Vomiting in Pregnancy
Tony Hollingworth in Differential Diagnosis in Obstetrics and Gynaecology: An A-Z, 2015
Vomiting and nausea are caused by physiological changes during pregnancy, and are nearly the most common symptoms of early pregnancy, second only to amenorrhoea. It affects up to 50–90 per cent of pregnant women. Hyperemesis gravidarum (HG) is a severe form of vomiting in pregnancy and effects one per cent of pregnant women. The features of HG include intractable vomiting associated with weight loss of more than five per cent of pre-pregnancy weight, ptyalism and associated spitting, dehydration, electrolyte imbalances, ketosis, and the need for admission to hospital. Gastroenteritis and food poisoning are common causes of vomiting in pregnancy. The onset of vomiting is abrupt and related to the ingestion of food. Pre-existing allergies to food products, such as eggs or nuts, can cause intractable vomiting after inadvertent ingestion. Gallstones may be commonly associated with pregnancy, and can cause both hyperacidity and vomiting.
Improvement of Cognitive Function in Patients with Alzheimer’s Disease using Ketogenic Diets
Abhai Kumar, Debasis Bagchi in Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
This chapter discusses the principles and impacts of ketogenic diets and medium-chain fatty acids on cognitive function. The completers achieved ketosis and their cognitive function was significantly improved compared to baseline despite reverting to baseline after the washout period. The subjects showed significant improvements on the immediate and delayed logical memory test and digit-symbol coding test compared to baseline. However, the effects of coconut oil supplementation on cognitive function in patients with AD have also been examined. Some clinical trials have demonstrated that classic and MCT ketogenic diets improve cognitive functions in patients with mild AD. The impacts of ketogenic diets on the cognitive function of patients with AD should also be analyzed by well-designed studies using large cohorts. Cognition is the mental act of acquiring knowledge and understanding through thoughts, experiences, and sensations. In other words, cognitive function includes thinking, reasoning, and remembering.
Multiple acyl CoA dehydrogenase deficiency/glutaric aciduria type II ethylmalonic-adipic aciduria
William L. Nyhan, Georg F. Hoffmann, Aida I. Al-Aqeel, Bruce A. Barshop in Atlas of Inherited Metabolic Diseases, 2020
Glutaric aciduria type II was first reported in 1976 by Przyrembel et al . in an infant with severe hypoglycemia and profound metabolic acidosis without ketosis. Patients with this form of the disorder have overwhelming illness in the neonatal period that has been uniformly fatal. The fundamental molecular defect is in the mitochondrial transport of electrons from the acylCoAs to ubiquinone of the main electron transport chain. An infant with classic multiple acyl CoA dehydrogenase deficiency (MADD) presents with life-threatening illness in the first days of life. Infants without dysmorphic features and abnormal organogenesis have also presented early in life with tachypnea, acidosis, hypoglycemia, and an abnormal odor. Many have had hepatomegaly. The diagnosis in all forms of MADD has usually been made on the basis of the unusual pattern of organic acid excretion in which a large number of organic acids are found in the urine.
Canagliflozin use in Type I diabetes mellitus
Published in Postgraduate Medicine, 2017
Peters et al documented the appearance of diabetic ketoacidosis without significant elevation of serum glucose in patients treated with Canagliflozin. They solicited patient reports from their practice and from other colleagues’ practices and identified nine patients, mainly with Type I Diabetes. Erondu et al evaluated the Canagliflozin development data base to describe the rate and appearance of ketoacidosis in the study patients. They found that in the research patients with Type 2 Diabetes, the rate of ketoacidosis in Canagliflozin patients was uncommon and similar to the reported rate in Type 2 patients not receiving Canagliflozin. Finally, Henry et al reported on a research program that added Canagliflozin onto insulin therapy in Type I patients, finding that there were only modest improvements in HgBA1 C levels and weight, while this therapy produced increased levels of ketosis and 6% rate of ketoacidosis in Canagliflozin patients. This information strongly suggests that Canagliflozin, and possibly the other SGLT-2 inhibitors, are not proper therapy for patients with Type I Diabetes.
Evaluation and management of ketosis-prone diabetes
Published in Expert Review of Endocrinology & Metabolism, 2019
Ruchi Gaba, Paras Mehta, Ashok Balasubramanyam
Introduction: Patients presenting with diabetic ketoacidosis (DKA) who lack the classic phenotype of autoimmune type 1 diabetes have become increasingly identified in recent decades. This has led to the recognition of heterogeneous syndromes of ‘ketosis-prone diabetes’ (KPD). Evaluation and optimal management of KPD differs from that of ‘typical’ type 1 or type 2 diabetes. Awareness of these differences and a systematic approach to diagnosis and treatment can improve glycemic control and prevent both acute and chronic complications of diabetes. Areas covered: This article reviews the Aß classification scheme (‘A’ for autoantibody status and ‘ß’ for beta cell functional reserve) which accurately delineates subgroups of KPD, and addresses the relevance of defining these subgroups for clinical outcomes and long-term insulin dependence. Subsequently, the detailed evaluation and management of KPD patients after their index DKA episode is described. Expert commentary: Among patients presenting with DKA, it is important to diagnose specific subgroups of KPD and not assume that they represent exclusively patients with autoimmune type 1 diabetes. The Aß classification is an accurate aid to diagnosis, and permits optimal management of the subgroups (e.g., insulin treatment for the ß- subgroups; follow-up testing and a range of treatment options for the ß+ subgroups).
The present and future treatment of pediatric type 2 diabetes
Published in Expert Review of Endocrinology & Metabolism, 2018
Michelle Anne Van Name, Cindy Guandalini, Amy Steffen, Anisha Patel, William Tamborlane
Introduction: Treatment of type 2 diabetes (T2D) in children and adolescents is particularly challenging. Metformin monotherapy is the standard initial treatment for youth with T2D, once metabolic control is restored with insulin in patients who present with ketosis and/or marked hyperglycemia. Insulin, the only other drug approved for use in youth with T2D, is also used as add-on therapy when patients fail metformin mono-therapy. Areas covered: In this paper, we will summarize the current use of both metformin and insulin in the treatment of pediatric type 2 diabetes, as well as comment on their limitations. Given the rapid progression of T2D in youth, there is also considerable interest in treating youth with new oral and injectable agents that have been approved for use in adults with T2D. The potential for improving clinical outcomes of each of the main classes of new drugs for the treatment of pediatric T2D will be summerized. Expert commentary: We will conclude by reviewing why phase 3 randomized clinical trials examining the safety and efficacy of these medications in the pediatric population have been difficult to complete and discuss a potential pathway to overcome these obstacles to regulatory approval for these drugs for adolescents with T2D.