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Poor nutrition among children is the primary health problem plagueing developing countries. The problem stems primarily from the social and economic inequalities extant in the world today and could be ameliorated by reducing unemployment and urban migration through rural and village level development keyed to the needs and desires of the community. The major nutritional problems facing the developing countries are described and suggestions for preventing the problems and for treating specific nutritional diseases are made. Major nutritional problems include: 1) Maternal nutritional anemia; 2) protein energy malnutrition; 3) vitamin A deficiency; 4) lactation failure; 5) addiction to milk feeding; and 6) inadequate preparation and use of artificial milk products. Maternal nutritional anemia increases the frequency of low weight births in developing countries. Protein energy malnutrition afflicts approximately 100 million children under the age of 5 and can permanently affect the physical and mental development of these children. Vitamin A deficiency is one of the major causes of preventable blindness. The economic loss resulting from preventable blindness is tremendous; this loss could be prevented by spending only 10 cents a day to supplement the diet of each malnourished child. Lactation failure is especially devasting for babies born to poor women and all practices, such as temporary bottle feeding, which contribute toward lactation failure should be halted. Inappropriate use of artificial milk products increases nutritional deficiency and gastrointestional problems among babies in the developing countries.
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PMID:Nutritional problems in developing countries. 11 62

This work is a retrospective study of 50 cases of DHX, collected over a period of 27 years. 24 children died, 26 are still alive. The prognosis for DHX was neither dependent on age (usually occurring in children under 2 years) nor on histological findings but on the extent of the lesions. It was possible to establish a clinical staging system distinguishing 2 groups. One, where the disease was severe and almost always fatal, often included the combined symptoms of thrombocytopenia, spontaneous anemia, jaundice, hepatosplenomegaly, respiratory insufficiency and absence of osteolytic lesions. The other, with a favorable prognosis, was characterized by skin lesions, diabetes insipidus, exclusively radiological pulmonary involvement and multiple bone lesions. In cases where death did not occur, DHX was often chronic, frequently persisting for 2 years or more and leading to serious sequelae such as diabetes insipidus, growth stunting, intellectual retardation, blindness or deafness.
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PMID:Disseminated histiocytosis X: analysis of prognostic factors based on a retrospective study of 50 cases. 31 67

It is important to establish the diagnosis of temporal arteritis because the disease is treatable; treatment may prevent blindness and even death. Temporal arteritis usually occurs in people older than 51 years of age, although very rarely, histologically documented disease occurs in younger people. The onset may be occult, so that there are few findings. A multitude of signs and symptoms may occur such as fever, headaches, malaise, weight loss, anemia, stroke, cranial nerve palsies, polymyalgia rheumatica, aortitis and other large vessel involvement. The eye may suffer from ischemic optic neuropathy (anterior or posterior), central or cilio-retinal arterial occlusion, ophthalmic artery ischemia, or extraocular muscle palsies. An arterial biopsy showing giant cell arteritis establishes the diagnosis. However, a negative biopsy does not rule out the disease because of the occasional presence of skip areas. Arteriography has only rarely yielded a positive temporal artery biopsy when the initial biopsy done elsewhere was negative. As a diagnostic parameter, the erythrocyte sedimentation rate is nonspecific, being elevated in diseases other than temporal arteritis and sometimes being falsely lowered by technical factors. Furthermore, the temporal artery biopsy is occasionally positive despite a normal erythrocyte sedimentation rate. Treatment is aimed at relieving the patient's symptoms and normalizing the erythrocyte sedimentation rate. Because of the wide spectrum of clinical and laboratory finding in temporal arteritis, no one specific treatment regimen with systemic corticosteroids works for all patients. Temporal arteritis is a well known disease of the elderly which ir rarely fatal but results in significant visual morbidity (Hinzpeter & Naumann, 1976; Spencer & Hoyt, 1960). Since Hutchinson's (1890) description, more than a thousand articles have been written on the subject (Cohen & Smith, 1974). Despite this, many unanswered questions and controversies remain concerning the diagnosis, prognosis and treatment of temporal arteritis. My goal is to review these questions and areas of controversy.
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PMID:Controversies regarding giant cell (temporal, cranial) arteritis. 39 20

