Tirotoxicosis por enfermedad trofoblástica gestacional: revisión a partir de 3 casos / Thyrotoxicosis due to gestational trophoblastic disease: clinical cases

La enfermedad trofoblástica gestacional (ETG) es una complicación del embarazo poco común. Corresponde a un espectro de lesiones proliferativas del tejido trofoblástico: Mola Hidatiforme (MH) en sus formas parcial y completa, Coriocarcinoma, Tumor Trofoblástico y Tumor Trofoblástico Epiteloide. Los distintos tipos de ETG presentan en común la hipersecreción de gonadotrofina coriónica humana (hCG). La hCG es una hormona glicoproteica con una estructura muy similar a la TSH, por lo cual puede estimular la función tiroidea en condiciones fisiológicas y en algunas condiciones patológicas. La ETG puede cursar con hipertiroidismo, el cual puede variar en intensidad, desde una presentación asintomática con alteración leve de hormonas tiroideas a un cuadro de hipertiroidismo manifiesto. Se presentan 3 casos clínicos de pacientes con ETG, específicamente MH que evolucionaron con tirotoxicosis transitoria. Los casos presentaron un cuadro leve de hipertiroidismo con pocos síntomas asociados. La taquicardia fue el único síntoma en la mayoría de los casos. En todas las pacientes las hormonas tiroideas se normalizaron después del tratamiento de la ETG. Conclusión: Se debe tener presente la posibilidad de hipertiroidismo en toda paciente con ETG. Un alto nivel de sospecha permitirá identificar a aquellas pacientes que cursen con hipertiroidismo, permitiendo así un diagnóstico y tratamiento oportuno.

Gestational trophoblastic disease (GTD) is a rare complication of pregnancy. GTD includes a group of proliferative lesions of trophoblastic tissue: partial and complete hydatidiform mole, choriocarcinoma, epithelioid trophoblastic tumor, and placental site trophoblastic tumor. The different types of GTD have in common the hypersecretion of human chorionic gonadotropin (hCG). HCG is a glycoprotein hormone with a similar structure to TSH. In physiological and pathological conditions hCG can stimulate thyroid function. GTD can present with hyperthyroidism, which can vary in intensity, from an asymptomatic presentation with mild alteration of thyroid hormones to a manifest hyperthyroidism. We present 3 clinical cases of patients with GTD thyrotoxicosis. All cases presented mild hyperthyroidism. Tachycardia was the only symptom in most cases. In all patients thyroid hormones return to normal after treatment of GTD. Conclusion: In patients with GTD the possibility of hyperthyroidism should be kept in mind. A high level of suspicion will allow to identifying patients with hyperthyroidism.

Endothelial nitric oxide synthase G894T gene polymorphism in Chilean subjects with coronary artery disease and controls.

BACKGROUND: Nitric oxide (NO) from the endothelium, produced by oxidation of l-arginine to L-citruline for the action at the endothelial nitric oxide synthase (eNOS), is considered an important atheroprotective factor. The Glu298Asp (G894T) polymorphic variant of the eNOS gene has been implicated in the development of coronary artery disease (CAD). We investigated the association between occurrence of CAD documented by angiography and the G894T polymorphism of the NOS3 gene in Chilean individuals. METHODS: A total of 112 unrelated patients with diagnosis of CAD and 72 controls were included in this study. G894T gene polymorphism was analyzed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). RESULTS: The frequency of TT homozygous genotype for G894T polymorphism was 7% in CAD patients and 1% in the control group. However, the genotype distribution and allele frequencies were not significantly different between CAD and control subjects (P>0.05). Moreover, the odds ratio for CAD associated with the T variant failed to reach statistical significance (OR=1.5; 95% CI: 0.87-2.59, P>0.05). CONCLUSION: These findings suggest that the G894T polymorphism of the eNOS gene was not associated with CAD in Chilean individuals.