefore our objective was to analyze the reversibility of these anomalies. MATERIALS AND METHODS: We analyzed the impact of levothyroxine treatment on lipid parameters, fibrinogen, platelet count, D-dimers, alpha2 antiplasmin activity, plasminogen activity, tissue plasminogen activator antigen (t-PA Ag), plasminogen activator inhibitor type 1 antigen (PAI-1 Ag) and coagulation factors (factor VIII coagulant, von Willebrand factor antigen, von Willebrand factor and factor IX) in 23 patients with severe hypothyroidism (TSH level > 50 mU/ I). RESULTS: Mean fibrinogen levels increased by 14.2% while t-PA Ag and PAI-1 Ag increased by 42.6 and 69%, respectively, after correction of hypothyroidism. Interestingly, post-treatment PAI-1 Ag levels tended to be higher in patients with normal-high final TSH levels than in patients with normal-low final TSH levels. Our results suggest that normalization of fibrinolysis is obtained after a transient decrease of fibrinolytic activity. We also confirmed the correction of coagulation factor abnormalities upon levothyroxine replacement therapy. CONCLUSIONS: We demonstrated that the coagulation disorders and the hyperfibrinolytic status of severe hypothyroid patients were corrected upon levothyroxine therapy. However, the clinical consequences of the transient decrease of the fibrinolytic activity during the course of TSH normalization need further studies.     

Effect of levothyroxine replacement therapy on improving diffused left ventricular myocardial lesions in patients with hypothyroidism

<正>Objective To study the effect of levothyroxine replacement therapy on improving diffused left ventricular myocardial lesions and cardiac function in patients with hypothyroidism.Methods Our research included 2groups:Hypothyroidism group,n=20,newly diagnosed patients and Control group,n=17,normal healthy subjects.Diffused left ventricular myocardial lesions were     

Lipoprotein and apolipoprotein levels in subclinical hypothyroidism. Effect of levothyroxine therapy

To assess whether subclinical hypothyroidism is associated with changes in lipoprotein fractions, 13 patients maintained in a stable state of subclinical hypothyroidism for at least 3 months were studied prior to and 2 and 4 months following restoration of a euthyroid state with incremental levothyroxine sodium therapy. Thyrotropin levels ( +/- SEM) had decreased from 16.6 +/- 3.2 mU/L to 3.1 +/- 0.7 mU/L and 3.2 +/- 0.7 mU/L at 2 months and 4 months. At 2 months, levothyroxine treatment led to a decrease in levels of total cholesterol from 5.5 +/- 0.3 mmol/L (213 +/- 12 mg/dL) to 4.8 +/- 0.3 mmol/L (186 +/- 12 mg/dL), in low-density lipoprotein cholesterol (LDL-C) from 3.7 +/- 0.3 mmol/L (143 +/- 12 mg/dL) to 2.9 +/- 0.3 mmol/L (112 +/- 12 mg/dL), and in apolipoprotein B from 91 +/- 8 mg/dL to 74 +/- 7 mg/dL. At 4 months, levels of LDL-C and apolipoprotein B remained significantly lower than pretreatment values (2.9 +/- 0.2 mmol/L [112 +/- 8 mg/dL] and 75 +/- 6 mg/dL, respectively). While high-density lipoprotein cholesterol (HDL-C), HDL3-C, and apolipoprotein A-I were not significantly affected by levothyroxine therapy, there was a slight trend of increase in HDL2-C during levothyroxine substitution. There was also a tendency for a decrease in triglyceride levels from 1.3 +/- 0.2 mmol/L (115 +/- 18 mg/dL) to 0.9 +/- 0.1 mmol/L (80 +/- 9 mg/dL) at 4 months of levothyroxine therapy. Levels of HDL-C tended to decrease from 4.8 +/- 0.4 mmol/L (186 +/- 15 mg/dL) to 4.5 +/- 0.5 mmol/L (174 +/- 19 mg/dL) at 2 months and to 3.9 +/- 0.4 mmol/L (151 +/- 15 mg/dL) at 4 months. The LDL-C/HDL-C ratio also decreased from 3.3 +/- 0.3 mmol/L (128 +/- 12 mg/dL) to 2.9 +/- 0.5 mmol/L (112 +/- 19 mg/dL) and 2.5 +/- 0.3 mmol/L (97 +/- 12 mg/dL) at 2 months and 4 months, respectively. These results suggest that long-term levothyroxine therapy in patients with subclinical hypothyroidism is associated with a decrease in LDL-C and apolipoprotein B levels that are reflected in a trend of decreases in cholesterol/HDL-C and LDL-C/HDL-C ratios known to have a relationship with coronary artery disease.     

