[Low-dose cinacalcet reduces serum calcium in patients with primary hyperparathyroidism not eligible for surgery]. / Dosis bajas de cinacalcet reducen el calcio sérico en pacientes con hiperparatiroidismo primario no subsidiario de tratamiento quirúrgico.

We present our experience with low-dose cinacalcet to normalize serum calcium in patients with primary hyperparathyroidism (PHPT) not eligible for surgery. We analyzed the impact of this drug on various parameters of calcium-phosphorus metabolism and its tolerability profile. We recruited 17 patients diagnosed with PHPT who had hypercalcemia and also met one or more of the following inclusion criteria: elevated risk for parathyroidectomy, persistent/recurrent PHPT after previous parathyroid surgery or refusal to undergo surgery. The starting dose of cinacalcet was 30 or 60 mg/day, which was adjusted depending on the degree of calcemia reduction and tolerance to the drug. We observed a reduction in serum calcium that was already evident in the first post-treatment test. Appropriate dose adjustment was performed when required and normal serum calcium levels were achieved in most patients, remaining stable during follow-up. Parathyroid hormone was reduced but not normalized in most patients. Calciuria decreased while serum phosphate and alkaline phosphatase levels increased. Cinacalcet tolerance was generally good at the doses used. The most common adverse effects were weakness, dizziness and asthenia, leading to treatment withdrawal in only one patient. We conclude that low-dose cinacalcet reduces serum calcium efficiently, normalizes calcium levels in most patients with PHPT not eligible for surgical treatment and has a good tolerability profile.

Dosis bajas de cinacalcet reducen el calcio sérico en pacientes con hiperparatiroidismo primario no subsidiario de tratamiento quirúrgico / Low-dose cinacalcet reduces serum calcium in patients with primary hyperparathyroidism not eligible for surgery

Presentamos nuestra experiencia con cinacalcet a dosis bajas, en pacientes con hiperparatiroidismo primario (HPTP) no subsidiario de tratamiento quirúrgico con el objetivo principal de normalizar la calcemia. Analizamos el impacto del fármaco sobre diversos parámetros del metabolismo calcio-fósforo y su perfil de tolerancia. Reclutamos un total de 17 pacientes diagnosticados de HPTP que presentaban hipercalcemia y que reunían además alguno de los siguientes criterios de inclusión: riesgo elevado para paratiroidectomía, HPTP persistente/recurrente tras cirugía paratiroidea previa o rechazo del paciente a la intervención quirúrgica. La dosis inicial de cinacalcet fue de 30 o 60mg/día, la cual se ajustó en función del grado de reducción de la calcemia y la tolerancia al fármaco. Observamos una reducción del calcio sérico que ya resultaba evidente en el primer control postratamiento. Tras el ajuste pertinente de dosis cuando fue preciso, se consiguió normalizar la calcemia en una mayoría de los pacientes, la cual se mantuvo estable a lo largo del seguimiento. La PTH se redujo, aunque no se normalizó en la mayor parte de los pacientes. La calciuria descendió mientras que la fosforemia y la fosfatasa alcalina sérica aumentaron. La tolerancia a cinacalcet fue buena en general a las dosis utilizadas. Los efectos secundarios más frecuentes fueron debilidad, mareos y astenia, y solamente en un paciente motivaron la suspensión del tratamiento. Concluimos que cinacalcet a dosis bajas reduce la calcemia de forma eficaz y consigue una normalización de la misma en una mayoría de pacientes con HPTP no subsidiarios de tratamiento quirúrgico con un buen perfil de tolerancia al fármaco (AU)

