Pellagra in African Children
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Familial Pellagra-Like Skin Rash with Neurological Manifestations
Arch Dis Child: first published as 10.1136/adc.56.2.146 on 1 February 1981. Downloaded from 146 Freundlich, Statter, and Yatziv Familial pellagra-like skin rash with neurological manifestations E FREUNDLICH, M STATTER, AND S YATZIV Department ofPaediatrics, Government Hospital, Nahariya, Israel, and Paediatric Research Unit and Department ofPaediatrics, Hadassah University Hospital, Jerusalem, Israel development was normal, although the skin rash SUMMARY A 14-year-old boy of Arabic origin was noted several times. On one occasion a skin presented with a pellagra-like rash and neurological biopsy was performed and reported to be compatible manifestations including ataxia, dysarthria, nystag- with pellagra. A striking improvement was again mus, and coma. There was a striking response to oral noticed after nicotinamide administration. nicotinamide. The laboratory findings were not The last admission was at age 14 years in late typical of Hartnup disease: aminoaciduria and November (as were all previous admissions). At indicanuria were absent and there was no evidence this time, he presented with mild confusion, diplopia, of tryptophan malabsorption. Tryptophan loading dysarthria, ataxia, and a pellagroid skin rash. His did not induce tryptophanuria nor did it increase general condition deteriorated during the next few excretion of xanthurenic or kynurenic acids. These days; he became unable to walk or stand, and both findings support the possibility of a block in trypto- horizontal and vertical nystagmus were observed. phan degradation. The family history suggests a He became apathetic and entered into deep coma genetically-determined disorder. 4 days after admission. The electroencephalogram showed a markedly abnormal tracing with short We report a patient with familial pellagra-like skin bursts of high voltage 2 5 per second activity with manifestations and laboratory rash, with neurological superimposed sharp waves, mainly over the posterior copyright. -
THE PATHOLOGIC PHYSIOLOGY of PELLAGRA: V. the Circulating Blood Volume
THE PATHOLOGIC PHYSIOLOGY OF PELLAGRA: V. The Circulating Blood Volume Roy H. Turner J Clin Invest. 1931;10(1):111-120. https://doi.org/10.1172/JCI100332. Find the latest version: https://jci.me/100332/pdf THE PATHOLOGIC PHYSIOLOGY OF PELLAGRA V. THE CIRCULATING BLOOD VOLUME By ROY H. TURNER (From the Department of Medicine, Tulane University of Louisiana School of Medicine, and the Medical Services of the Charity Hospital, New Orleans) (Received for publication October 27, 1930) Determination of circulating blood volume was undertaken as a part of a study of the disturbed physiology in pellagra, chiefly for the purpose of finding out whether shrinkage of plasma volume existed in patients who were suffering from a disease frequently characterized by severe diarrhea. Such a shrinkage would be of great importance of itself, and would obviously have a bearing upon the interpretation of the composition of the plasma determined at the same time. The existence of anemia can hardly be established nor its severity estimated -so long as we are in ignorance- of the plasma volume. It was also considered possible that the magnitude of the circulating blood volume might be correlated with certain of the features of the skin lesions, such as the degree of exudation of serum. I have used the dye method of Keith, Rowntree and Geraghty (1) modified as follows: A 3 per cent aqueous solution of brilliant vital red (National Analine Company) was made up 'the afternoon before use, and sterilized at 100°C. for 8 minutes. With a sterile calibrated pipette the quantity of this solution for each patient was placed in a sterile 50 cc. -
Symptom Management for Cardiac Anorexia/Cachexia
Hospice Palliative Care HPC Consultation Services Waterloo Wellington Tip of the Month [email protected] May 2019 Palliative Approach to Care Tips: Symptom Management for Cardiac Anorexia/Cachexia • Focus interventions on treatment of Anorexia symptoms and reduction of psychological and social burden for patient and family. Anorexia is a syndrome characterized by loss of appetite, nausea, early satiety, weakness, fatigue, food aversion, and • Cachexia is not starvation. In cachexia, significant physical and/or psychological symptoms. Causes are complex and can include fatigue, dyspnea, medication side- effects, nausea, depression, anxiety and sodium-restricted diets, which are common to patients with