Rhabdomyolysis in a patient with hypothyroidism

We describe a case of rhabdomyolysis associating hypothyroidism. Hypothyroidism frequently leads to myalgias, muscle stiffness, cramps and sometimes elevated levels of muscle enzymes, but rhabdomyolysis is quite rare. This report describes a case of rhabdomyolysis associating hypothyroidism in a 19-year old man. Muscle enzyme levels were typical of rhabdomyolysis. Muscle biopsy and electromyographic findings were compatible with hypothyroid myopathy. Muscle functions completely recovered with levothyroxine therapy. The present case represents rhabdomyolysis secondary to undiagnosed hypothyroidism in a developed stage which manifests itself with rhabdomyolysis.     

左旋甲状腺素和维生素E干预对甲状腺功能减退大鼠心肌氧化应激和细胞凋亡的影响

目的 通过研究左旋甲状腺素(LT4)、维生素E(VitE)及二者联合治疗对甲状腺功能减退(甲减)大鼠氧化应激及心肌细胞凋亡的影响,进一步探讨甲减心肌损伤的发生机制及其治疗方法.方法 将SD雄性大鼠分为正常对照组、丙基硫氧嘧啶组(PTU)、LT4治疗组(PTU +LT4)、VitE治疗组(PTU+VitE)、LT4和VitE联合治疗组(PTU+LT4 +VitE).测定血清T3、T4、TSH水平以及血清、心肌组织超氧化物歧化酶(SOD)活性和丙二醛含量;用TUNEL法检测心肌细胞凋亡指数.结果 (1)与正常对照组比较,PTU组、PTU+VitE组T3、T4水平明显降低,TSH显著升高(P＜0.05);与PTU组比较,PTU+LT4组、PTU+LT4 +VitE组T3、T4水平明显升高,TSH显著降低(P＜0.05);PTU组与PTU+VitE组T3、T4、TSH水平差异无统计学意义(P＞0.05).(2)与正常对照组比较,PTU组血清及心肌组织丙二醛含量显著升高(P＜0.05),其他各组之间差异无统计学意义(P＞0.05);与正常对照组比较,PTU组血清SOD活性显著降低(P＜0.05),但心肌组织SOD活性各组之间差异无统计学意义(P＞0.05).(3)与正常对照组比较,PTU组、PTU+VitE组心肌细胞凋亡显著升高(P＜0.05);与PTU组比较PTU+LT4组、PTU+ LT4+ VitE组凋亡显著降低(P＜0.05).结论 LT4、VitE及二者联合治疗可降低甲减大鼠心肌细胞凋亡,其机制可能与甲状腺功能改善和氧化应激水平降低有关.     

Increased levothyroxine requirement in a woman with previously well-controlled hypothyroidism and intestinal giardiasis

The most common cause of apparent inefficiency or resistance to oral therapy with levothyroxine for hypothyroidism is nonadhesion. However, in some subjects in whom the control of hypothyroidism is extremely difficult, levothyroxine bioavailability defects should be considered. We report here the case of a 57-year-old woman with hypothyroidism that was well-controlled for the previous 6 years but suddenly presented with poor hormonal control and abdominal symptoms, despite repeatedly reporting good compliance to therapy. Adequate control of thyroid function was only obtained after intestinal giardiasis was diagnosed and treated.     

