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.

Drug-induced hypothyroidism in tuberculosis.

INTRODUCTION: Adverse reactions to tuberculosis treatment can impact patient adherence and prognosis. Hypothyroidism is a frequent adverse reaction caused using ethionamide, prothionamide, and para-aminosalicylic acid and is often underdiagnosed. AREAS COVERED: We searched Scielo, Scopus, and EMBASE databases, including 67 articles. Antitubercular drug-induced hypothyroidism has a prevalence of 17%. It occurs after 2 to 3 months of treatment and resolves within 4 to 6 weeks after discontinuation. It is postulated to result from the inhibition of thyroperoxidase function, blocking thyroid hormone synthesis. Symptoms are nonspecific, necessitating individualized thyroid-stimulating hormone measurement for detection. Specific guidelines for management are lacking, but initiation of treatment with levothyroxine, as is customary for primary hypothyroidism, is recommended. Discontinuation of antitubercular drugs is discouraged, as it may lead to unfavorable consequences. EXPERT OPINION: Antitubercular drug-induced hypothyroidism is more common than previously thought, affecting one in six MDR-TB patients. Despite diagnostic and treatment recommendations, implementation is hindered in low-income countries due to the lack of certified laboratories. New drugs for tuberculosis treatment may affect thyroid function, requiring vigilant monitoring for complications, including hypothyroidism.

Ifosfamide-induced nephrotoxicity in oncological patients.

INTRODUCTION: Ifosfamide is an alkylating chemotherapeutic agent used in the treatment of various neoplasms. Its main adverse effects include renal damage. AREAS COVERED: A comprehensive review was conducted, including 100 articles from the Scielo, Scopus, and EMBASE databases. Ifosfamide-induced nephrotoxicity is attributed to its toxic metabolites, such as acrolein and chloroacetaldehyde, which cause mitochondrial damage and oxidative stress in renal tubular cells. Literature review found a 29-year average age with no gender predominance and a mortality of 13%. Currently, no fully effective strategy exists for preventing ifosfamide-induced nephrotoxicity; however, hydration, forced diuresis, and other interventions are employed to limit renal damage. Long-term renal function monitoring is essential for patients treated with ifosfamide. EXPERT OPINION: Ifosfamide remains essential in neoplasm treatment, but nephrotoxicity, often compounded by coadministered drugs, poses diagnostic challenges. Preventive strategies are lacking, necessitating further research. Identifying timely risk factors can mitigate renal damage, and a multidisciplinary approach manages established nephrotoxicity. Emerging therapies may reduce ifosfamide induced nephrotoxicity.

Ifosfamide is a type of chemotherapy used to treat different types of cancers. However, one of its main side effects is kidney damage. Researchers reviewed 100 articles from medical databases to understand how ifosfamide affects the kidneys. The kidney damage is caused by harmful substances produced when ifosfamide is broken down in the body. These substances can harm the cells in the kidneys. Studies have shown that 13% of the patients treated with ifosfamide can die. Currently, there is no perfect way to prevent kidney damage from ifosfamide, but doctors try to protect the kidneys by giving patients plenty of fluids and using other treatments, so it's important for patients who receive ifosfamide to have their kidney function checked regularly. Although ifosfamide is effective against cancer, its potential kidney side effects should be carefully considered by doctors when deciding on the best treatment for each patient.

A comprehensive review of genetic causes of obesity.

BACKGROUND: Obesity is a multifactorial chronic disease with a high, increasing worldwide prevalence. Genetic causes account for 7% of the cases in children with extreme obesity. DATA SOURCES: This narrative review was conducted by searching for papers published in the PubMed/MEDLINE, Embase and SciELO databases and included 161 articles. The search used the following search terms: "obesity", "obesity and genetics", "leptin", "Prader-Willi syndrome", and "melanocortins". The types of studies included were systematic reviews, clinical trials, prospective cohort studies, cross-sectional and prospective studies, narrative reviews, and case reports. RESULTS: The leptin-melanocortin pathway is primarily responsible for the regulation of appetite and body weight. However, several important aspects of the pathophysiology of obesity remain unknown. Genetic causes of obesity can be grouped into syndromic, monogenic, and polygenic causes and should be assessed in children with extreme obesity before the age of 5 years, hyperphagia, or a family history of extreme obesity. A microarray study, an analysis of the melanocortin type 4 receptor gene mutations and leptin levels should be performed for this purpose. There are three therapeutic levels: lifestyle modifications, pharmacological treatment, and bariatric surgery. CONCLUSIONS: Genetic study technologies are in constant development; however, we are still far from having a personalized approach to genetic causes of obesity. A significant proportion of the affected individuals are associated with genetic causes; however, there are still barriers to its approach, as it continues to be underdiagnosed. Video Abstract (MP4 1041807 KB).

