Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One of the major factors in the development of severe protein-energy malnutrition (PEM) is infection, such as diarrhea, upper respiratory infection, and malaria. Social and environmental factors include family size, access to land and occupation of parents, and exposure of rural populations to urban centers. Breast milk has been shown to play a role in the prevention of infections; however, the mother must be well-nourished to provide the optimum product. Traditional foods available to rural children in most developing countries are difficult to digest and low in energy and protein and inadequate nutritional education prevents the inclusion of good protein sources in children's diets. Severe PEM, called marasmus and kwashiorkor is indicated by wasting of muscles, absence of subcutaneous fat, wrinkled skin, thin and sparse hair, and weakness. The basic treatment for severe PEM is dietary. Treatment of kwashiorkor and marasmus is divided into 3 stages: 1) attending to acute problems, 2) restoring nutritional balance, and 3) ensuring nutritional rehabilitation. Care must be taken to ensure a minimum daily intake of 3-4 gm of protein and 120-150 Kcal of energy/kg of body weight. There must be, in addition, replacement of vitamin A, zinc, potassium, magnesium, and iron. An initial regimen which has been advocated is based on dry skim milk, sugar, and vegetable oil, divided into 6-12 feedings/day, which prevents vomiting. It is not necessary to remove lactose from the diet, and other animal protein sources such as meat and meat extracts are also well accepted. Soy and vegetable protein have been used successfully. In treating mild and moderate PEM it is important to ensure the intake of these food supplements by the child and to avoid a major substitution effect in the household diet. It is crucial for the physicians, nutritionists, public health workers, and educators to convince parents about the safety of using foods that are fed only to adults and older children. In addition nutritional and health education must not be restricted to the rehabilitation of the child but the prevention of nutritonal deterioration of the entire family and sometimes to the entire community.
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PMID:Infantile malnutrition in the tropics. 681 12

The physiologic effects of habitual vomiting mimic the metabolic abnormalities seen in Bartter's syndrome, ie, hypokalemic metabolic alkalosis and increased plasma renin and aldosterone levels with kaliuresis. However, in habitual vomiting, the 24-hour urine chloride level will be lss than 10 mEq/liter owing to gastrointestinal loss and in Bartter's syndrome it will be greater than 20 mEq/liter owing to defective chloride reabsorption. The case is reported of a young woman whose self-induced vomiting caused metabolic abnormalities consistent with a diagnosis of Bartter's syndrome. The absence of urinary chloride wasting, ie, level less than 10 mEq/liter, was the only finding distinguishing her condition from Bartter's syndrome and leading to the correct diagnosis.
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PMID:Self-induced vomiting presenting as Bartter's syndrome. 714 83

Magnesium (Mg) deficiency occurs frequently in chronic alcoholism and may contribute to the increased incidence of osteoporosis and cardiovascular disease seen in this population. Mg deficiency is primarily due to renal Mg-wasting and is exacerbated by dietary Mg deprivation, gastrointestinal losses with diarrhea or vomiting, as well as concomitant use of drugs such as diuretics and aminoglycosides. Osteoporosis is prevalent in the alcoholic population. Mg deficiency may contribute to increased bone loss by its effects on mineral homeostasis. In Mg depletion, there is often hypocalcemia due to impaired parathyroid hormone (PTH) secretion, as well as renal and skeletal resistance to PTH action. Serum concentrations of 1,25-vitamin D are also low. These changes are seen with even mild degrees of Mg deficiency and may contribute to the metabolic bone disease seen in chronic alcoholics. Hypomagnesemia in alcoholics may also contribute to increased cardiovascular disease by altering platelet function. Mg deficiency has been demonstrated to enhance platelet reactivity. In these studies, Mg was shown to inhibit platelet aggregation against various aggregation agents. Patients with Mg deficiency were shown to have increased platelet aggregation that was normalized with Mg therapy. The antiplatelet effect of Mg may be related to the finding that Mg inhibits the synthesis of thromboxane A2 and 12-hydroxyeicosatetraenoic acid, eicosanoids thought to be involved in platelet aggregation. Mg also inhibits the thrombin-induced Ca2+ influx in platelets, as well as stimulates synthesis of prostaglandin I2, the potent antiaggregatory eicosanoid. Therefore, Mg deficiency may increase platelet aggregation and cause increased hypertension and atherosclerotic cardiovascular disease in alcoholics.
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PMID:Magnesium deficiency in alcoholism: possible contribution to osteoporosis and cardiovascular disease in alcoholics. 784 87

A 24-year-old man with anorexia, repeated bouts of vomiting, and wasting was found to have florid thyrotoxicosis and hypercalcaemia. Pamidronate promptly reduced the serum calcium concentration to normal, and simultaneously abated the abdominal symptoms, which did not recur in spite of continuing severe hyperthyroidism, which was eventually controlled by radioactive iodine ablation of thyroid activity.
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PMID:Abdominal symptoms, hypercalcaemia and apathetic hyperthyroidism: treatment with pamidronate. 774 97