heart failure. catabolism and subsequent weight loss continue to occur, even if caloric intake is Cachexia maintained or increased. Cachexia is a syndrome characterized by severe body weight, fat and muscle loss and increased protein catabolism due to • Educate patient/family about the underlying disease. This occurs in both chronic right-sided heart failure and the advanced stages of heart failure. difference between weight loss related to How is cachexia diagnosed? The patient with cachexia has: cachexia versus diuresis. • >5% non-edematous weight loss in <12 months; or body mass index (BMI) <20kg/m2; and • Artificial nutrition in the context of • 3 out of 5 of the following: fatigue, decreased muscle strength, anorexia, low muscle mass, abnormal biochemistry advanced cachexia is ineffective and will Screening not improve quality of life. • Screen with Edmonton Symptom Assessment System (ESAS-r) for issues with appetite, nausea, fatigue, depression. Assessment Figure 1: Understanding the Effects • of the Cachexia Cycle Obtain a thorough history of nutritional intake, weight loss, and symptoms (nausea, early satiety, dyspnea, poor oral hygiene, dysphagia, malabsorption, bowel habits). -
Cachexia: the Physical and Psychosocial Impact
Cachexia: The physical and psychosocial impact Caroline Quilty RD, MSc Specialist Palliative Care Dietitian/Therapies Services Manager Aims What is cachexia & why should we be concerned about it? Consider the impact of anorexia in cachexia What are the physical and psychosocial effects of cachexia Identify our role in the management of patients with cachexia What is Cachexia? Cachexia in any disease refers to a state of severely and pathologically low weight, due principally to the loss of mass of tissues other than fat • a serious and under-recognised consequence of cancer (von Haeling and Ankers 2010) • Cachexia is a hallmark of certain diseases including cancer and COPD (Wagner 2008) What is cachexia? “a multifactorial syndrome characterised by an ongoing loss of skeletal muscle mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutrition support, and progressive functional impairment. The pathophysiology is characterised by a negative protein and energy balance driven by a variable combination of reduced food intake and abnormal metabolism.” Fearon et al 2011 Prevalence Prevalence of cancer cachexia is high, ranging from 50-80% in advanced cancer (von Haeling and Ankers 2014) 20 – 40% of people with COPD have cachexia (von Haeling 2010) What does cachexia look like? The word cachexia has Greek roots, “kakos” meaning bad and “hexus” meaning habit, appearance, condition. Cachexia has been known for centuries (von Haehling 2010) and was described by Hippocrates “…the shoulders, clavicles, chest and thighs melt away” (Katz and Katz 1962). Some terms: Term Definition Ref Anorexia loss of appetite and diminished intake. Poole and Prevalent in cachexia Frogatt 2002 Malnutrition A state of nutrition in which a deficiency of energy, Elia 2003 protein and/or other nutrients causes measurable adverse effects on tissue/body form, composition, function or clinical outcome. -
High-Dose Vitamin C in Advanced-Stage Cancer Patients
nutrients Review High-Dose Vitamin C in Advanced-Stage Cancer Patients Anna Zasowska-Nowak 1,* , Piotr Jan Nowak 2 and Aleksandra Ciałkowska-Rysz 1 1 Department of Palliative Medicine, Chair of Oncology, Medical University of Lodz, Ul. Zeromskiego 113, 90-549 Lodz, Poland; [email protected] 2 Department of Nephrology, Hypertension and Kidney Transplantation, Medical University of Lodz, Ul. Pomorska 251, 92-213 Lodz, Poland; [email protected] * Correspondence: [email protected] Abstract: High-dose intravenously administered vitamin C (IVC) is widely used in cancer patients by complementary and alternative medicine practitioners. The most frequent indications for IVC therapy result from the belief in its effectiveness as a potent anti-cancer agent which additionally enhances chemosensitivity of cancer cells and reduces chemotherapy-related toxicities and fatigue intensity. In this narrative review, we decided to deal with this issue, trying to answer the question whether there is any scientific evidence supporting the rationale for application of high-dose IVC therapy in advanced-stage cancer patients. Although results obtained from preclinical studies demon- strated that millimolar ascorbate plasma concentrations achievable only after IVC administration were cytotoxic to fast-growing malignant cells and inhibited tumor growth as well as prolonged the survival of laboratory animals, such positive effects were not found in human studies with advanced-stage cancer patients. We also have not found the rationale for the use of IVC to increase the effectiveness of chemotherapy and to reduce the chemotherapy-induced toxicity in the above mentioned group. Nevertheless, in palliative care, high-dose IVC might be considered as a ther- apy improving the quality of life and reducing cancer-related symptoms, such as fatigue and bone Citation: Zasowska-Nowak, A.; pain. -