Thyroid dysfunction and female infertility. A comprehensive review.

INTRODUCTION: Female infertility is defined as the inability to achieve pregnancy following one year of consistent, unprotected sexual intercourse. Among the various endocrine factors contributing to this complex issue, thyroid dysfunction assumes a pivotal and noteworthy role. METHODS: A narrative review, encompassing 134 articles up to 2023, was conducted utilizing the PubMed/Medline, EMBASE, and Scielo databases. The primary focus of this review was to investigate the effects of thyroid dysfunction on female infertility. RESULTS: Thyroid disorders exert a significant influence on folliculogenesis, fertilization, and implantation processes. Thyroid autoimmunity, although associated with diminished ovarian reserve, does not typically necessitate levothyroxine therapy. On the other hand, both subclinical and overt hypothyroidism often require levothyroxine treatment to enhance fertility and optimize obstetric outcomes. Hyperthyroidism warrants prompt intervention due to its heightened risk of miscarriage. Furthermore, thyroid dysfunction exerts notable effects on assisted reproductive technologies, underscoring the importance of achieving euthyroidism prior to ovarian stimulation. CONCLUSION: Women presenting with thyroid dysfunction must undergo meticulous and individualized assessments since fertility outcomes, whether achieved through natural conception or assisted reproductive technologies, can be significantly influenced by thyroid-related factors.

Refractory Hypothyroidism: Unraveling the Complexities of Diagnosis and Management.

INTRODUCTION: Refractory hypothyroidism (RH) represents a challenge in the diagnosis and treatment within the field of thyroidology. It is defined as the inability to achieve disease control despite using levothyroxine (LT4) doses of 1.9 µg/kg/d or higher. METHODS: A comprehensive review, encompassing 103 articles, was conducted using the Scielo, Scopus, and EMBASE databases, providing an approach to evaluation and diagnosis of this condition. RESULTS: LT4 disintegrates and dissolves within an acidic gastric environment before being absorbed in the jejunum and ileum. It then extensively binds to serum transporter proteins and undergoes deiodination to yield tri-iodothyronine, the biologically active hormone. There are various nonpathological causes of RH, such as noncompliance with treatment, changes in the brand of LT4, food and drug interferences, as well as pregnancy. Pathological causes include lactose intolerance, Helicobacter pylori infection, giardiasis, among others. The diagnosis of RH involves conducting a thorough medical history and requesting relevant laboratory tests to rule out causes of treatment resistance. The LT4 absorption test allows for the identification of cases of malabsorption. The treatment of RH involves identifying and addressing the underlying causes of noncompliance or malabsorption. In cases of pseudomalabsorption, supervised and weekly administration of LT4 may be considered. DISCUSSION: Early recognition of RH and correction of its underlying cause are of utmost importance, as this avoids the use of excessive doses of LT4 and prevents cardiovascular and bone complications associated with this condition.

Endocrine factors associated with infertility in women: an updated review.

INTRODUCTION: Infertility is defined as the inability to conceive after unprotected sexual intercourse for at least 12 consecutive months. Our objective is to present an updated narrative review on the endocrine causes of infertility in women. AREAS COVERED: A comprehensive review was conducted using Scielo, Scopus, and EMBASE databases, comprising 245 articles. The pathophysiology of infertility in women was described, including endocrinopathies such as hypothalamic amenorrhea, hyperprolactinemia, polycystic ovary syndrome, primary ovarian insufficiency, obesity, thyroid dysfunction, and adrenal disorders. The diagnostic approach was outlined, emphasizing the necessity of hormonal studies and ovarian response assessments. Additionally, the treatment plan was presented, commencing with non-pharmacological interventions, encompassing the adoption of a Mediterranean diet, vitamin supplementation, moderate exercise, and maintaining a healthy weight. Subsequently, pharmacological treatment was discussed, focusing on the management of associated endocrine disorders and ovulatory dysfunction. EXPERT OPINION: This comprehensive review highlights the impact of endocrine disorders on fertility in women, providing diagnostic and therapeutic algorithms. Despite remaining knowledge gaps that hinder more effective treatments, ongoing research and advancements show promise for improved fertility success rates within the next five years. Enhanced comprehension of the pathophysiology behind endocrine causes and the progress in genetic research will facilitate the delivery of personalized treatments, thus enhancing fertility rates.

Cushing disease in pediatrics: an update.

