Diagnosis and Treatment > Signs and Symptoms

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Marcela Rodríguez Flores Obesity and Eating Disorders Clinic, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

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Ruth Carmina Cruz Soto Nutrition and Obesity Center, Centro Médico ABC

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Verónica Vázquez Velázquez Obesity and Eating Disorders Clinic, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

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Reina Ruth Soriano Cortés Obesity and Eating Disorders Clinic, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

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Carlos Aguilar Salinas Metabolic Diseases Research Unit, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico
Endocrinology and Metabolism Department, Instituto Tecnológico de Estudios Superiores de Monterrey Tec Salud, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Mexico City, Mexico

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Eduardo García García Obesity and Eating Disorders Clinic, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

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Summary

In patients with gastric bypass (GB), high glucose variability (GV) and hypoglycemia have been demonstrated, which could impact the metabolic status and eating behavior. We describe the glucose patterns determined through continuous glucose monitoring (CGM) in two patients with >5 years follow-up after GB and significant weight recovery, who reported hypoglycemic symptoms that interfered with daily activities, and their response to a nutritional and psycho-educative prescription. Case 1: A 40-year-old woman without pre-surgical type 2 diabetes (T2DM) and normal HbA1c, in whom CGM showed high GV and hypoglycemic episodes that did not correlate with the time of hypoglycemic symptoms. Her GV reduced after prescription of a diet with low glycemic index and modification of meal patterns. Case 2: A 48-year-old male with pre-surgical diagnosis of T2DM and current normal HbA1c, reported skipping meals. The CGM showed high GV, 15% of time in hypoglycemia and hyperglycemic spikes. After prescription of a low glycemic index diet, his GV increased and time in hypoglycemia decreased. Through the detailed self-monitoring needed for CGM, we discovered severe anxiety symptoms, consumption of simple carbohydrates and lack of meal structure. He was referred for more intensive psychological counseling. In conclusion, CGM can detect disorders in glucose homeostasis derived both from the mechanisms of bariatric surgery, as well as the patient’s behaviors and mental health, improving decision-making during follow-up.

Learning points:

  • High glycemic variability is frequent in patients operated with gastric bypass.

  • Diverse eating patterns, such as prolonged fasting and simple carbohydrate ingestion, and mental health disorders, including anxiety, can promote and be confused with worsened hypoglycemia.

  • CGM requires a detailed record of food ingested that can be accompanied by associated factors (circumstances, eating patterns, emotional symptoms). This allows the detection of particular behaviors and amount of dietary simple carbohydrates to guide recommendations provided within clinical care of these patients.

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Jose León Mengíbar Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Ismael Capel Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Teresa Bonfill Medical Oncology Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Isabel Mazarico Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Laia Casamitjana Espuña Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Assumpta Caixàs Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Mercedes Rigla Endocrinology and Nutrition Department, Parc Taulí University Hospital, Sabadell, Barcelona, Spain

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Summary

Durvalumab, a human immunoglobulin G1 kappa monoclonal antibody that blocks the interaction of programmed cell death ligand 1 (PD-L1) with the PD-1 and CD80 (B7.1) molecules, is increasingly used in advanced neoplasias. Durvalumab use is associated with increased immune-related adverse events. We report a case of a 55-year-old man who presented to our emergency room with hyperglycaemia after receiving durvalumab for urothelial high-grade non-muscle-invasive bladder cancer. On presentation, he had polyuria, polyphagia, nausea and vomiting, and laboratory test revealed diabetic ketoacidosis (DKA). Other than durvalumab, no precipitating factors were identified. Pre-durvalumab blood glucose was normal. The patient responded to treatment with intravenous fluids, insulin and electrolyte replacement. Simultaneously, he presented a thyroid hormone pattern that evolved in 10 weeks from subclinical hyperthyroidism (initially attributed to iodinated contrast used in a previous computerised tomography) to overt hyperthyroidism and then to severe primary hypothyroidism (TSH: 34.40 µU/mL, free thyroxine (FT4): <0.23 ng/dL and free tri-iodothyronine (FT3): 0.57 pg/mL). Replacement therapy with levothyroxine was initiated. Finally, he was tested positive for anti-glutamic acid decarboxylase (GAD65), anti-thyroglobulin (Tg) and antithyroid peroxidase (TPO) antibodies (Abs) and diagnosed with type 1 diabetes mellitus (DM) and silent thyroiditis caused by durvalumab. When durvalumab was stopped, he maintained the treatment of multiple daily insulin doses and levothyroxine. Clinicians need to be alerted about the development of endocrinopathies, such as DM, DKA and primary hypothyroidism in the patients receiving durvalumab.

Learning points:

  • Patients treated with anti-PD-L1 should be screened for the most common immune-related adverse events (irAEs).

  • Glucose levels and thyroid function should be monitored before and during the treatment.

  • Durvalumab is mainly associated with thyroid and endocrine pancreas dysfunction.

  • In the patients with significant autoimmune background, risk–benefit balance of antineoplastic immunotherapy should be accurately assessed.

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Verena Schwetz Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria

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Felix Aberer Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria

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Claudia Stiegler Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria

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Thomas R Pieber Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria

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Barbara Obermayer-Pietsch Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria

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Stefan Pilz Clinical Division of Endocrinology and Metabolism, Department of Internal Medicine, Medical University of Graz, Graz, Austria

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Summary

Cushing's syndrome (CS) due to ectopic ACTH production accounts for about 10% of all types of CS and is frequently associated with metabolic alkalosis. Treatment of CS involves surgical resection and/or medical therapy to control hypercortisolism. We present the case of an 80-year-old woman affected by CS due to an unknown cause. The patient had severe metabolic alkalosis with refractory hypokalemia. To treat the underlying CS, fluconazole was initiated due to unavailability of ketoconazole. In spite of markedly decreasing cortisol levels, metabolic alkalosis persisted. Treatment of metabolic alkalosis with acetazolamide was thus initiated and pH levels successfully lowered. This case report shows that hypercortisolism can be effectively treated with fluconazole in cases where ketoconazole is unavailable or not tolerated and that persistent severe metabolic alkalosis caused by glucocorticoid excess can be safely and successfully treated with acetazolamide.

Learning points

  • Hypercortisolism can be effectively treated with fluconazole where ketoconazole is unavailable or not tolerated.

  • Glucocorticoid excess can cause severe metabolic alkalosis.

  • Persistent severe metabolic alkalosis can be safely and successfully treated with acetazolamide.

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