RESUMEN
SUMMARY: Anaplastic thyroid cancer (ATC) is the type of thyroid cancer that has the worst prognosis. It usually presents as a rapidly growing cervical mass that generates compressive symptoms. Its association with thyrotoxicosis is rare. A 76-year-old woman, with no contributory history, presented with a 3-month course of fast-growing cervical tumor, associated with tenderness, cough, and weight loss. Physical examination revealed goiter, localized erythema, and a painful and stone tumor dependent on the right thyroid lobe. Due to the malignant findings of the thyroid ultrasound, the patient underwent a thyroid core needle biopsy, which indicated ATC. Laboratory tests revealed leukocytosis, decreased thyroid-stimulating hormone, elevated free thyroxine (fT4), and increased thyroperoxidase (TPO) antibodies. At the beginning, we considered that the etiology of thyrotoxicosis was secondary to subacute thyroiditis (SAT) after SARS-CoV-2 infection, due to the immunochromatography result and chest tomography findings. The result of markedly elevated TPO antibodies left this etiology more remote. Therefore, we suspected Graves' disease as an etiology; however, thyroid histopathology and ultrasound did not show compatible findings. Therefore, we suspect that the main etiology of thyrotoxicosis in the patient was the destruction of the thyroid follicles caused by a rapid invasion of malignant cells, which is responsible for the consequent release of preformed thyroid hormone. ATC is a rare endocrine neoplasm with high mortality; it may be associated with thyrotoxicosis, whose etiology can be varied; therefore, differential diagnosis is important for proper management. LEARNING POINTS: Anaplastic thyroid cancer is the thyroid cancer with the worst prognosis and the highest mortality. The association of anaplastic thyroid cancer with thyrotoxicosis is rare, and a differential diagnosis is necessary to provide adequate treatment. Due to the current pandemic, in patients with thyrotoxicosis, it is important to rule out SARS-CoV-2 as an etiology. Anaplastic thyroid cancer, due to its aggressive behavior and rapid growth, can destroy thyroid follicular cells, generating preformed thyroid hormone release, being responsible for thyrotoxicosis.
RESUMEN
SUMMARY: Type B insulin resistance syndrome (TBIR) is a rare autoimmune disease caused by antibodies against the insulin receptor. It should be considered in patients with dysglycaemia and severe insulin resistance when other more common causes have been ruled out. We report a case of a 72-year-old male with a 4-year history of type 2 diabetes who presented with hypercatabolism, vitiligo, acanthosis nigricans, and hyperglycaemia resistant to massive doses of insulin (up to 1000 U/day). Detection of anti-insulin receptor antibodies confirmed TBIR. The patient received six pulses of methylprednisolone and daily treatment with cyclophosphamide for 6 months. Response to treatment was evident after the fourth pulse of methylprednisolone, as indicated by weight gain, decreased glycosylated haemoglobin and decreased requirement of exogenous insulin that was later discontinued due to episodes of hypoglycaemia. Remission was eventually achieved and the patient is currently asymptomatic, does not require insulin therapy, has normal glycaemia and is awaiting initiation of maintenance therapy with azathioprine. Thus, TBIR remitted without the use of rituximab. This case highlights the importance of diagnosis and treatment in a timely fashion, as well as the significance of clinical features, available laboratory findings and medication. Large controlled studies are required to standardise a therapeutic protocol, particularly in resource-constrained settings where access to rituximab is limited. LEARNING POINTS: Type B insulin resistance syndrome is a rare autoimmune disorder that should be considered in patients with dysglycaemia, severe insulin resistance and a concomitant autoimmune disease. Serological confirmation of antibodies against the insulin receptor is not necessary in all cases due to the high associated mortality without timely treatment. Although there is no standardised immunosuppressive treatment, a protocol containing rituximab, cyclophosphamide and steroids has shown a significant reduction in previously reported mortality rates. The present case, reports successful remission in an atypical patient using cyclophosphamide and methylprednisolone, which is an effective therapy in countries in which rituximab is not covered by health insurance. When there is improvement in the hypercatabolic phase, the insulin dose should be reduced and/or discontinued to prevent hypoglycaemia; a mild postprandial hyperglycaemic state should be acceptable.
RESUMEN
Se estudió retrospectivamente 79 pacientes con Enfermedad de Graves que recibieron yodo-131. Se encontró 62 mujeres y 17 hombres. La dosis de 1-131 administrada fue en promedio de 6.29 más menos 1.37mCi. Se observo S3 (67.1 por ciento) pacientes curados(hipotiroideos o eutiroideos) y 26(32.9 por ciento) no curados (hipertiroideos) posterior al radioyodo. Los pacientes curados recibieron mayor dosis de radioyodo (6.49 mCi) que los no curados (S.904 mCi) (p menor que O.OS). Además se observó que 3S (44.3 por ciento) pacientes pasaron a hipotiroidismo después de la primera dosis deradioyodo. De los pacientes curados el 43.5 por ciento suspendió metimazol mas de S días antes del tratamiento con radioyodo a diferencia del 6.S por ciento que lo suspendió menos de 5 días (p menor que 0.05). Las variables edad, tiempo de enfermedad, grado de bocio, índice de crooks, captación de yodo a las 2,5,24 y 48 horas, TSH, T4L y metimazol post yodo no presentaron asociación significativa con la evolución a hipotiroidismo, eutiroidismo o hipertiroidismo.
A descriptive retrospective study of 79 patients with Graves' Disease that received radioiodine 131. Of the 79 patients, 62 patients were women and 17 were men. The 1-131 dose administered was 6.29 more less 1.37mCi. After radioiodine treatment,S3(67.1 per cent) pacientes were cured (hypothyroids and euthyroids) and 26(32.9 per cent) patients were not cured (hyperthyroids). The patients cured received a bigger mean dose ofradioiodine (6.49 mCi) than the patients not cured (S.88 mCi) (p less than O.OS). Thirtyfive (44.3 per cent) patients developed hypothyroidism after the first radioiodine dose. Of the patients cured and who had received metimazol previously, 43.5 per cent patients stopped metimazol more than 5 days before receiving radioiodine while 6.5 per cent patients stopped metimazol less than 5 days (p less than 0.05).Finally, the variables age, time of disease, degree of goiter, crooks 'index, 2 hour and 24 hour radioiodine uptake , TSH, T4L and metimazol treatment did not display significant association with the clinical evolution.