Anorexia/Cachexia Heart Failure Symptom Management Guideline for Adults, Age 19 and Older in British Columbia
Anorexia/Cachexia Heart Failure Symptom Management Guideline For adults, age 19 and older in British Columbia What is anorexia? Anorexia is a syndrome characterized by some or all of the following symptoms: loss of appetite, nausea, early satiety, weakness, fatigue, food aversion, and significant physical and/or psychological symptoms. Causes of anorexia are multifactorial and include fatigue, dyspnea, medication side-effects, nausea, depression, anxiety and sodium restricted diets, which may all be found in patients with heart failure. What is cachexia? Cachexia is a syndrome characterized by severe body weight, fat and muscle loss and increased protein catabolism due to underlying disease. The prevalence of cachexia is 16–42% in the heart failure population and is associated with a 50%, 18 month mortality risk independent of variables such as ejection fraction, age and functional ability. How is cachexia diagnosed? Chronic condition with >5% weight loss in <12 months; or body mass index (BMI) <20kg/m2; and 3 out of 5 additional criteria: 1) Fatigue, 2) Decreased muscle strength, 3) Anorexia, 4) Low muscle mass, 5) Abnormal biochemistry *Blood testing to diagnose cachexia in advanced stages of disease is not advocated. Reminder: Malnutrition also affects prognosis in patients with heart failure and is often found in early transitions of the disease. However this symptom management guideline will focus on the assessment and treatment of anorexia and cachexia. Approach to Managing Anorexia/Cachexia Assessment History: When did weight loss begin? How much weight was lost? Obtain baseline (dry) weight. How is [the patients] appetite? What do they eat or drink on a typical day? How has weight loss affected mood? Ask about: nausea, early satiety, dyspnea, poor oral hygiene, dysphagia, malabsorption, bowel habits. -
Rickets: Not a Disease of the Past LINDA S
Rickets: Not a Disease of the Past LINDA S. NIELD, M.D., West Virginia University School of Medicine, Morgantown, West Virginia PRASHANT MAHAJAN, M.D., M.P.H., Wayne State University School of Medicine, Detroit, Michigan APARNA JOSHI, M.D., Children’s Hospital of Michigan, Detroit, Michigan DEEPAK KAMAT, M.D., PH.D., Wayne State University School of Medicine, Detroit, Michigan Rickets develops when growing bones fail to mineralize. In most cases, the diagnosis is established with a thorough his- tory and physical examination and confirmed by laboratory evaluation. Nutritional rickets can be caused by inadequate intake of nutrients (vitamin D in particular); however, it is not uncommon in dark-skinned children who have limited sun exposure and in infants who are breastfed exclusively. Vitamin D–dependent rickets, type I results from abnor- malities in the gene coding for 25(OH)D3-1-a-hydroxylase, and type II results from defective vitamin D receptors. The vitamin D–resistant types are familial hypophosphatemic rickets and hereditary hypophosphatemic rickets with hyper- calciuria. Other causes of rickets include renal disease, medications, and malabsorption syndromes. Nutritional rickets is treated by replacing the deficient nutrient. Mothers who breastfeed exclusively need to be informed of the recom- mendation to give their infants vitamin D supplements beginning in the first two months of life to prevent nutritional rickets. Vitamin D–dependent rickets, type I is treated with vitamin D; management of type II is more challenging. Familial hypophosphatemic rickets is treated with phosphorus and vitamin D, whereas hereditary hypophosphatemic rickets with hypercalciuria is treated with phosphorus alone. -
341 Nutrient Deficiency Or Disease Definition/Cut-Off Value