There are increasing challenges for the practising gastroenterologist in treating AIDS-related gastrointestinal diseases. The differential diagnoses of dysphagia and odynophagia include cytomegalovirus (CMV) and herpes simplex virus (HSV) infection, non-specific aphthous ulceration and non-AIDS oesophageal diseases, especially reflux oesophagitis. Chronic subacute abdominal pain with nausea, vomiting, early satiety and weight loss is suggestive of an obstructive lesion caused by lymphoma or Kaposi's sarcoma. Severe acute abdominal pain can indicate pancreatitis or intestinal perforation due to cytomegalovirus. Right upper quadrant pain (with or without fever, vomiting or abnormal liver function tests with a cholestatic profile) is suggestive of hepatobiliary pathology including cholecystitis, cholangitis, acalculous cholecystitis and AIDS cholangiopathy. Diarrhoea is the most common gastrointestinal symptom of AIDS, affecting 50-90% of patients. Causes of AIDS diarrhoea include protozoa (Cryptosporidium parvum, Isospora belli, Enterocytozoon bieneusi, Septata intestinalis, Cyclospora spp, Entamoeba histolytica and Giardia lamblia), bacteria (Mycobacterium avium-intracellulare, Clostridium difficile, Salmonella, Shigella and Campylobacter jejuni), and viruses (CMV, HSV and possibly HIV). Chronic diarrhoea, malnutrition and weight loss can shorten the life-span of patients with AIDS. Elemental diets, isotonic formulas, medium chain triglycerides and total parenteral nutrition have been tried with little success in AIDS patients with severe diarrhoea and wasting.
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PMID:AIDS and the gut. 805 32

Although gout and hyperuricaemia are usually thought of as conditions of indulgent male middle age, in addition to the well-known uricosuria of the newborn, there is much of importance for the paediatric nephrologist in this field. Children and infants may present chronically with stones or acutely with renal failure from crystal nephropathy, as a result of inherited deficiencies of the purine salvage enzymes hypoxanthine-guanine phosphoribosyltransferase (HPRT) and adenine phosphoribosyltransferase (APRT) or of the catabolic enzyme xanthine dehydrogenase (XDH). Genetic purine overproduction in phosphoribosylpyrophosphate synthetase superactivity, or secondary to glycogen storage disease, can also present in infancy with renal complications. Children with APRT deficiency may be difficult to distinguish from those with HPRT deficiency because the insoluble product excreted, 2,8-dihydroxyadenine (2,8-DHA), is chemically very similar to uric acid. Moreover, because of the high uric acid clearance prior to puberty, hyperuricosuria rather than hyperuricaemia may provide the only clue to purine overproduction in childhood. Hyperuricaemic renal failure may be seen also in treated childhood leukaemia and lymphoma, and iatrogenic xanthine nephropathy is a potential complication of allopurinol therapy in these conditions. The latter is also an under-recognised complication of treatment in the Lesch-Nyhan syndrome or partial HPRT deficiency. The possibility of renal complications in these three situations is enhanced by infection, the use of uricosuric antibiotics and dehydration consequent upon fever, vomiting or diarrhoea. Disorders of urate transport in the renal tubule may also present in childhood. A kindred with X-linked hereditary nephrolithiasis, renal urate wasting and renal failure has been identified, but in general, the various rare types of net tubular wasting of urate into the urine are recessive and relatively benign, being found incidentally or presenting as colic from crystalluria. However, the opposite condition of a dominantly inherited increase in net urate reabsorption is far from benign, presenting as familial renal failure, with hyperuricaemia either preceding renal dysfunction or disproportionate to it. Paediatricians need to be aware of the lower plasma urate concentrations in children compared with adults when assessing plasma urate concentrations in childhood and infancy, so that early hyperuricosuria is not missed. This is of importance because most of the conditions mentioned above can be treated successfully using carefully controlled doses of allopurinol or means to render urate more soluble in the urine. Xanthine and 2,8-DHA are extremely insoluble at any pH. Whilst 2,8-DHA formation can also be controlled by allopurinol, alkali is contraindicated. A high fluid, low purine intake is the only possible therapy for XDH deficiency.
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PMID:Gout, uric acid and purine metabolism in paediatric nephrology. 843 71

Bartter's syndrome (BS) is a disease with severe hypokalaemia due to renal potassium wasting. The potassium loss is due to lesions at different sites within the renale tubule. Additional features include metabolic alkalosis, excess renal production of prostaglandins, hyperreninaemia, hyperaldosteronism and impaired pressor responses to exogenous angiotensin II. These secondary features are the result of renal potassium wasting. Symptoms are due to potassium deficiency, but many adult patients feel well despite marked hypokalaemia. The hypocalciuric variant of BS is called Gitelman's syndrome. These patients have a more benign course. The diagnosis of BS is one of exclusion, mainly of surreptitious vomiting, diuretic or laxative abuse. The primary treatment is potassium supplementation often in combination with potassium-sparing diuretics, prostaglandin inhibitors or ACE-inhibitors. With coexisting magnesium deficiency, magnesium supplementation might be effective.
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PMID:[Bartter's syndrome. A condition with chronic hypokalemia]. 896 74

