Refractory Hypoglycemia in T-Cell Lymphoma
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MEDICAL DIRECTIVE Point of Care Glucose Meter Testing And
MEDICAL DIRECTIVE Point of Care Glucose Meter Testing and Treatment for Out-Patients with Suspected Hypoglycemia in the Diabetes Education Program Approved by/Date: Medical Advisory Comm. – June 25, 2013 Authorizing physician(s) Dr. Rachel Chong Dr. Angeline Chong Dr. Theodore Monchesky Authorized to whom Nurses and dietitians working in the diabetes education program at LH who have received education and validation of glucose meter testing according to Ontario Laboratory Accreditation Standards (OLA). Patient Description / Population Any outpatient 18 years of age or older at LH exhibiting signs or symptoms of hypoglycemia. Any outpatient 18 years of age or older suspected of having hypoglycemia. Medical Directive Description/Physician’s Order The nurse/dietitian will obtain a capillary blood sample from a patient’s finger upon suspecting hypoglycemia. The nurse/dietitian will perform a blood glucose meter test, and treat hypoglycemia as per protocol outlined below. Patient/Population Description: All LH Patients 18 years and over registered with the LH Diabetes Education Program. Contraindications to implementing the Protocol: • Patients unwilling or unable to provide blood sample. • Patient less than 18 years of age • Refusal of patient/family consent for testing and/or treatment; call code blue and 911 immediately Originating Committee: RNS Program Council – Feb 26, 2013 Medical Advisory Committee: June 25, 2013 This material has been prepared solely for the use at Lakeridge Health. Lakeridge Health accepts no responsibility for use of this material by any person or organization not associated with Lakeridge Health. No part of this document may be reproduced in any form for publication without the permission of Lakeridge Health. -
Diabetes Control in Thyroid Disease
In Brief Thyroid disease is commonly found in most types of diabetes. This article defines the prevalence of thyroid disease in diabetes and elucidates through case studies the assessment, diagnosis, and clinical management of thyroid disease in diabetes. Diabetes Control in Thyroid Disease Thyroid disease is a pathological state abnormality. Several studies, including that can adversely affect diabetes con- the Colorado study, have documented trol and has the potential to negative- a higher prevalence of thyroid disease Jennal L. Johnson, MS, RNC, FNP, ly affect patient outcomes. Thyroid in women, with prevalence rates rang- BC-ADM, CDE disease is found commonly in most ing from 4 to 21%, whereas the rate in forms of diabetes and is associated men ranges from 2.8 to 16%.1 with advanced age, particularly in Thyroid disease increases with age. In type 2 diabetes and underlying the Colorado study, the 18-year-olds autoimmune disease in type 1 dia- had a prevalence rate of 3.5% com- betes. This article defines the preva- pared with a rate of 18.5% for those lence of thyroid disease in diabetes, ≥ 65 years of age. discusses normal physiology and The prevalence of thyroid disease in screening recommendations for thy- diabetes has been estimated at 10.8%,2 roid disease, and elucidates through with the majority of cases occurring as case studies the assessment, diagnosis, hypothyroidism (~ 30%) and subclini- and clinical management of thyroid cal hypothyroidism (~ 50%).2 Hyper- disease and its impact on diabetes. thyroidism accounts for 12%, and postpartum thyroiditis accounts for Thyroid Disease Prevalence 11%.2 Of the female patients with The prevalence of thyroid disease in type 1 diabetes, 30% have thyroid dis- the general population is estimated to ease, with a rate of postpartum thy- be 6.6%, with hypothyroidism the roid disease three times that of the most common malady.1 Participants normal population. -
CANINE INSULINOMA: DIAGNOSIS, TREATMENT, & STAGING Eliza Reiss Grant, DVM, and Kristine E
