Disfunción tiroidea subclínica / Subclinical thyroid dysfunction

La disfunción tiroidea subclínica es una alteración funcional de alta prevalencia en las consultas médicas de los centros de salud, observable solo mediante la realización de pruebas complementarias de laboratorios, caracterizadas por una elevación de la TSH mayor a 4.0mU/L ó menor a 0.4mU/L con valores normales de T3 y T4 libres, aunque existe la tendencia actual a la disminución de estos rangos de referencia según estudios epidemiológicos en cada población en particular; su tratamiento y control por el especialista son mandatorios en aquellos individuos con valores séricos de TSH superiores a 10mU/L ó menores de 0.1mU/L. La presente revisión bibliográfica tiene como propósito resumir los conocimientos actuales con relación a la prevalencia, factores de riesgo, diagnóstico, clasificación, tratamiento y seguimiento de las patologías incluidas en la disfunción tiroidea subclínica (hipotiroidismo e hipertiroidismo) y sus consecuencias sistémicas(AU)

Thyroid dysfunction is highly prevalent in the health consultation and it is only proven by laboratory essays, were TSH is higher than 4 mU/L, with a normal T3 and free T4; although there is a current tendency to take in account lower values depending of the epidemiological studies of each population. The diagnosis and treatment are mandatory in subjects with a TSH higher than 10 mU/L or lower than 0,1mU/L. This review has the purpose of summarizing the current knowledge of prevalence, risk factors, diagnosis, treatment and follow-up of hypo and hyperthyroidism, as well as their sistemic consequences(AU)

The usage of low dose of cholestyramine in the preoperotive preparation in hyperthyroidism / 重庆医科大学学报

Objective:To investigate the effect of lowdose of cholestyramine in the preoperotive preparation in hyperthroidism(HT).Methods:Sixty-seven patients with HT were randomly and double blindedly divided into group A and group B,the former were give low dose of cholestyramine and thioureas,the latter were given tapazole(MMI)and Logul's liquid.Four weeks later,the level of TH and basic metabolism rate(BMR)were comparised between two groups.Results:The level of FT3,FT4,BMR,and the preoperotive preparation time were significantly priorier than those of group B(P0.05).Conclusion:It suggests that lowdose of(cholestyramine is beneficial for the preoperotive preparation in HT.

Hepatic Injury during Treatment with Antithyroid Drugs in Patients with Hyperthyroidism / 대한내분비학회지

BACKGROUND: Propylthiouracil (PIV) and methimazole (MMI) were widely used for the treatment of hyperthyroidism. Hepatic injury caused by these agents is a rare but serious complication. This study is to investigate the clinical features of hepatotoxicity from antithyroid drugs. METHODS: We reviewed 17 cases of hepatic injury during treatment with antithyroid drugs in patients with hyperthyroidism. Included were 6 cases we experienced and 11 cases reported in Korean literature from 1986 to 1999. We analyzed the clinical features of hepatic injury. RESULTS: Of 17 cases of hepatic injury, 12 were PTU cases and 5 MMI cases. The mean age of PTU cases was 40 years with 6/12 patients over 40 years old and 2/5 MMI cases were over 40 years old. The dose of PTU was 300 mg/d or more in 10/12 cases (83%) and the dose of MMI was 30 mg/d in 3/5 cases (60%). The hepatic injury occurred within 3 months in 8/12 PTU cases (67%) and within 2 months in 4/5 MMI cases (80%). The duration of hepatic injury tended to be longer in MMI cases than in PTV cases (median; 80 vs 41 days, p=0.102). In PTU cases, the duration of hepatic injury was correlated with the duration of drug use before hepatic injury (p<0.05). All of 8 biopsied cases who took PTU had predominantly hepatocellular necrosis. Two biopsied cases who took MMI had cholestatic jaundice and nonspecific abnormality, respectively. Biochemical findings of all MMI cases were compatible with cholestatic jaundice. As to the treatment of hyperthyroidism after hepatic injury, 4/12 PTU cases were treated with RAI therapy, 5 with MMI and one with surgery, and treatment was unknown in two. On the other hand 3/5 MMI cases interestingly entered into spontaneous remission after hepatic injury and 2/5 had RAI therapy. Hepatic dysfunction recurred in each one whom treatment by changing to MMI or PTU was tried on. CONCLUSION: Most of hepatic injury during treatment with antithyroid drugs developed within two to three months of drug use. The hepatic injury related to PTU was mainly cytotoxic whereas that related to MMI was cholestatic. Since there is a cross-reaction between PTU and MMI in hepatotoxicity, RAI therapy or operation shoud be considered as an alternative treatment of hyperthyroidism after hepatic injury.