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Pathophysiology of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Neonatal diabetes affects infants and their ability to produce or use insulin. It is a monogenic condition that is controlled by a single gene. Neonatal diabetes develops within the first 6 months of life. Since there is not enough insulin produced, the glucose levels increase. This rare disease only occurs in 1 of every 100,000–500,000 live births. It can be mistaken for type 1 diabetes. There are two types of neonatal diabetes. The permanent form is lifelong, while the transient form disappears during infancy. However, the transient form can recur later in life. Onset of neonatal diabetes can be linked to abnormal pancreatic development and the speeds of beta cell dysfunction. The condition can be genetically linked between patients and offspring. Symptoms include polydipsia, polyuria, dehydration, dry mouth, tiredness, and dark-colored urine. When dehydration is severe, signs include hypotension, sunken eyes, weak pulse, tachycardia, and fatigue. Ketoacidosis develops if the disease is severe. Related to neonatal diabetes is intrauterine growth restriction, with the fetus not growing to reach a normal weight within the womb. After birth, the infant may have hyperglycemia or hypoglycemia. Permanent and transient neonatal diabetes are both genetically inherited from the mother or father.
Endocrine Disorders
Published in Praveen S. Goday, Cassandra L. S. Walia, Pediatric Nutrition for Dietitians, 2022
Lisa Spence, Nana Adwoa Gletsu Miller, Tamara S. Hannon
Diabetes insipidus is rare in children but can occur due to a genetic abnormality or secondary to hypothalamic or pituitary tumors or following neurosurgery. Unlike diabetes mellitus, blood glucose concentrations are normal in diabetes insipidus. Rather, common symptoms for both conditions are frequent urination (polyuria) and constant thirst (polydipsia). In the case of diabetes insipidus, the urine is dilute and odorless while for diabetes mellitus, the urine is concentrated with glucose. The etiology of diabetes insipidus involves disruption of hormonal regulation of water balance, most often due to abnormal production or function of vasopressin. Vasopressin (also called anti-diuretic hormone) is made in the hypothalamus and its function is to increase fluid balance by reducing the excretion of water from the kidney. Thus, a main complication of diabetes insipidus is dehydration that results from water loss through excessive urination. Treatment of diabetes insipidus aims to address the primary cause, whether a tumor or hormonal. Treatment also focuses on drinking sufficient water to avoid dehydration.
Investigation of Pituitary Disease
Published in John C Watkinson, Raymond W Clarke, Louise Jayne Clark, Adam J Donne, R James A England, Hisham M Mehanna, Gerald William McGarry, Sean Carrie, Basic Sciences Endocrine Surgery Rhinology, 2018
Thozhukat Sathyapalan, Stephen L. Atkin
Decreased secretion or action of AVP causes diabetes insipidus and is characterized by the production of abnormally large volumes of dilute urine. The 24-hour urine volume is >50 mL/kg body weight and the osmolarity is <300 mOsmol/L. The polyuria produces symptoms of urinary frequency, enuresis, and/or nocturia, which may disturb sleep and cause mild daytime fatigue or somnolence. It is also associated with thirst and a commensurate increase in fluid intake (polydipsia). Clinical signs of dehydration are uncommon unless fluid intake is impaired.
Effects of cinnamaldehyde on glucose-6-phosphate dehydrogenase activity, some biochemical and hematological parameters in diabetic rats
Published in Biomarkers, 2022
Remzi Çelik, Handan Mert, Bahat Comba, Nihat Mert
In this study, it was determined that all hematological parameters except RDWC decreased in the diabetes group compared to other groups. MCV values in diabetes + cinnamaldehyde group was increased compared to diabetes groups. The decrease in the value of haematocrit in diabetes group seems to be more remarkable. This may be due to excessive water intake (polydipsia) in diabetes. In cases where the body receives excess fluid, an increase in blood plasma is seen, which leads to a reduction in indirect haematocrit and reduces the viscosity of the blood. Sinnamaldehyde may be caused by elevation of haematocrit in diabetes, decreased fluid intake, or increased fluid excretion from the kidneys. Thus, while the use of cinnamaldehyde in diabetes improves erythrocyte, haemoglobin, haematocrit, MCV, MCHC and RDWC values slightly, it is thought that especially if the MCV values are significantly increased, the use of cinnamaldehyde increases in diabetic patients, the changes of these parameters may be statistically significant and contribute to the healing process of diabetic patients.
Successful management of germanium poisoning-induced multiple organ dysfunctions by combined blood purification therapy
Published in Current Medical Research and Opinion, 2020
Luyun Wang, Changlong Zheng, Daqiang Zhao
A 58-year-old male was admitted to a local hospital due to polydipsia, polyuria, and weight loss (3 kg) for 2 months. He had no history of nephritis, hepatitis, alcoholism, and overeating or drinking. Until 2 months ago, he continued to feel thirsty and polyuria, then he visited the hospital. The results of the blood test were as follows: fasting blood glucose = 17.59 mmol/L; 2-h postprandial blood glucose = 24.9 mmol/L; Glycated hemoglobin (HbA1c) = 10.6%, serum creatinine (Scr) = 115 μmol/L. The patient was diagnosed with diabetes mellitus and received regular blood glucose control therapy. A week ago, he felt fatigued, nausea, vomiting, and drowsiness, blood tests in clinic showed random blood glucose = 16.2 mmol/L; blood potassium = 3.2 mmol/L; Scr = 342.9 μmol/L; ketonuria, carbondioxide combining power (CO2CP)=11.9 mmol/L, base excess (BE) −11.5 mmol/L, considering diabetes mellitus, ketoacidosis, and acute renal injury. The patient was transferred to a local hospital immediately.
A comprehensive review of the clinical utility of and a combined analysis of the clozapine/norclozapine ratio in therapeutic drug monitoring for adult patients
Published in Expert Review of Clinical Pharmacology, 2019
Georgios Schoretsanitis, John M. Kane, Can-Jun Ruan, Edoardo Spina, Christoph Hiemke, Jose de Leon
CLO is approved by the Food and Drug Administration (FDA) in monotherapy for treatment-resistant schizophrenia [3] and for suicide risk in schizophrenia [4]. Additional CLO off-label uses encompass: 1) augmentation treatment after partial response in treatment-resistant schizophrenia in co-prescription with other drugs [5,6] or electroconvulsive therapy [7]; 2) acute schizophrenia in adults [8], children and adolescents [9]; 3) schizophrenia with aggressive behavior [10]; 4) schizophrenia with comorbid substance abuse [11]; 5) tardive dyskinesia [12]; 6) treatment-resistant bipolar disorder [13]; 7) polydipsia associated with severe mental illness [14]; 8) aggression in patients with intellectual disability who do not respond to other treatments [14,15]; and 9) psychosis in Parkinson’s disease [16].