We present our experience with low-dose cinacalcet to normalize serum calcium in patients with primary hyperparathyroidism (PHPT) not eligible for surgery. We analyzed the impact of this drug on various parameters of calcium-phosphorus metabolism and its tolerability profile We recruited 17 patients diagnosed with PHPT who had hypercalcemia and also met one or more of the following inclusion criteria: elevated risk for parathyroidectomy, persistent/recurrent PHPT after previous parathyroid surgery or refusal to undergo surgery. The starting dose of cinacalcet was 30 or 60mg/day, which was adjusted depending on the degree of calcemia reduction and tolerance to the drug.We observed a reduction in serum calcium that was already evident in the first post-treatment test. Appropriate dose adjustment was performed when required and normal serum calcium levels were achieved in most patients, remaining stable during follow-up. Parathyroid hormone was reduced but not normalized in most patients. Calciuria decreased while serum phosphate and alkaline phosphatase levels increased. Cinacalcet tolerance was generally good at the doses used. The most common adverse effects were weakness, dizziness and asthenia, leading to treatment withdrawal in only one patient. We conclude that low-dose cinacalcet reduces serum calcium efficiently, normalizes calcium levels in most patients with PHPT not eligible for surgical treatment and has a good tolerability profile (AU)

99MTc-sestamibi as sole technique in selection of primary hyperparathyroidism patients for unilateral neck exploration.

BACKGROUND: Unilateral neck exploration (UNE) is becoming the procedure of choice for treatment of primary hyperparathyroidism (PHPT). The aim of this study was to evaluate the role of (99m)Tc-sestamibi (MIBI) parathyroid scintigraphy as the sole technique in selecting patients for UNE. METHOD: We selected 136 consecutive PHPT patients who had only 1 solitary uptake at a MIBI were for UNE. The technique was a single dual-phase using MIBI and a subtraction technique with (99m)Tc-pertechnetate. Imaging data were correlated with surgical results. RESULTS: In 3 cases, the sestamibi scan was falsely positive, 1 had a contralateral location relative to the uptake, and 2 had multiglandular hyperplasia. Overall, the positive predictive value (PPV) of MIBI for detecting a solitary parathyroid adenoma in patients with 1 solitary uptake was 97.8. Sixteen patients (12%) had evidence of multinodular goiter. Overall, the PPV of MIBI was 98.4% (2 false positive among 120 cases) in patients with no multinodular thyroid disease (MNG) and 93.7% (1 false negative among 16 cases) in patients with MNG. The mean duration of the surgical procedure was 34.17 minutes. Mean hospitalization was 0.6 days. Conversion to bilateral neck exploration was performed in 5 patients. After a period of follow-up of 40 months (range, 6-72 months), the cure rate was 98%. CONCLUSION: Patients with PHPT and unequivocally positive preoperative (99m)Tc-sestamibi can safely be managed with UNE without additional localizing techniques.

Fibrosis quística, bocio e hipertiroidismo / Cystic fibrosis, goiter and hyperthyroidism

El aumento de tamaño de la glándula tiroidea por depósito de material amiloide, conocido como bocio amiloide, es una rara entidad clínica. En la mayoría de los casos publicados, los pacientes presentan una función tiroidea normal; menos frecuente es la presencia de hipofunción tiroidea, y aún más infrecuente la asociación con hiperfunción tiroidea. Comunicamos un caso de bocio amiloide e hipertiroidismo primario, secundario a amiloidosis sistémica, en un paciente con fibrosis quística, sin síntomas compresivos y clínica de hiperfunción tiroidea. A continuación, realizamos una breve revisión de este proceso y su tratamiento (AU)

Thyroid gland enlargement due to amyloid infiltration, known as amyloid goitre, is a rare clinic entity. In most reported cases, patients' thyroid function is normal; less frequent is the presentation with thyroid hypofunction, and exceedingly rare is its association with thyroid hyperfunction. We hereby report a case of amyloid goitre and primary hyperthyroidism, due to systemic amyloidosis, in a patient with cystic fibrosis, without compressive symptoms. Then, we provide a brief review of this entity and its therapeutic management (AU)

[New approaches in obesity treatment: the gastrointestinal tract as an endocrine organ]. / Nuevas perspectivas en el tratamiento de la obesidad: el aparato digestivo como órgano endocrino.