Cushing disease (CD) is the main cause of endogenous Cushing syndrome (CS) and is produced by an adrenocorticotropic hormone (ACTH)-producing pituitary adenoma. Its relevance in pediatrics is due to the retardation of both growth and developmental processes because of hypercortisolism. In childhood, the main features of CS are facial changes, rapid or exaggerated weight gain, hirsutism, virilization, and acne. Endogenous hypercortisolism should be established after exogenous CS has been ruled out based on 24-hour urinary free cortisol, midnight serum or salivary cortisol, and dexamethasone suppression test; after that, ACTH dependence should be established. The diagnosis should be confirmed by pathology. The goal of treatment is to normalize cortisol level and reverse the signs and symptoms. Treatment options include surgery, medication, radiotherapy, or combined therapy. CD represents a challenge for physicians owing to its multiple associated conditions involving growth and pubertal development; thus, it is important to achieve an early diagnosis and treatment in order to control hypercortisolism and improve the prognosis. Its rarity in pediatric patients has led physicians to have limited experience in its management. The objective of this narrative review is to summarize the current knowledge about the pathophysiology, diagnosis, and treatment of CD in the pediatric population.

Thyrotoxic Cardiomyopathy: State of the Art.

Thyroid hormones, mainly triiodothyronine, have genomic and non-genomic effects on cardiomyocytes related to the contractile function of the heart. Thyrotoxicosis, which is the set of signs and symptoms derived from the excess of circulating thyroid hormones, leads to increased cardiac output and decreased systemic vascular resistance, increasing the volume of circulating blood and causing systolic hypertension. In addition, the shortening of the refractory period of cardiomyocytes produces sinus tachycardia and atrial fibrillation. This leads to heart failure. Approximately 1% of patients with thyrotoxicosis develop thyrotoxic cardiomyopathy, a rare but potentially fatal form of dilated cardiomyopathy. Thyrotoxic cardiomyopathy represents a diagnosis of exclusion, and prompt identification is crucial as it is a reversible cause of heart failure, and heart function can be recovered after achieving a euthyroid state using antithyroid drugs. Radioactive iodine therapy and surgery are not the best initial therapeutic approach. Moreover, it is important to manage cardiovascular symptoms, for which beta blockers are the first-line therapeutic option.

[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.

Pleuropericardial compromise associated with Graves' disease - a diagnostic challenge.

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Liothyronine use in primary hypothyroidism - current concepts.

Hypothyroidism is an endocrine disorder whose management raises many challenges in clinical practice. Its standard treatment is levothyroxine (LT4). The goal of the treatment is to normalize signs and symptoms, as well as to achieve thyroid-stimulating hormone (TSH) concentrations within the reference range, on an individual basis. It is known that 5-10% of hypothyroid patients remain symptomatic, despite achieving the target TSH levels, which, in turn, affects their quality of life. After ruling out other causes of non-thyroid origin for this persistence, it is suggested that these patients could benefit from the use of liothyronine (LT3), added to LT4, especially if polymorphism of the deiodinase 2 (D2) genes is documented. There exist a variety of LT3 preparations, whose concentrations vary from 5 to 50 ug, with the recommended LT4/LT3 ratio of 13:1-20:1. The goals of combination therapy should be to achieve a physiological ratio of free triiodothyronine/free thyroxine (FT3/FT4) and non-suppression of TSH. Because there is currently no guide that makes evidence-based recommendations on the use of LT3 in primary hypothyroidism, more clinical studies are needed to be able to identify hypothyroid patients who may benefit from the use of LT3, by identifying new biomarkers.

Therapeutic challenge: Unusual coexistence of idiopathic central diabetes insipidus and diabetes mellitus in a male with vitiligo.

BACKGROUND: Idiopathic central diabetes insipidus (DI) is a rare endocrine disorder that results from total or partial deficiency of vasopressin secretion. It is idiopathic when the cause is unknown, but in many cases, is associated with autoimmune disorders. CASE PRESENTATION: We present the case of a 44-year-old male with vitiligo and a family history of diabetes mellitus and thyroid disease. The patient presented with polydipsia and polyuria greater than 8 L/day. After water deprivation test, the patient was diagnosed with partial central diabetes insipidus. Contrast-enhanced pituitary magnetic resonance imaging showed decreased brightness of the neurohypophysis and normal thickness of the pituitary stalk. Because desmopressin was not initially available, the patient was managed with chlorpropamide, carbamazepine, and hydrochlorothiazide, and afterwards substituted. During his outpatient checkups, he presented many episodes of polyuria, the last after 13 years, with polyuria of up to 15 L associated with weight loss, and abnormal blood glucose levels; anti-GAD 65 and IA-2 antibodies were negative. He was subsequently diagnosed with diabetes mellitus and received metformin and insulin; this latter was suspended in subsequent check-ups due to hypoglycemic episodes. CONCLUSION: We highlight the importance of treatment and adequate control of these pathologies, since they share similar clinical manifestations, can easily have electrolyte imbalance and represent a challenge for endocrinologists and internists.

Late Diagnosis of Partial Androgen Insensitivity Syndrome in a Peruvian Child.

