From liver to hormones: The endocrine consequences of cirrhosis.

Hepatocrinology explores the intricate relationship between liver function and the endocrine system. Chronic liver diseases such as liver cirrhosis can cause endocrine disorders due to toxin accumulation and protein synthesis disruption. Despite its importance, assessing endocrine issues in cirrhotic patients is frequently neglected. This article provides a comprehensive review of the epidemiology, pathophysiology, diagnosis, and treatment of endocrine disturbances in liver cirrhosis. The review was conducted using the PubMed/Medline, EMBASE, and Scielo databases, encompassing 172 articles. Liver cirrhosis is associated with endocrine disturbances, including diabetes, hypoglycemia, sarcopenia, thyroid dysfunction, hypogonadotropic hypogonadism, bone disease, adrenal insufficiency, growth hormone dysfunction, and secondary hyperaldosteronism. The optimal tools for diagnosing diabetes and detecting hypoglycemia are the oral glucose tolerance test and continuous glucose monitoring system, respectively. Sarcopenia can be assessed through imaging and functional tests, while other endocrine disorders are evaluated using hormonal assays and imaging studies. Treatment options include metformin, glucagon-like peptide-1 analogs, sodium-glucose co-transporter-2 inhibitors, and insulin, which are effective and safe for diabetes control. Established standards are followed for managing hypoglycemia, and hormone replacement therapy is often necessary for other endocrine dysfunctions. Liver transplantation can address some of these problems.

[Clinical-epidemiological profile of patients with thyrotoxic periodic paralysis in two peruvian hospitals]. / Perfil clínico-epidemiológico de pacientes con parálisis periódica tirotóxica en dos hospitales peruanos.

Background: Thyrotoxic Periodic Paralysis (PPT) is an uncommon complication of hyperthyroidism, it is the most frequent cause of acute flaccid paralysis in adults. Material and methods: A retrospective observational study was carried out in 2 reference hospitals of the social security in Lima-Peru, which included 22 patients diagnosed with PPT during the period 2014-2021. Results: the average age at diagnosis was 35.77 ± 9.6 years, all of mixed race, in 82% of the patients the diagnosis of hyperthyroidism was established from this entity, the etiology in 95% was autoimmune (Graves-Basedow) except for one whose etiology was toxic multinodular goiter. The triggering event reported in 54% of patients was the intake of copious food high in carbohydrates, followed by exercise (27%), the most frequent presentation time was during the morning (41% of the cases), the main weakness pattern compromised lower limbs (45% paraplegia, 18% paraparesis), only 36% were diagnosed with PPT in their first episode of motor weakness. Conclusions: We consider that this condition should be suspected in any young male patient of any ethnicity with acute muscle weakness, associated with low serum potassium levels and symptoms of thyrotoxicosis, although its absence should not rule out the diagnosis. The precipitating factor should be identified as much as possible and initial therapy with propanolol with or without intravenous or oral potassium replacement should be established, with adequate subsequent monitoring to minimize the risk of rebound hyperkalemia.

Introducción: la paralisis periodica tirotóxica (PPT) es una complicación poco común del hipertiroidismo, corresponde la causa más frecuente de parálisis aguda flácida del adulto. Material y métodos: se realizó un estudio observacional retrospectivo en 2 hospitales referenciales del seguro social en Lima-Perú, que incluyo a 22 pacientes (21 hombres, 1 mujer) diagnosticados con PPT durante el periodo 2014-2021. Resultados: la edad promedio al diagnóstico fue de 35.77 ± 9.6 años, todos de raza mestiza, en 82% de los pacientes el diagnostico de hipertiroidismo fue establecido a partir de esta entidad, la etiología en el 95% fue autoinmune (enfermedad de Graves-Basedow) excepto uno cuya etiología fue bocio multinodular tóxico. El evento desencadenante reportado en 54% de pacientes fue la ingesta de comida copiosa alta en carbohidratos, seguido del ejercicio (27%), el horario más frecuente de presentación fue durante la mañana ( 41% de los casos), el patrón de debilidad principal comprometió miembros inferiores(45% paraplejia, 18% paraparesia), solo 36% fue diagnosticado de PPT en su primer episodio de debilidad motora. Conclusiones: consideramos que se debe sospechar esta condición en cualquier paciente varón joven de cualquier etnia con debilidad muscular aguda, asociado a niveles séricos bajos de potasio y síntomas de tirotoxicosis, aunque su ausencia no debe descartar el diagnostico. Se debe identificar en lo posible el factor precipitante e instaurar terapia inicial con propanolol con o sin reemplazo de potasio endovenoso u oral, con monitoreo posterior adecuado que minimice el riesgo de hiperpotasemia de rebote.

New-onset thyrotoxicosis in a patient with anaplastic thyroid carcinoma: a diagnostic challenge.

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.

Successful remission of type B insulin resistance syndrome without rituximab in an elderly male.

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.