Twenty-seven dogs with lead poisoning were admitted to the University of Pennsylvania Veterinary Hospital from July, 1963, to April, 1975. The major source of the lead was paint. A common history was ingestion of plaster or paint scrapings during room renovation. Most of the dogs were less than 1 year old and had clinical signs referable to the gastrointestinal or the nervous system, or both. The gastrointestinal signs, in order of frequency, were vomiting, anorexia, tender abdomen, diarrhea, and constipation. The neurologic signs, in order of frequency, were hysteria, convulsions, ataxia, blindness, and mydriasis. The finding of many nucleated erythrocytes without severe anemia was nearly pathognomonic for lead poisoning. Of 14 affected dogs subjected to abdominal radiography, 9 had evidence of ingested radiopaque material. A mean blood lead concentration of 18.8 mug/100 ml, with a range of 0 to 50 mug/100 ml, was found for 26 dogs that were hospitalized for problems unrelated to lead poisoning. Of the 27 dogs with lead poisoning, 22 had their blood analyzed for lead. This group had blood lead values ranging from 40 to 530 mug/100 ml. Seven of the affected dogs were monitored throughout their period of treatment with calcium ethylenediaminetetraacetate. The concentration of lead in the blood decreased quickly after the initiation of treatment but leveled off after 2 or 3 days. The initial rapid phase probably corresponded to the removal of weakly bound or extracellular lead, whereas the slow phase probably corresponded to strongly bound or intracellular lead.
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PMID:Lead poisoning in dogs at the University of Pennsylvania Veterinary Hospital. 81 31

1. Malabsorptions and anemia can be used by ulceration or stenosis of the anastomosis, also well known in other anastomotic techniques. 2. Long-term problems are seldom seen in children secondary to side-to-side anastomosis if the technique is satifactory. Blind pouches may result from unsatisfactory technique, or may develop just as in the adult. They may or may not be symptomatic. We surely have to ask whether the blind loop will really grow with the growing child. Nevertheless this study only has historical character because since 1965 we only use end-to-end anastomosis and its modifications with the well known good results.
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PMID:Late results following to side-to-side anastomosis of the small intestine in infancy and childhood. 86 90

Temporal arteritis (granulomatous inflammation) usually involves the temporal and ophthalmic arteries, but may be part of a more widespread inflammation of the medium and large vessels. The patient usually presents with an associated group of constitutional symptoms (fever, malaise, anorexia, weight loss, anemia) and rheumatic complaints (polymyalgia rheumatic complaints (polymyalgia rheumatica). The diagnosis should be considered in any patient over 55 years old in whom these symptoms develop or in whom there is evidence of recent onset of headache, visual loss of localized arterial involvement. The diagnosis is also to be considered when the erythrocyte sedimentation rate is over 50 mm/hr, and the presence of arteritis is confirmed by temporalartery biopsy findings. Visual loss may occur in 50 percent of affected patients; other serious complications are less common. A strong clinical suspicion of temporal arteritis will permit diagnosis of the more uncommon and atypical presentations of the syndrome. Although cases of temporal arteritis may be self-limited, treatment is imperative because of the threat of blindness. Patients respond well to steroid (prednisone) therapy, which should be maintained for a prolonged period.
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PMID:Temporal arteritis. 90 43

Currently major nutrition supplementation programs in India are: 1) Integrated Child Development Services Scheme (ICDS); 2) Mid-day meal Programs (MDM); 3) Special Nutrition Programs (SNP); 4) Wheat Based Nutrition Programs (WNP); 5) Applied Nutrition Programs (ANP); 6) Balwadi Nutrition Programs (BNP); 7) National Nutritional Anaemia Prophylaxis Program (NNAPP); 8) National Program for Prevention of Blindness due to Vitamin A Deficiency; and 9) National Goiter Control Program (NGCP). The history of the respective programs, their beneficiaries, objectives, activities, organization, and evaluation are detailed. The ICDS beneficiaries are children below 6 years, pregnant and lactating mothers, and women aged 15-44 years, who are provided the following: supplementary nutrition; immunization; health check-ups; referral services; treatment of minor illnesses; pre-school education to children aged 3-6 years. The MDM program's intended beneficiaries are children attending the primary school. Children belonging to backward classes, scheduled caste, and scheduled tribe families are given priority. The SNP is to provide supplementary nutrition and health care services including supply of vitamin A solution and iron and folic acid tablets to pre-school children, and pregnant and lactating mothers of poor groups in urban slums and tribal areas. The ANP strives to make people conscious of their nutritional needs and to provide supplementary nutrition to children aged between 3-6 years and to pregnant and lactating mothers. The beneficiaries of the WNP scheme are children of pre-school age and nursing and expectant mothers in areas with high infant mortality such as urban slums and backward rural areas. The program of BNP aims to supply about one-third of the calorie and half of the protein requirements of pre-school children between the age of 3-5 years to improve the nutritional status. The NNAPP scheme beneficiaries are children in the 1-5 age group and pregnant and nursing mothers, female acceptors of terminal methods of family planning and IUDs. The NGCP aims to supply iodized salt to the entire country by 1992.
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PMID:National nutrition supplementation programmes. 129 17