Disorders of sexual differentiation are congenital pathologies characterized by atypical development of genetic, gonadal, or phenotypic sex. These are caused by the alteration of any primordial phases of sexual development and may be evident at birth or in the later stage of life. Here, we present the case of a nine-year-old Peruvian school patient who has female gender assigned at birth, has no contributory antecedents and was found to have clitoromegaly and hypospadia on physical examination. In the blood tests, anti-Müllerian hormone and testosterone were found, and 46 XY karyotype and sex-determining region Y (SRY) genes were present. On abdominal ultrasound, testicles were found in the inguinal canals. The human chorionic gonadotropin (HCG) stimulation test was conducted, which allowed us to rule out defects in testosterone biosynthesis and enzyme defects in dihydrotestosterone production; the main suspected diagnosis was partial androgen insensitivity syndrome (PAIS). A multidisciplinary medical meeting was held, accepting the patient's desire to opt for the male gender, after acceptance by the parents. Thus, the patient underwent bilateral orchidopexy and genitoplasty. He is currently receiving therapy with testosterone, with an adequate response to the treatment and the molecular study confirmed the androgen-receptor gene mutation. In conclusion, we highlight the importance of a timely multidisciplinary diagnosis and management of disorders of sexual differentiation to avoid premature gender assignment and major social and family repercussions that it implies.

Surgical Remission of Diabetes in a Patient With Mutation of RET Proto-Oncogene.

OBJECTIVE: In pheochromocytomas, accelerated catecholamine production can cause secondary diabetes. The gene responsible for multiple endocrine neoplasia type 2 (MEN2)-related pheochromocytomas is the RET proto-oncogene. The objective of this report is to describe a unique case of surgical remission of misdiagnosed type 2 diabetes mellitus (T2DM) in a woman with bilateral pheochromocytoma and RET proto-oncogene mutation. METHODS: Clinical examination, urinary metanephrine level, triple-phase abdominal computed tomography (CT) with adrenal protocol, positron emission tomography with 18F-fluorodeoxyglucose integrated with CT, surgical pathology, and genetic testing were performed. RESULTS: A 46-year-old woman with a 5-year history of apparent T2DM complicated by neuropathy, without a contributory family history, presented with occasional headaches, weight loss, and abdominal pain. A 24-hour urinary metanephrine of 5 mg (reference range, 0.05-1 mg) was found. Abdominal CT showed bilateral adrenal masses with <60% washout. Positron emission tomography with 18F-fluorodeoxyglucose integrated with CT showed a left solid-cystic lesion with low metabolic activity and a right nodular lesion with a higher metabolic activity, which was conclusive of bilateral pheochromocytoma. The remission of diabetes was achieved 1 year after a bilateral adrenalectomy. In addition, a multinodular goiter was found, and a fine-needle aspiration biopsy confirmed that it was a medullary thyroid carcinoma. A heterozygous pathogenic variant of the RET proto-oncogene was found and MEN2A was confirmed. CONCLUSION: This is the first report of a patient with a RET proto-oncogene mutation experiencing remission of diabetes after surgical resection of bilateral pheochromocytomas. Timely recognition and treatment of the underlying condition are important to potentially achieve diabetes remission and prevent its long-term complications.

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.

Diabetic gastroenteropathy: An underdiagnosed complication.

This article is an extensive review that provides an update on the pathophysiology, symptoms, diagnosis, and treatment of diabetic gastroenteropathy. There is no reported prevalence, but it has been described that patients with type 1 diabetes have a cumulative incidence at 10 years of 5.2%, and type 2 patients, 1%. Also, in the group of type 1 diabetes, it has been observed that women are more likely to present this condition (5.8% vs 3.5%). Many factors are associate with its development (e.g., hyperglycemia, vagal dysfunction, loss of expression of neural nitric oxide synthase in the myenteric plexus, alterations in the Cajal interstitial cell network, and oxidative stress). Gastrointestinal discomfort could be perceived 70% higher in diabetic patients, describing that 25% of diabetic patients experience gastrointestinal symptoms. Diabetic enteropathy could affect any portion of the gastrointestinal tract, but esophageal alterations were described in more than 60% of diabetic patients, also 60% of them present constipation, and 20%, diarrhea. Gastric emptying scintigraphy is useful to evaluate gastroparesis, therefore, gastric retention of more than 60% at 2 h has a sensitivity of 100% and specificity of 20% for diagnosis; however, other studies such as breath tests, with a sensitivity of 89% and a specificity of 80%, or the endoscopic capsule contribute to the diagnosis. There is no cure; however, management must be multidisciplinary, focused on slowing the progression of diabetic gastroenteropathy, reducing symptoms, and restoring function; that includes nutritional recommendation, maintain glucose levels kept below 180 mg/dL, use of prokinetics, anti-emetics; nowadays, it has been special interest in surgical treatment, such as pyloroplasty, also gastric electrical stimulation appears to be another alternative.