Primary amenorrhea and pseudoprolactinoma in a patient with primary hypothyroidism. Reversal of clinical, biochemical, and radiologic abnormalities with levothyroxine

A 15-year-old girl presented with primary amenorrhea, galactorrhea, hyperprolactinemia and an enlarged pituitary gland. She proved to have primary hypothyroidism. Therapy with levothyroxine resulted in prompt induction of regular menses, normalization of hormone levels, and a reduction in the size of the pituitary. Although hypothyroidism is known to produce secondary amenorrhea, hyperprolactinemia, and pituitary enlargement, this is believed to be the first computed tomographic documentation of such a "pseudoprolactinoma" presenting as primary amenorrhea.     

Effects of levothyroxine treatment on biochemical and hemostasis parameters in patients with hypothyroidism

OBJECTIVE: The aims of the study were to evaluate the disturbances in the coagulation system in patients with overt hypothyroidism (OH), to assess the effects of levothyroxine (LT4) on the coagulation parameters, and to determine whether subclinical hypothyroidism (SH) affects concentrations of coagulation markers and several biochemical parameters, thereby supporting early substitution. DESIGN: The study included 15 patients with SH (TSH levels 5-10 mU/l), 15 patients with OH and 15 euthyroid controls. METHODS: Blood urea nitrogen, creatinine, creatine phosphokinase, aspartate aminotransferase, lactate dehydrogenase, total-cholesterol, high density lipoprotein-cholesterol, low density lipoprotein-cholesterol and triglyceride levels, and bleeding time, prothrombin time (PT), activated partial thromboplastin time (APTT), factor VIII activity, von Willebrand factor activity (vWF), platelet count and clotting time were evaluated just before and three months after the maintenance of euthyroidism with LT4 treatment. RESULTS: Factor VIII and vWF activities were lower in patients with SH than in controls (P < 0.01). Increased bleeding time, PT, APTT and clotting time and decreased factor VIII activity and vWF activity were observed in patients with OH when compared with controls. Bleeding time, PT, APTT and clotting time decreased and factor VIII activity, vWF and platelet count increased after LT4 in patients with OH. Increases in factor VIII activity and vWF (P < 0.01) were detected also in the SH group with treatment. CONCLUSIONS: OH is associated with significant abnormalities in clotting parameters which are reversed by LT4. In contrast, SH is associated with minor changes in factor VIII activity and vWF which are reversible by LT4. Serum lipids and other measured parameters are not improved by LT4 in patients with TSH < 10 mU/l and these data fail to demonstrate a need to treat such patients.     

Effect of levothyroxine on cardiac function and structure in subclinical hypothyroidism: a double blind, placebo-controlled study

Subclinical hypothyroidism (sHT) affects 5-15% of the general population; however, the need of lifelong L-T(4) therapy is still controversial. As myocardium is a main target of thyroid hormone action, we investigated whether sHT induces cardiovascular alterations. Twenty sHT patients were randomly assigned to receive placebo or L-T(4) therapy and were followed for 1 yr. Twenty sex- and age-matched normal subjects served as controls. Doppler echocardiography and videodensitometric analysis were performed in all subjects. Myocardium textural parameters were obtained as mean gray levels, which were then used to calculate the cyclic variation index (CVI; percent systolic/diastolic change in mean gray levels). Patients had a significantly higher isovolumic relaxation time (3.1 +/- 0.5 vs. 2.6 +/- 0.6; P < 0.03), peak A (0.77 +/- 0.16 vs. 0.56 +/- 0.13 m/s; P < 0.01), and preejection/ejection time (PEP/ET) ratio (0.72 +/- 0.05 vs. 0.57 +/- 0.06; P < 0.03) and a lower CVI (P < 0.0001) than controls. CVI was inversely related to TSH level (P < 0.0001) and PEP/ET ratio (P < 0.01). L-T(4)-treated patients showed a significant reduction of the PEP/ET ratio (P < 0.05), peak A (P < 0.05), and isovolumic relaxation time (P < 0.05) along with a normalization of CVI. Conversely, no changes were observed in the placebo-treated group. In conclusion, sHT affects both myocardial structure and contractility. These alterations may be reversed by L-T(4) therapy.