Cytomegalovirus retinitis, the major cause of blindness in patients with the acquired immunodeficiency syndrome, can be arrested by early detection and treatment. We identified 9 screening indices for early CMV retinitis: T-4/T-8 ratio less than 0.11, T-4 count less than 30, T-8 count less than 500, leukocytes less than 4,200, platelets less than 240,000, hemoglobin less than 11.6, hematocrit less than 35, less than 6 for a diagnostic profile which incorporates these 7 indices, and less than 2 for the IA-sum which compounds T-cell inversion and anemia. A threshold value was determined for each index, identified by retrospective review of charts of 15 patients with CMV retinitis and 30 without. Sensitivity, specificity, positive predictive value, negative predictive value, and receiver operating characteristic curve area was calculated. The best screening index was the T-cell ratio, which had the highest sensitivity (0.93), negative predictive value (0.94-0.99) and receiver operating characteristic curve area (0.89), and a positive predictive value among the highest (0.50-0.82).
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PMID:Screening indices for cytomegalovirus retinitis in patients with human immunodeficiency virus. 131 Mar 46

The earliest written report of selenium poisoning is thought to be the description by Marco Polo of a necrotic hoof disease of horses that occurred in China in 13. century. However recognition of Se as toxic principle come in the early 1930s. Severity of Se poisoning depends on chemical forms of the element, species of animals and routes of administration. The soluble Se salts (Na2SeO3 and Na2SeO4) appear to be among the more toxic compounds; the Se inherent in grains and selenoamino acids (selenomethionine and selenocystine) appear to have relative moderate toxicity; the poorly soluble forms (e.g., elemental Se, Na2Se, SeS2 and diphenyl selenide) are among the least toxic of the Se compounds. In general, toxicity of Se compounds are substantially less when they are administered orally than when they are given parenterally. Rosenfeld and Beath described three clinical types of Se intoxication: acute selenosis, subacute selenosis (i.e., blind staggers type), and chronic selenosis (i.e., alkali disease type). Acute poisoning occurs when high Se content plants are consumed in large quantities within short period. Accidental acute poisoning occurs as consequence of errors in formulation of a Se supplemented diet. The most characteristic sign of acute selenosis is garlic breath due to the pulmonary excretion of volatile Se metabolites. Other signs include lethargy, excessive salivation, vomiting, dyspnea, muscle tremors and respiratory distress. Pathological findings are: congestion of the liver and kidney, fatty degeneration and focal necrosis of the liver, endocarditis and myocarditis. Subacute selenosis ("blind staggers") occurs as a consequence of exposure to large doses of Se over a longer period of time and manifests with neurological signs (e.g., blindness, ataxia, disorientation) and respiratory distress. This form of selenosis is most frequently observed in grazing animals that have consumed Se-accumulated plants. Chronic selenosis ("alkali disease") comes about when animals consume moderate levels of Se (more than 5 mg/kg and less than 40 mg/kg) for period of weeks or months. The usual clinical signs of chronic selenosis in horses, cattle and swine are: loss of hair (horses and cattle lose long hair from the mane and tails), emaciation, hoof lesions and lameness. In advanced cases liver cirrhosis, atrophy of the heart and anemia occur. In swine symmetrical poliomyclomalacia of cervical and lumbal/sacral spinal cord segment has been seen. Sheep seen to be more tolerant and get milder form of the disease. They lose appetite and have reduced gain. In growing chicks reduced gain and feed intake, rough feathers, and characteristics of nervousness has been observed. Reduced egg production, embryonic deformations and reduced hatchability has been observed in hens.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Selenium toxicity in domestic animals]. 134 Apr 80

Hunger and malnutrition in Africa have been on the increase since the 1960s. During the 1970s, it is estimated that 30 million people were directly affected by famine and malnutrition. About 5 million children died in 1984 alone. In Mozambique during the 1983-84 famine, about 100,000 people perished. In Ethiopia, Sudan, Somalia, Liberia, and Angola armed conflicts compound the problem. Ethiopia alone had 9 million famine victims in 1983. The most common form of malnutrition in Africa is protein energy deficiency affecting over 100 million people, especially 30-50 million children under 5 years of age. Almost another 200 million are at risk. Iron deficiency, commonly called anemia, also affects 150 million people, mostly women and children. Iodine deficiency leads to disorders like mental retardation, cretinism, deafness, abortion, low resistance to disease, and goiter and this affects 60 million with about 150 million more at risk. Vitamin A deficiency causes blindness and low resistance to disease and affects about 10 million. Protein energy deficiency is treated by using donated foods in hospitals, rehabilitation centers, day care centers, and feeding centers. There are no community programs for anemia, or vitamin A or iodine deficiencies. Vaccines for preventing and drugs for treating diseases that cause malnutrition are imported. Therefore, African food and nutrition professionals met in 1988 and created the Africa Council for Food and Nutrition Sciences (AFRONUS) to eliminate famine and malnutrition in Africa. Activities have started in: 1) developing contacts between the workers in food and nutrition; 2) assessing the situation of food and nutrition in Africa; 3) developing an action plan; 4) implementing the plan; and 5) monitoring progress. Food and Nutrition Policy Guidelines have also been prepared by AFRONUS for food and nutrition workers. Africa has enough natural resources to solve the problem of hunger and malnutrition, but these resources have to be harnessed.
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PMID:Hunger and malnutrition: the determinant of development: the case for Africa and its food and nutrition workers. 139 7


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