The World Health Organization (WHO) has developed a diagnostic and treatment algorithm to facilitate the rapid identification and management of severely ill children in developing countries. 13 indicators are listed on Sick Child Charts: inability to drink, abnormal mental status (e.g., sleepiness), convulsions, wasting, edema, chest wall retraction, stridor, abnormal skin turgor, repeated vomiting, stiff neck, tender swelling behind the ear, pallor of the conjunctiva, and corneal ulceration. These indicators target the principal causes of child mortality: acute respiratory infection, malaria, measles, diarrheal disease, and malnutrition. The usefulness of the WHO algorithm was evaluated in 4 clinics in western Kenya's Siaya district and in the pediatric outpatient and inpatient departments of Siaya District Hospital. 770 (28%) of the 2799 children (mean age, 13 months) seen in these rural outpatient clinics had 1 or more of the 13 signs, most frequently repeated vomiting (13%). Children with any of these signs had a 2.3 times higher odds of hospitalization than those without such signs; however, 424 admitted children (54%) had none of the 13 signs. Pallor and chest wall retraction were most highly associated with hospital admission (odds ratio [OR], 8.6 and 5.3, respectively). Among the 1139 inpatients, 666 (58%) presented with at least 1 sign and 75 (7%) died, 67 (89%) of whom had at least 1 clinical sign at admission. Overall, the mortality risk associated with having at least 1 sign was 6.5 times higher than that for children with none of the signs. The signs most associated with mortality were abnormal mental status (OR, 59.6), poor skin turgor (OR, 5.6), pallor (OR, 4.3), repeated vomiting (OR, 3.6), chest wall retraction (OR, 2.7), and edema (OR, 2.4). Although studies in other settings are required to validate the WHO logarithm, this schema appears to be a feasible means for identifying high-risk children in developing countries.
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PMID:An evaluation of clinical indicators for severe paediatric illness. 906 Feb 22

A squirrel monkey (Saimiri sciureus) presented with wasting, vomiting and diarrhoea. Haematology revealed elevation of creatinine phosphokinase, lactic dehydrogenase, alanine aminotransferase, amylase and lipase, together with azotaemia and hypoalbuminaemia. Prominent findings were chronic pancreatitis with acinar and ductal plugs, granulomatous and necrotizing peripancreatic steatitis, degenerative myopathy, testicular atrophy, candidiasis and bacterial necrotizing glossitis. Antioxidant analyses revealed low concentrations of serum vitamin E (and apparently A), hepatic selenium and hair zinc. Pancreatitis may have caused malabsorption and maldigestion, associated with deficiency of multiple antioxidants.
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PMID:Antioxidant status in a squirrel monkey (Saimiri sciureus) with chronic pancreatitis and degenerative myopathy. 1103 77

Epidemiological studies have demonstrated a marked negative relationship between diarrhoea and physical growth and development of a child. Each day of illness due to diarrhoea produces a weight deficit of 20-40 gms. Poor nutrition is associated with more serious prolonged diarrhoea. 'Catch-up growth' often does not occur in malnourished children. Malnutrition, particularly wasting, is a strong predictor of diarrhoeal duration and the prolonged illness could exacerbate nutritional faltering, thereby increasing the subsequent risk of death. Poor appetite, vomiting, deliberate withholding of food resulting in poor intake; malabsorption of macro and micronutrients; hastening of intestinal transit time; disturbance of metabolic and endocrine functions; and direct loss of protein and other nutrients in gastrointestinal tract are some of the known mechanisms which have an impact on the nutrition during an episode of diarrhea. In addition diarrhoea of infectious origin causes cytokine induced malnutrition which results from the actions of proinflammatory cytokines like tumour necrosis factor and interleukin 1, 6 and 8. Preexisting malnutrition is associated with decreased turnover of epithelial cells resulting in delayed recovery which may prolong an episode of infectious diarrhoea by itself as well as by promoting tissue invasion by other enteropathogens. Malnutrition may also alter protective host factors and thereby favour intestinal colonization by the pathogenic microbes. Mucosal damage varying from moderately severe changes to flat lesions indistinguishable from those of celiac disease may occur in kwashiorkar. Diarrhoea malnutrition interaction represents a dangerous web which can be distangled by prevention of disease transmission by promoting exclusive breast feeding, hygienic weaning practices, safe drinking water and handwashing, improved host defences by breast feeding, improved nutrition, measles vaccine and other vaccines against enteropathogens in the offing; and promotion of standard case management with special emphasis on nutritional support and rehabilitation.
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PMID:Diarrhoea and malnutrition interaction. 1113 59


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