10/2019 341 Nutrient Deficiency or Disease Definition/Cut-off Value Any currently treated or untreated nutrient deficiency or disease. These include, but are not limited to, Protein Energy Malnutrition, Scurvy, Rickets, Beriberi, Hypocalcemia, Osteomalacia, Vitamin K Deficiency, Pellagra, Xerophthalmia, and Iron Deficiency. Presence of condition diagnosed, documented, or reported by a physician or someone working under a physician’s orders, or as self-reported by applicant/participant/caregiver. See Clarification for more information about self-reporting a diagnosis. Participant Category and Priority Level Category Priority Pregnant Women 1 Breastfeeding Women 1 Non-Breastfeeding Women 6 Infants 1 Children 3 Justification Nutrient deficiencies or diseases can be the result of poor nutritional intake, chronic health conditions, acute health conditions, medications, altered nutrient metabolism, or a combination of these factors, and can impact the levels of both macronutrients and micronutrients in the body. They can lead to alterations in energy metabolism, immune function, cognitive function, bone formation, and/or muscle function, as well as growth and development if the deficiency is present during fetal development and early childhood. The Centers for Disease Control and Prevention (CDC) estimates that less than 10% of the United States population has nutrient deficiencies; however, nutrient deficiencies vary by age, gender, and/or race and ethnicity (1). For certain segments of the population, nutrient deficiencies may be as high as one third of the population (1). Intake patterns of individuals can lead to nutrient inadequacy or nutrient deficiencies among the general population. Intakes of nutrients that are routinely below the Dietary Reference Intakes (DRI) can lead to a decrease in how much of the nutrient is stored in the body and how much is available for biological functions. -
VITAMIN DEFICIENCIES in RELATION to the EYE* by MEKKI EL SHEIKH Sudan VITAMINS Are Essential Constituents Present in Minute Amounts in Natural Foods
Br J Ophthalmol: first published as 10.1136/bjo.44.7.406 on 1 July 1960. Downloaded from Brit. J. Ophthal. (1960) 44, 406. VITAMIN DEFICIENCIES IN RELATION TO THE EYE* BY MEKKI EL SHEIKH Sudan VITAMINS are essential constituents present in minute amounts in natural foods. If these constituents are removed or deficient such foods are unable to support nutrition and symptoms of deficiency or actual disease develop. Although vitamins are unconnected with energy and protein supplies, yet they are necessary for complete normal metabolism. They are, however, not invariably present in the diet under all circumstances. Childhood and periods of growth, heavy work, childbirth, and lactation all demand the supply of more vitamins, and under these conditions signs of deficiency may be present, although the average intake is not altered. The criteria for the fairly accurate diagnosis of vitamin deficiencies are evidence of deficiency, presence of signs and symptoms, and improvement on supplying the deficient vitamin. It is easy to discover signs and symptoms of vitamin deficiencies, but it is not easy to tell that this or that vitamin is actually deficient in the diet of a certain individual, unless one is able to assess the exact daily intake of food, a process which is neither simple nor practical. Another way of approach is the assessment of the vitamin content in the blood or the measurement of the course of dark adaptation which demon- strates a real deficiency of vitamin A (Adler, 1953). Both tests entail more or less tedious laboratory work which is not easy in a provincial hospital. -
Pathogenesis and Diagnostic Criteria for Rickets and Osteomalacia
Endocrine Journal 2015, 62 (8), 665-671 OPINION Pathogenesis and diagnostic criteria for rickets and osteomalacia —Proposal by an expert panel supported by Ministry of Health, Labour and Welfare, Japan, The Japanese Society for Bone and Mineral Research and The Japan Endocrine Society Seiji Fukumoto1), Keiichi Ozono2), Toshimi Michigami3), Masanori Minagawa4), Ryo Okazaki5), Toshitsugu Sugimoto6), Yasuhiro Takeuchi7) and Toshio Matsumoto1) 1)Fujii Memorial Institute of Medical Sciences, Tokushima University, Tokushima 770-8503, Japan 2)Department of Pediatrics, Osaka University Graduate School of Medicine, Suita 565-0871, Japan 3)Department of Bone and Mineral Research, Research Institute, Osaka Medical Center for Maternal and Child Health, Izumi 594-1101, Japan 4)Department of Endocrinology, Chiba Children’s Hospital, Chiba 266-0007, Japan 5)Third Department of Medicine, Teikyo University Chiba Medical Center, Ichihara 299-0111, Japan 6)Internal Medicine 1, Shimane University Faculty of Medicine, Izumo 693-8501, Japan 7)Division of Endocrinology, Toranomon Hospital Endocrine Center, Tokyo 105-8470, Japan Abstract. Rickets and osteomalacia are diseases characterized by impaired