Peer Reviewed PRACTICAL ONCOLOGY CANINE INSULINOMA: DIAGNOSIS, TREATMENT, & STAGING Eliza Reiss Grant, DVM, and Kristine E. Burgess, DVM, Diplomate ACVIM (Oncology) Tufts University An insulinoma is a malignant pancreatic tumor that DIAGNOSIS inappropriately secretes excessive insulin, resulting in Aside from a histologic confirmation of insulinoma, profound hypoglycemia.1 no currently available diagnostic test provides a de- Pancreatic tumors are classified as: finitive diagnosis of insulinoma. Existing techniques • Exocrine, which includes adenocarcinomas of may help increase suspicion for an insulin-secreting ductular or acinar origin tumor but, with most diagnostic testing, it is im- • Endocrine, which arise from the islets of perative to interpret all results in the context of the Langerhans. coexisting clinical signs. Insulinomas are functional neuroendocrine tumors that originate in the beta cells of the islets Differential Diagnosis of Langerhans.1 A complete work-up, including careful patient history, physical examination, bloodwork, and PRESENTATION diagnostic imaging tests, should be performed to Signalment rule out other causes of hypoglycemia, such as Any breed of dog can be affected, but large sepsis, hepatic failure, adrenal cortical insufficiency, breeds tend to be overrepresented.1 While, in toxin ingestion, and other forms of neoplasia. humans, insulinomas affect females far more frequently than males, there is no apparent sex Laboratory Tests predilection in dogs.1-3 Dogs also commonly Blood Glucose present with a malignant variant, while humans A simple fasting blood glucose level of less than often have a benign adenoma (80%).1 Insulino- 40 mg/dL can suggest hyperinsulinemia, although ma is rare in cats.4 careful monitoring of a fasted dog with suspected insulinoma is strongly recommended due to high Clinical Signs risk for seizure activity. -
Clinical and Histopathological Features of Renal Maldevelopment in Boxer Dogs: a Retrospective Case Series (1999–2018) †
animals Article Clinical and Histopathological Features of Renal Maldevelopment in Boxer Dogs: A Retrospective Case Series (1999–2018) † Maria Alfonsa Cavalera 1, Floriana Gernone 1, Annamaria Uva 1, Paola D’Ippolito 2, Xavier Roura 3 and Andrea Zatelli 1,* 1 Department of Veterinary Medicine, University of Bari, 70010 Valenzano, Italy; [email protected] (M.A.C.); fl[email protected] (F.G.); [email protected] (A.U.) 2 Veterinary diagnostic Lab ACV Triggiano, 70019 Triggiano, Italy; [email protected] 3 Hospital Clínic Veterinari, Universitat Autònoma de Barcelona, 08193 Bellaterra, Spain; [email protected] * Correspondence: [email protected]; Tel.: +39-080-4679804 † This study was partially presented as oral communication at the 11th ECVIM-CA/ESVIM Congress, Dublin (Ireland) as “Congenital nephrotic syndrome with renal glomerular immaturity in 7 Boxer dogs”. Zatelli, A., Domenech, O., Bussadori, C., Lubas, G., Del Piero, F. Simple Summary: This study describes clinical findings in Boxer dogs with renal maldevelopment and proposes a possible mode of inheritance. Medical records of 9 female Boxer dogs, older than 5 months and with a clinical diagnosis of proteinuric chronic kidney disease prior to one year of age, showed the presence of polyuria and polydipsia, decreased appetite, weight loss, lethargy and weakness in all affected dogs. Common laboratory findings were proteinuria and diluted urine, non- regenerative anemia, azotemia, hyperphosphatemia, hypoalbuminemia and hypercholesterolemia. Citation: Cavalera, M.A.; Gernone, Histopathology of the kidneys identified the presence of immature glomeruli in all dogs. In 7 out F.; Uva, A.; D’Ippolito, P.; Roura, X.; of 9 related dogs, the pedigree analysis showed that a simple autosomal recessive trait may be a Zatelli, A. -
Hypoglycemia, Hepatic Dysfunction, Muscle Weakness, Cardiomyopathy
Pediatr. Res. 17: 319-326 (1983) Hypoglycemia, Hepatic Dysfunction, Muscle Weakness, Cardiomyopathy, Free Carnitine Deficiency and Long-Chain Acylcarnitine Excess Responsive to Medium Chain Triglyceride Diet ALLEN M. GLASGOW,'~~'ANDREW G. ENGEL, DENNIS M. BIER, LOWELL W. PERRY, MARY DICKIE, JANE TODARO, BARBARA I. BROWN, AND MERTON F. UTTER Departments of Endocrinology and Metabolism [A.M.G.], Gastroenterology [J. TI, Cardiology [L. W.P.] and Dietary [M.B.], Children's Hospital National Medical Center, Washington, D.C.; Department of Neurology, and the Neuromuscular Research Laboratory [A. G.E.], Mayo Clinic and Mayo Foundation, Rochester, Minnesota USA; Departments of Medicine and Pediatrics [D. M. B.] and Biochemistry [B. I. B.], Washington University, School of Medicine, St. Louis, Missouri, USA; and Department of Biochemistry [MI U.],Case Western Reserve, Cleveland, Ohio, USA Summary Hepatic long-chain acyl CoA carnitine transferase deficiency (4), multiple acyl CoA dehydrogenase deficiency (glutaric aciduria Fraternal twins who had fasting hypoglycemia, hypoketonemia, type 11) (18), and systemic carnitine deficiency (3,9, 12, 17, 24, 37, muscle weakness, and hepatic dysfunction are reported. The he- 43), all of which are associated with impaired fatty acid oxidation, patic dysfunction occurred only during periods of caloric depriva- have hypoglycemia as a major clinical manifestation. tion. The surviving patient developed a cardiomyopathy. In this The purpose of this paper is twofold: (1) to report fraternal sibling, muscle weakness and cardiomyopathy were markedly im- proved by a diet high in medium chain triglycerides. There was a twins with free carnitine deficiency and long-chain acylcarnitine marked deficiency of muscle total carnitine and a mild deficiency excess in whom hypoglycemia, hepatic dysfunction, muscle weak- of hepatic total carnitine. -