The gastrointestinal tract, besides digesting and processing nutrients, is now regarded as an endocrine organ able to modulate appetite, satiety, and carbohydrate metabolism. Several enteroendocrine cells produce numerous peptides codifying either orexigenic (ghrelin, orexins) or anorexigenic signals (pancreatic polypeptide, peptide YY, cholecystokinin, amylin, bombesin homologs, apolipoprotein A-IV, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, oxyntomodulin), which interact in a complex network with other peripheral signals of energy balance and with different neuropeptides involved in the central control of appetite and energy homeostasis. The growing knowledge of the actions of these gastrointestinal peptides on appetite regulation and carbohydrate metabolism, and subsequent synthesis of analogs, particularly those derived from amylin and incretins, herald a new era in the therapy of 2 closely related diseases, obesity and type 2 diabetes mellitus.

Nuevas perspectivas en el tratamiento de la obesidad: el aparato digestivo como órgano endocrino / New approaches in obesity treatment: the gastrointestinal tract as an endocrine organ

El aparato digestivo, más allá de la digestión y absorción de nutrientes, es un órgano endocrino modulador del apetito, la saciedad y el metabolismo hidrocarbonado mediante la producción, por parte de diversas células enteroendocrinas, de numerosos péptidos codificadores de señales orexígenas (ghrelina, orexinas) o anorexígenas (polipéptido pancreático, péptido YY, colecistoquinina, amilina, homólogos de bombesina, apolipoproteína A-IV, polipéptido insulinotrópico dependiente de la glucosa, péptido similar al glucagón tipo 1, oxintomodulina). El conocimiento de las acciones reguladoras del apetito y el metabolismo energético de estos péptidos, a través de su compleja interacción con otras señales periféricas (leptina, adiponectina) y con distintos neuropéptidos centrales, así como la síntesis de análogos, en especial los derivados de la amilina e incretinas, proporciona nuevos enfoques terapéuticos para 2 trastornos íntimamente relacionados: la obesidad y la diabetes mellitus tipo 2

The gastrointestinal tract, besides digesting and processing nutrients, is now regarded as an endocrine organ able to modulate appetite, satiety, and carbohydrate metabolism. Several enteroendocrine cells produce numerous peptides codifying either orexigenic (ghrelin, orexins) or anorexigenic signals (pancreatic polypeptide, peptide YY, cholecystokinin, amylin, bombesin homologs, apolipoprotein A-IV, glucose-dependent insulinotropic polypeptide, glucagon-like peptide 1, oxyntomodulin), which interact in a complex network with other peripheral signals of energy balance and with different neuropeptides involved in the central control of appetite and energy homeostasis. The growing knowledge of the actions of these gastrointestinal peptides on appetite regulation and carbohydrate metabolism, and subsequent synthesis of analogs, particularly those derived from amylin and incretins, herald a new era in the therapy of 2 closely related diseases, obesity and type 2 diabetes mellitus

Dilated cardiomyopathy as a presenting feature of Cushing's syndrome.

Patients with Cushing's syndrome can rarely present with systolic heart failure as the mainstay feature. In these patients, heart failure is usually secondary to left ventricular hypertrophy (LVH) and not to dilated cardiopathy. We herewith report a patient with Cushing's syndrome, who presented with systolic ventricular failure secondary to dilated myocardiopathy and signs of proximal myopathy as predominant features. All symptoms regressed after successful treatment.

Acute pancreatitis, hepatic cholestasis, and erythema nodosum induced by carbimazole treatment for Graves' disease.

A 33-year old female was diagnosed as Graves' disease and started on carbimazole. One month later when she was already euthyroid only on carbimazole therapy, she developed acute pancreatitis associated with mild cholestatic hepatitis and erythema nodosum. Carbimazole therapy was interrupted, pancreatic and liver function gradually improved and became normalized two weeks later. Other potential etiological causes of acute pancreatitis, hepatitis and erythema nodosum were excluded. Rechallenge with a single dose of carbimazole led to a new episode of acute pancreatitis and cholestatic hepatitis one day later. The appearance of different hypersensitivity reactions including pancreatitis, hepatitis and erythema nodosum, together with the observation that the interval between drug intake and onset of symptoms became shorter with repeated exposure to carbimazole, point to an immune-mediated mechanism. Carbimazole has to be added to the list of drugs capable of inducing acute pancreatitis, and should be emphasized the need to discontinue this medication as soon as there is evidence of pancreatic dysfunction.