mineralization of bone matrix. Recent investigations revealed that the causes for rickets and osteomalacia are quite variable. While these diseases can severely impair the quality of life of the affected patients, rickets and osteomalacia can be completely cured or at least respond to treatment when properly diagnosed and treated according to the specific causes. On the other hand, there are no standard criteria to diagnose rickets or osteomalacia nationally and internationally. Therefore, we summarize the definition and pathogenesis of rickets and osteomalacia, and propose the diagnostic criteria and a flowchart for the differential diagnosis of various causes for these diseases. -
Cancer Cachexia and Fatigue
CME Palliative care Cancer cachexia and mechanisms (Fig 1). The cachectic Other cachectic factors patient is analogous to an accelerating Cachexia can occur in the absence of car running out of petrol. The anorexia anorexia, suggesting that catabolic fatigue component of cancer cachexia reduces mediators produced by tumour or host fuel supply (by ca 300–500 kcal/day) cells are involved in the cancer cachexia whilst accelerated metabolic cycling Grant D Stewart BSc(Hons) MBChB MRCS(Ed), process.9 Experimental cachexia models drives hypermetabolism (by ca Surgical Research Fellow suggest pro-inflammatory cytokines, 100–200 kcal/day). There are also the Richard JE Skipworth BSc(Hons) MBChB such as tumour necrosis factor- , inter- direct catabolic effects of muscle proteol- α MRCS(Ed), Surgical Research Fellow leukin (IL)-6, IL-1 and interferon- , can ysis and lipolysis. These changes underlie γ Kenneth CH Fearon MBChB(Hons) MD all play a role. Activation of the neuro- a key paradox of cachexia: whilst meta- FRCS(Glas) FRCS(Ed) FRCS(Eng), Professor of endocrine stress response is also thought bolic rate may be increased, overall (or Surgical Oncology to be important. Potential mediators total) energy expenditure is decreased Department of Clinical and Surgical Sciences include increased adrenergic activity, ele- due to a fall in physical activity.7 (Surgery), University of Edinburgh, Royal vated cortisol, low insulin and increased Infirmary, Edinburgh activity of the renin-angiotensin system.1 Anorexia With regard to tumour-specific Clin Med 2006;6:140–3 The anorexia component of cancer cachectic factors, proteolysis-inducing cachexia has both a neurohumoral mech- factor (PIF) is produced by tumours and anism due to disturbance of the central excreted in the urine of patients with Background physiological mechanisms controlling cancer cachexia. -
Nutritional Dermatoses in the Hospitalized Patient
HOSPITAL CONSULT IN PARTNERSHIP WITH THE SOCIETY FOR DERMATOLOGY HOSPITALISTS Nutritional Dermatoses in the Hospitalized Patient Melissa Hoffman, MS; Robert G. Micheletti, MD; Bridget E. Shields, MD Nutritional deficiencies may arise from inadequate nutrient intake, abnormal nutrient absorption, or improper nutrient PRACTICE POINTS utilization.4 Unfortunately, no standardized algorithm for • Nutritional deficiencies are common in hospitalized screening and diagnosing patients with malnutrition exists, patients and often go unrecognized. making early physical examination findings of utmost • Awareness of the risk factors predisposing patients importance. Herein, we present a review of acquired nutri- to nutritional deficiencies and the cutaneous manifes- tional deficiency dermatoses in the inpatient setting. tations associated with undernutrition can promote copy early diagnosis. Protein-Energy Malnutrition • When investigating cutaneous findings, undernutri- tion should be considered in patients with chronic Protein-energy malnutrition (PEM) refers to a set of infections, malabsorptive states, psychiatric illness, related disorders that include marasmus, kwashiorkor and strict dietary practices, as well as in those using (KW), and marasmic KW. These conditions frequently are certain medications. seen in developing countries but also have been reported 5 • Prompt nutritional supplementation can prevent patient in developed nations. Marasmus occurs from a chronic morbidity and mortality and reverse skin disease. deficiencynot of protein and calories. Decreased insulin pro- duction and unopposed catabolism result in sarcopenia and loss of bone and subcutaneous fat.6 Affected patients include children who are less than 60% ideal body weight Cutaneous disease may be the first manifestation of an underlying nutri- 7 tional deficiency, highlighting the importance of early recognition by der- (IBW) without edema or hypoproteinemia.