Cases reported "Kwashiorkor"

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1/10. A case of kwashiorkor in the UK.

    A case of kwashiorkor in a British child of Caucasian origin is described. The 5-year-old boy was referred to hospital for investigation of a persistent anaemia, but on examination was found to have classical features of kwashiorkor. He was stunted with both height and weight below the fifth centile and had mild pitting oedema in both legs. His hair was pale and easily pluckable and a soft liver edge was palpable. plasma albumin concentration was 16 g/l and the plasma amino acid pattern, which revealed markedly reduced levels of essential but normal to high non-essential amino acids, was similar to that described in kwashiorkor in uganda. A dietary history revealed that for about 2 years the child's diet had contained very little protein but adequate energy and had been supplemented with multivitamin pills. There was no evidence of other pathology, neglect or abuse and the child responded rapidly to refeeding with a balanced diet.
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2/10. Malnutrition in infants receiving cult diets: a form of child abuse.

    Severe nutritional disorders, including kwashiorkor, marasmus, and rickets, were seen in four children and were due to parental food faddism, which should perhaps be regarded as a form of child abuse. All disorders were corrected with more normal diets and vitamin supplements. In view of the potentially serious consequences of restricted diets being fed to children, families at risk should be identified and acceptable nutritional advice given. When children are found to be suffering from undernutrition due to parental food faddism a court order will normally be a necessary step in providing adequate treatment and supervision.
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3/10. Severe nutritional deficiencies in toddlers resulting from health food milk alternatives.

    It is widely appreciated that health food beverages are not appropriate for infants. Because of continued growth, children beyond infancy remain susceptible to nutritional disorders. We report on 2 cases of severe nutritional deficiency caused by consumption of health food beverages. In both cases, the parents were well-educated, appeared conscientious, and their children received regular medical care. Diagnoses were delayed by a low index of suspicion. In addition, nutritional deficiencies are uncommon in the united states and as a result, US physicians may be unfamiliar with their clinical features. Case 1, a 22-month-old male child, was admitted with severe kwashiorkor. He was breastfed until 13 months of age. Because of a history of chronic eczema and perceived milk intolerance, he was started on a rice beverage after weaning. On average, he consumed 1.5 L of this drink daily. Intake of solid foods was very poor. As this rice beverage, which was fallaciously referred to as rice milk, is extremely low in protein content, the resulting daily protein intake of 0.3 g/kg/day was only 25% of the recommended dietary allowance. In contrast, caloric intake was 72% of the recommended energy intake, so the dietary protein to energy ratio was very low. A photograph of the patient after admission illustrates the typical features of kwashiorkor: generalized edema, hyperpigmented and hypopigmented skin lesions, abdominal distention, irritability, and thin, sparse hair. Because of fluid retention, the weight was on the 10th percentile and he had a rotund sugar baby appearance. Laboratory evaluation was remarkable for a serum albumin of 1.0 g/dL (10 g/L), urea nitrogen <0.5 mg/dL (<0.2 mmol/L), and a normocytic anemia with marked anisocytosis. Evaluation for other causes of hypoalbuminemia was negative. Therapy for kwashiorkor was instituted, including gradual refeeding, initially via a nasogastric tube because of severe anorexia. Supplements of potassium, phosphorus, multivitamins, zinc, and folic acid were provided. The patient responded dramatically to refeeding with a rising serum albumin and total resolution of the edema within 3 weeks. At follow-up 1 year later he continued to do well on a regular diet supplemented with a milk-based pediatric nutritional supplement. The mortality of kwashiorkor remains high, because of complications such as infection (kwashiorkor impairs cellular immune defenses) and electrolyte imbalances with ongoing diarrhea. Children in industrialized countries have developed kwashiorkor resulting from the use of a nondairy creamer as a milk alternative, but we were unable to find previous reports of kwashiorkor caused by a health food milk alternative. We suspect that cases have been overlooked. Case 2, a 17-month-old black male, was diagnosed with rickets. He was full-term at birth and was breastfed until 10 months of age, when he was weaned to a soy health food beverage, which was not fortified with vitamin d or calcium. Intake of solid foods was good, but included no animal products. Total daily caloric intake was 114% of the recommended dietary allowance. Dietary vitamin d intake was essentially absent because of the lack of vitamin d-fortified milk. The patient lived in a sunny, warm climate, but because of parental career demands, he had limited sun exposure. His dark complexion further reduced ultraviolet light-induced endogenous skin synthesis of vitamin d. The patient grew and developed normally until after his 9-month check-up, when he had an almost complete growth arrest of both height and weight. The parents reported regression in gross motor milestones. On admission the patient was unable to crawl or roll over. He could maintain a sitting position precariously when so placed. Conversely, his language, fine motor-adaptive, and personal-social skills were well-preserved. Generalized hypotonia, weakness, and decreased muscle bulk were present. Clinical features of rickets present on examination included: frontal bossing, an obvious rachitic rosary (photographed), genu varus, flaring of the wrists, and lumbar kyphoscoliosis. The serum alkaline phosphatase was markedly elevated (1879 U/L), phosphorus was low (1.7 mg/dL), and calcium was low normal (8.9 mg/dL). The 25-hydroxy-vitamin d level was low (7.7 pg/mL) and the parathyroid hormone level was markedly elevated (114 pg/mL). The published radiographs are diagnostic of advanced rickets, showing diffuse osteopenia, frayed metaphyses, widened epiphyseal plates, and a pathologic fracture of the ulna. The patient was treated with ergocalciferol and calcium supplements. The published growth chart demonstrates the dramatic response to therapy. Gross motor milestones were fully regained within 6 months. The prominent neuromuscular manifestations shown by this patient serve as a reminder that rickets should be considered in the differential diagnosis of motor delay. (ABSTRACT TRUNCATED)
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4/10. Tropical calcific pancreatitis presenting as kwashiorkor.

