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Q: Why is Kwashiorkor most common in poor developing countries? Write your answer Related questions. Where in the world is Kwashiorkor most common? Where is kwashiorkor most common? What continent has most developing countries? Are most countries in Africa developed or developing? What causes iron deficiency anemia in developing countries? Which is the most common non-commercial biological fuel in a large number of developing countries? What are similarities between Caribbean countries?
What health effects occur if you are protein deficient? What is the most common victim for typhoid fever prey on? What is diarrhea vaccine? What features characterize most developing countries? Kwashiorkor can be fatal if it's left untreated for too long because children become very vulnerable to infections. The main cause of kwashiorkor is not eating enough protein or other essential vitamins and minerals. It's most common in developing countries with a limited food supply, poor hygiene, and a lack of education about the importance of giving babies and children an adequate diet.
Kwashiorkor is rare in developed countries such as the UK, but it can occasionally happen as a result of severe neglect, long-term illness, a lack of knowledge about good nutrition, or a very restricted diet. Kwashiorkor can often be diagnosed based on a child's physical appearance and questions about their diet and care. However, a blood test and urine test may be done to rule out other conditions.
This can include tests to:. Other tests may include growth measurements, calculating body mass index BMI , measuring body water content, taking a sample of skin biopsy or hair for testing.
If kwashiorkor is found early, it can be treated with either specially formulated milk-based feeds or ready-to-use therapeutic food RUTF. RUTF is typically made up of peanut butter, milk powder, sugar, vegetable oil, and added vitamins and minerals. More intensive treatment in hospital is needed in severe cases or where there are already complications, such as infections.
The diagnoses were based on the characteristic rash and the overall clinical presentation. The rash consisted of an erosive, crusting, desquamating dermatitis sometimes with classic "pasted-on" scale—the so-called flaky paint sign. Most cases were due to nutritional ignorance, perceived milk intolerance, or food faddism.
Half of the cases were the result of a deliberate deviation to a protein-deficient diet because of a perceived intolerance of formula or milk. Financial and social stresses were a factor in only 2 cases, and in both cases social chaos was more of a factor than an absolute lack of financial resources.
Misleading dietary histories and the presence of edema masking growth failure obscured the clinical picture in some cases. Conclusions Physicians should consider the diagnosis of kwashiorkor in children with perceived milk allergies resulting in frequent dietary manipulations, in children following fad or unorthodox diets, or in children living in homes with significant social chaos.
The presence of edema and "flaky paint" dermatitis should prompt a careful dietary investigation. We report 12 cases of kwashiorkor in infancy and early childhood seen over 9 years by pediatric dermatologists throughout the United States, and discuss common causative themes.
The medical records of 12 patients with kwashiorkor were reviewed. The patients were seen over a 9-year period. All cases were diagnosed by pediatric dermatologists at major medical centers based on the characteristic rash and the overall clinical presentation, including elements of the medical history, laboratory values, other physical examination findings, skin biopsy results, and response to therapy.
Patient 5 was a 5-month-old white girl who was referred to the Dermatology Clinic, University of California, San Francisco, with a 3-day history of swelling of the lower extremities and vomiting and a 3-week history of a worsening rash on the face, trunk, and diaper area. The rash had been unsuccessfully treated with empirical systemic and topical corticosteroids, topical antifungal agents, antihistamines, and emollients.
Her medical history was significant for chronic constipation. She had been breastfed for 6 weeks and had been switched to a vegan formula of brown rice emulsion, black strap molasses, chlorophyll, acidophilus extract, flaxseed oil, and vitamins. Her family was vegan. Her 3-year-old brother apparently thrived on the same formula but was breastfed longer. On physical examination, she was an irritable edematous infant.
Her height, head circumference, and weight were significantly decreased for her age. She had diffuse, fine, reddish brown scale over her abdomen in a reticulated pattern Figure 1. Crusting and superficial erosions were noted in the diaper area Figure 2. Her lower extremities had extensive desquamation and edema Figure 3.