SIRS Is Valid in Discriminating Between Severe and Moderate Diabetic Foot Infections
Pathophysiology/Complications ORIGINAL ARTICLE SIRS Is Valid in Discriminating Between Severe and Moderate Diabetic Foot Infections 1 2 DANE K. WUKICH, MD KATHERINE MARIE RASPOVIC, DPM best of our knowledge, the use of SIRS 2 3 KIMBERLEE B. HOBIZAL, DPM BEDDA L. ROSARIO, PHD has not yet been validated as a method of discriminating between moderate and severe DFI. OBJECTIVEdThis retrospective, single-center study was designed to distinguish severe di- The aim of this study was to classify abetic foot infection (DFI) from moderate DFI based on the presence or absence of systemic fl infectionseverityinagroupofhospital- in ammatory response syndrome (SIRS). ized diabetic patients based on the pres- RESEARCH DESIGN AND METHODSdThe database of a single academic foot and ence or absence of SIRS. The reason for ankle program was reviewed and 119 patients were identified. Severe DFI was defined as local hospitalization in this group of patients infection associated with manifestation of two or more objective findings of systemic toxicity was their DFI. Our hypotheses are that using SIRS criteria. patients with DFI who manifest SIRS (i.e., severe infection) will have longer hospital RESULTSdPatients with severe DFI experienced a 2.55-fold higher risk of any amputation – – stays and higher rates of major amputa- (95% CI 1.21 5.36) and a 7.12-fold higher risk of major amputation (1.83 41.05) than patients tion than patients who don’tmanifest with moderate DFI. The risk of minor amputations was not significantly different between the two groups (odds ratio 1.02 [95% CI 0.51–2.28]). The odds of having a severe DFI was 7.82 SIRS (i.e., moderate infection). -
National Coverage Determination Procedure Code: 82977 Gamma Glutamyl Transferase CMS Policy Number: 190.32 Back to NCD List
National Coverage Determination Procedure Code: 82977 Gamma Glutamyl Transferase CMS Policy Number: 190.32 Back to NCD List Description: Gamma glutamyl transferase (GGT) is an intracellular enzyme that appears in blood following leakage from cells. Renal tubules, liver, and pancreas contain high amounts, although the measurement of GGT in serum is almost always used for assessment of Hepatobiliary function. Unlike other enzymes which are found in heart, skeletal muscle, and intestinal mucosa as well as liver, the appearance of an elevated level of GGT in serum is almost always the result of liver disease or injury. It is specifically useful to differentiate elevated alkaline phosphatase levels when the source of the alkaline phosphatase increase (bone, liver, or placenta) is unclear. The combination of high alkaline phosphatase and a normal GGT does not, however, rule out liver disease completely. As well as being a very specific marker of Hepatobiliary function, GGT is also a very sensitive marker for hepatocellular damage. Abnormal concentrations typically appear before elevations of other liver enzymes or biliuria are evident. Obstruction of the biliary tract, viral infection (e.g., hepatitis, mononucleosis), metastatic cancer, exposure to hepatotoxins (e.g., organic solvents, drugs, alcohol), and use of drugs that induce microsomal enzymes in the liver (e.g., cimetidine, barbiturates, phenytoin, and carbamazepine) all can cause a moderate to marked increase in GGT serum concentration. In addition, some drugs can cause or exacerbate liver dysfunction (e.g., atorvastatin, troglitazone, and others as noted in FDA Contraindications and Warnings.) GGT is useful for diagnosis of liver disease or injury, exclusion of hepatobiliary involvement related to other diseases, and patient management during the resolution of existing disease or following injury. -
Can Hyperuricemia Predict Glycogen Storage Disease (Mcardle's Disease) in Rheumatology Practice? (Myogenic Hyperuricemia)