    Tropical clacific pancreatitis can be accompanied by varying degrees of malnutrition but full-blown kwashiorkor is an extremely rare presentation. We report the case of a 10-year-old male who presented with clinical features of severe kwashiorkor. He had extensive pancreatic clacification and exocrine pancreatic deficiency. The child was treated with pancreatic enzyme replacement, and enteral nutrition supplemented with vitamins and micronutrients. Following therapy, he started gaining weight, the skin changes partly disappeared and his hair resumed its normal black colour.
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5/10. A case of kwashiorkor.

    kwashiorkor is part of the spectrum of protein-energy malnutrition. The condition results from a lack of nutritional protein coupled with carbohydrate excess. Protein malnutrition is much more common in the Third World; however, it is also the most common form of nutritional deficiency among hospitalized patients in the united states. Cutaneous clues to the diagnosis of protein deficiency include the "flag sign," hypochromotrichia, alopecia, "crazy pavement" dermatosis, pallor, and glossitis. Systemic manifestations include peripheral edema, liver disease, neurologic changes, diarrhea, weight loss, and hypoalbuminemia. We report here a case of profound kwashiorkor in a nonhospitalized patient who presented with multiple cutaneous and systemic findings indicative of protein malnutrition.
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keywords = deficiency
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6/10. Two unusual cases of kwashiorkor: can protein deficiency explain the mystery?

    Two children with unusual features of kwashiorkor are reported. One, an exclusively breastfed 7-month-old girl, had been admitted earlier, treated for pneumonia and discharged 3 weeks before she presented with kwashiorkor. The other was an identical twin who was admitted for kwashiorkor and gastro-enteritis. The twin sister was underweight but relatively well. Both children died. Potent aflatoxins were detected in the organs of these children on post-mortem examination. The occurrence of kwashiorkor in a fully breastfed infant and in an identical twin does not accord with the extant belief that the aetiology of kwashiorkor is wholly nutritional, but suggests a disease probably of multifactorial origin.
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7/10. Community-acquired pseudomonas aeruginosa infection in an infant.

    A 7-month-old infant presented at a tertiary centre with a 6-day history of a skin rash, fever and diarrhoea. Clinical features included pyrexia, kwashiorkor, extensive ulcerating skin lesions suggestive of ecthyma gangrenosum, hepatomegaly, meningismus, neutropenia and iron deficiency anaemia. blood and skin aspirate cultures yielded a positive growth of pseudomonas aeruginosa. Apart from severe protein energy malnutrition, no other causes of immunodeficiency were found. He responded well to parenteral antibiotic therapy with gentamicin and piperacillin.
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keywords = deficiency
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8/10. Hypoinsulinaemia has an important role in the development of oedema and hepatomegaly during malnutrition.

    Various alterations in hormonal levels have been suggested to contribute to the development of nutritional oedema and fatty liver in children with kwashiorkor. We present an infant who underwent near-total pancreatectomy at the age of 4 weeks and developed kwashiorkor after 11 weeks. The sequence of events following surgery can be divided into two phases. The first phase was characterized by hyperinsulinaemia and hypoglycaemia before feeds. During this phase, although the weight gain was slow (10 g/day) serum albumin (32 g/I) and prealbumin (0.23 g/I) concentrations were maintained with no oedema or hepatomegaly. In the second phase, insulin deficiency prevailed and he was receiving the same amount of milk (protein)/day (enriched with starch). During that phase he rapidly developed hypoalbuminaemia (18 g/l), hypoprealbuminaemia (0.1 g/l), oedema, hepatomegaly, and dermatosis. This case demonstrates clearly the important role of defective insulin secretion in the development of nutritional oedema and hepatomegaly.
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9/10. Central pontine myelinolysis associated with acquired folate depletion.

    After long-standing malnutrition a 15-month-old boy with signs of kwashiorkor was admitted in a moribund state with serious hyponatraemic dehydration, hypothermia, somnolence, and signs of a pontine disconnection syndrome. folic acid levels were below the detection level in the presence of normal cobalamin levels. MRI of the brain showed global volume loss and signal abnormalities on the T2-weighted images suggestive for central pontine myelinolysis (CPM). Brainstem acoustic evoked responses have remained normal. The serious metabolic and nutritional derangements required substitution of folic acid, vitamins and trace elements as well as slow correction of hyponatraemic dehydration with return of the sodium level over a period of four days. This therapeutic regimen resulted in complete neurological recovery. Follow-up MRI documented normalisation of the initial pathologic findings. The hypothesis was put forward linking the pathogenesis of CPM with the combination of folate depletion and superimposed hyponatraemic dehydration. The previously acquired folate depletion could affect normal appositional function of myelin basic protein molecules due to insufficient methylation of arginine in position 107. The subsequent development of intramyelinic edema and CPM will then be triggered by the superimposed hyponatraemic dehydration. The verification of this hypothesis requires further investigations.
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10/10. kwashiorkor-like zinc deficiency syndrome in anorexia nervosa.

    This report deals with a 26-year-old white woman exhibiting signs of both kwashiorkor (marasmus, pallor, hypopigmentation of hair and hepatomegaly) and acrodermatitis enteropathica (eczematous dermatitis predominantly on acral areas). Clinical and laboratory examinations excluded malabsorption syndrome and glucagonoma syndrome and revealed hypoproteinemia and marked zinc deficiency. Psychiatric examination disclosed anorexia nervosa. Substitution therapy led to rapid clearing of the skin lesions.
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