Patient 5. Extensive edema and desquamation over the lower extremities. Edema can mask decreased muscle mass and subcutaneous fat, making growth failure less evident. The results of the laboratory evaluation were unremarkable except for microcytic anemia, low albumin and total protein levels, and mildly elevated liver transaminase levels.
A skin biopsy was performed, and the results showed confluent parakeratosis and pallor in the upper third of the epidermis with a sparse superficial perivascular infiltrate Figure 4. These findings were consistent with the diagnosis of kwashiorkor.
This patient was briefly treated in the intensive care unit with antibiotics for an Escherichia coli urinary tract infection , albumin, diuretics, and parenteral and nasogastric nutrition.
Her rash and edema improved rapidly. She was switched to formula by mouth and was discharged after 7 days of hospitalization. The medical histories of all 12 patients are summarized in Table 1. There were 8 boys and 4 girls. Six patients were Hispanic, 2 were white, 2 were black, 1 was Native American, and 1 was East Indian.
None of the patients had any serious chronic illnesses. Two patients had a history of atopic dermatitis. One patient was born prematurely at 27 weeks and had a history of asthma and developmental delay.
Half of the cases patients were the result of a deliberate deviation from a standard diet because of a perceived intolerance of formula or milk.
The subsequent replacement diets were all deficient in protein. Two patients patients 1 and 2 had significant financial and social stresses directly contributing to the development of kwashiorkor. Three patients patients 3, 4, and 12 developed kwashiorkor as a result of parental nutritional ignorance. Other contributing factors included poor feeding skills, secondary ileitis, and suspected milk protein allergies.
The duration of symptoms ranged from 2 weeks to 5 months. The clinical findings and key laboratory values of the 12 cases are summarized in Table 2. Of the 12 patients, 9 were at or less than the 25th percentile for weight and 11 were less than the 25th percentile for height.
The most common physical examination findings were rash, irritability, and edema. The rash consisted of a diffuse, erythematous, crusting, erosive, desquamative dermatitis most prominent in the flexures, face, perioral area, and diaper area. Some patients had the classic "pasted-on" scale that has been called "flaky paint" dermatitis Figure 5 and Figure 6. Four patients had noticeably sparse hair, and 1 had mild depigmentation of his hair for the 3 months before presentation.
The classic "flag sign"—alternating light and dark bands of pigmentation along a single strand of hair—was not seen in any of our patients. Laboratory abnormalities included decreased total protein and albumin levels, elevated hepatic transaminase levels, and evidence of associated iron and zinc deficiency. Of the 5 patients with a low serum zinc level, patients 1, 5, and 8 improved without zinc supplementation, but patients 6 and 10 did receive zinc supplementation.
Patient 2 had increased IgA, IgM, and IgG levels, but these results were not believed to be contributory to the cause of the patient's condition, as the tests were drawn to rule out an immunodeficiency. Patient 6 had a positive radioallergosorbent test result to milk, soy, and barley.
Skin biopsy specimens were obtained in 7 of the 12 patients and revealed findings consistent with kwashiorkor with either confluent parakeratosis with pallor of the outer third of the epidermis or confluent parakeratosis and psoriasiform hyperplasia.
Initial diagnostic impressions by the referring physicians included atopic dermatitis, viral exanthem, staphylococcal scalded skin syndrome, zinc deficiency, scabies, tinea corporis, Langerhans cell histiocytosis, epidermolysis bullosa, and hypothyroidism.
Therapeutic trials of empirical oral and topical therapy had failed in several patients before referral to pediatric dermatologists, which led to delays of up to several weeks in diagnosis. Eleven patients had a dramatic improvement of their symptoms and signs with caloric and protein supplementation. Patient 12 died of heart failure in the pediatric intensive care unit. The results of an autopsy revealed an enlarged fatty liver, pneumocystis infection of the lung, herpes esophagitis, and bacterial and candidal superinfection of the skin and esophagus.
Patient 5 was treated for an E coli urinary tract infection and had a dramatic response to antibiotics and caloric and protein supplementation.
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