Clinical Rheumatology (2019) 38:2941–2948 https://doi.org/10.1007/s10067-019-04572-8 CASE BASED REVIEW Can hyperuricemia predict glycogen storage disease (McArdle’s disease) in rheumatology practice? (Myogenic hyperuricemia) Döndü Üsküdar Cansu1 & Bahattin Erdoğan2 & Cengiz Korkmaz1 Received: 25 March 2019 /Revised: 17 April 2019 /Accepted: 18 April 2019 /Published online: 1 May 2019 # International League of Associations for Rheumatology (ILAR) 2019 Abstract Gout disease is an inflammatory arthritis that arises due to the accumulation of monosodium urate crystals (MSU) around the joints and in tissues. Clinical manifestation of metabolic diseases leading to secondary hyperuricemia most predominantly occurs in the form of gouty arthritis. Hyperuricemia and gout may develop during the course of glycogen storage diseases (GSD), particularly in GSD type I, which involves the liver. On the other hand, during the course of GSD type V (GSDV, McArdle’s disease), which merely affects the muscle tissue due to the deficiency of the enzyme myophosphorylase, hyperuricemia and/or gout is rarely an expected symptom. These patients may mistakenly be diagnosed as having idiopathic hyperuricemia and associated gout, leading to the underlying secondary causes be overlooked and thus, diagnostic delays may occur. In this case report, we present a premenopausal female patient who experienced flare-ups of chronic arthritis while on disease-modifying antirheumatic drugs and intraarticular steroids due to a diagnosis of undifferentiated arthritis. The patient was initially suspected of having gouty arthritis because elevated concentrations of uric acid were incidentally detected, but then, a diagnosis of asymptomatic GSDV was made owing to elevated concentrations of muscle enzymes during colchicine use. -
Fasting Study for the Evaluation of Hypoglycemia in Pediatric Patients: Inpatient Unit Management Clinical Guideline
Fasting Study for the Evaluation of Hypoglycemia in Pediatric Patients: Inpatient Unit Management Clinical Guideline This guideline was developed to ensure the proper diagnostic evaluation of hypoglycemia in pediatric patients. Please direct questions and patient referrals to Dr. Alan Morris or Dr. Jerry Olshan, Pediatric Endocrinologists at The Barbara Bush Children’s Hospital and Maine Pediatric Specialty Group, 207.662.5522. For management of neonatal hypoglycemia, see the guideline entitled “Newborn Hypoglycemia Guideline.” Autonomic Neuroglycopenic Definition: The definition of hypoglycemia in infants and children Symptoms Symptoms continues to be controversial. The physiologic nadir of plasma glucose occurs in the first 2 - 4 hours life, but, normally, increases • Sweating • Fatigue to values > 60 mg/dL by 6 hours of life. Any documented plasma • Hunger • Weakness glucose level ≤ 40 mg/dL at any time after the physiologic nadir • Paresthesias • Dizziness warrants further evaluation. • Tremors • Confusion • Pallor • Headache • Normal > 70 mg/dL • Anxiety • Irritability • Hypoglycemia < 60 mg/dL • Nausea • Coma • With illness or fasting < 50 mg/dL • Seizures Duration of Predominant Purpose of the fasting study: The Disorders Fasting Fuel purpose of a fasting study is to systematically pinpoint the etiology of the 0 - 2 hours Sugars from meals Malabsorption hypoglycemia (first, by confirming the Hyperinsulinism hypoglycemic state and, then, by obtaining 2 - 6 hours Glycogen Glycogen storage disease critical blood and urine samples). The key (GSD) historical clue to the etiology of Hyperinsulinism hypoglycemia is the duration of fasting Glucagon Deficiency before hypoglycemia occurs. The duration 6 - 12 hours Gluconeogenesis Hyperinsulinism of fasting may direct the laboratory studies Gluconeogenesis disorder you order. -
Low Blood Glucose (Hypoglycemia)
Low Blood Glucose (Hypoglycemia) Hypoglycemia, also known as low blood Hunger, nausea glucose (blood sugar), is when your blood Color draining from skin (pallor) glucose levels have fallen low enough that you need to take action to bring them back Feeling sleepy to your target range. This is usually when your blood glucose is less than 70 mg/dL. However, Feeling weak, having no energy talk to your doctor about your own blood Blurred/impaired vision glucose targets, and what level is too low for you. Tingling or numbness in lips, tongue, cheeks Headaches When can it happen? Coordination problems, clumsiness Low blood glucose can happen if you’ve skipped a meal or snack, eaten less than usual, or been Nightmares or crying out in sleep more physically active than usual. If you don’t Seizures take steps to bring glucose levels back to normal, you could even pass out. What should you do? What are the symptoms? The 15-15 rule—have 15 grams of carbohydrate to raise your blood glucose and check it after Each person’s reaction to low blood glucose is 15 minutes. If it’s still below 70 mg/dL, have different. It’s important that you learn your own another serving. signs and symptoms when your blood glucose is low. Repeat these steps until your blood glucose is at least 70 mg/dL. Once your blood glucose is back Signs and to normal, eat a meal or snack to make sure it symptoms of doesn’t lower again. low blood glucose include: This may be: Feeling shaky Glucose tablets (see instructions) Being nervous Gel tube (see instructions) or anxious 4 ounces (1/2 cups) of juice or regular soda Sweating, chills, (not diet) clamminess 1 tablespoon of sugar, honey, or corn syrup Mood swings, irritability, impatience 8 ounces of nonfat or 1% milk Confusion Hard candies, jellybeans, or gumdrops—see Fast heartbeat food label for how many to consume Feeling light-headed or dizzy Continued » Visit diabetes.org or call 800-DIABETES (800-342-2383) for more resources from the American Diabetes Association. -
Drug-Induced Hyperglycemia Risk Factors Presentation Causative Agents Mallory Linck, Pharm.D
9/29/12 Outline Drug-Induced Hyperglycemia Risk Factors Presentation Causative Agents Mallory Linck, Pharm.D. Mechanisms Pharmacy Practice Resident Prevention University of Arkansas for Medical Sciences Management Risk Factors Presentation of Drug-Induced Hyperglycemia Mild-to-Moderate Severe disease General Diabetes risk factors, plus: Blurred vision Abdominal Pain, N/V Pre-existing or underlying Diabetes Excessive thirst Coma Higher doses of thiazides or corticosteroids Fatigue/weakness Dehydration Use of more than one drug that can induce Polydipsia Hypokalemia hyperglycemia Polyphagia Hypotension Polypharmacy Polyuria Kussmaul respiration and Unexplained weight loss fruity breath Increased Blood Glucose Lethargy Metabolic acidosis Causative Agents Mechanisms Atypical antipsychotics Nicotinic acid B-blockers Oral contraceptives Cyclosporine Pentamidine Diazoxide Phenothiazines Thiazide Diuretics Phenytoin Fish oil Protease inhibitors Glucocorticoids Rifampin Growth Hormone Ritodrine Interferons Tacrolimus Megesterol Terbutaline Thalidomide 1 9/29/12 Thiazide Diuretics High doses Hypokalemia “Each 0.5mEq/L decrease in serum potassium was associated with a 45% higher risk of new diabetes” DECREASE INSULIN SECRETION Plan: Use smaller doses (12.5-25mg/day HCTZ) and replace potassium Shafi T. Hypertension. 2009 Feb;53(2):e19. Immunosuppressants Overall incidence 4-46% Pre-disposing factors Genetics Metabolic syndrome Increasing age Most common in the first few months post- transplant -
Fructosamine Interpretive Summary
Fructosamine Interpretive Summary Description: Fructosamine is a complex of glucose and protein that can be used to assess the average blood glucose concentration in a dog or cat over the previous 2-3 weeks. It is used in the diagnosis and management of diabetes mellitus. Decreased Fructosamine Common Causes Prolonged hypoglycemia o Insulin overdose o Insulinoma Decreased albumin (dog) or total protein (cat) Hyperthyroidism Uncommon Causes Increased serum triglycerides Azotemia Sample handling – storage at room temperature Related Findings Prolonged hypoglycemia o Insulinoma . Normal to increased serum insulin with concurrent decreased blood glucose . Increased insulin:glucose ratio . Pancreatic mass may be seen on ultrasound (cats>dogs) . A decreased fructosamine is not diagnostic for insulinoma but can increase clinical suspicion Hyperthyroidism o Increased T4, free T4 and free T4 by equilibrium dialysis Increased Fructosamine Common Causes Diabetes Mellitus Hemolysis (certain methodologies) Insulin overdose with Somogyi rebound effect Uncommon Causes Hypothyroidism Increased albumin (dog) or total protein (cat) Related Findings Diabetes Mellitus o Increased blood glucose o Glucose in urine +/- ketones Generated by VetConnect® PLUS: Fructosamine Page 1 of 2 Additional Information Physiology Fructosamine correlates with the patient’s average blood glucose concentration over the last 2-3 weeks. o Fructosamine is not affected by short-term increases in serum glucose such as those that occur with excitement, stress or intravenous dextrose administration. Fructosamine is a ketoamine that is formed by an irreversible, nonenzymatic linking of glucose to proteins (most often albumin and IgG). o Formation of fructosamine is related to the degree and duration of hyperglycemia. o Removal of fructosamine from the blood is dependent on the loss or degradation of the parent molecule (albumin).