Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002895 (sickle cell disease)
 11,747 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mortality of infants aged 0-30 months was studied in a subdistrict of the eastern Ivory Coast with a population of 240,000 inhabitants. A cluster sample of the type recommended by the World Health Organization for evaluating progress of the expanded program of immunizations consisted of 2 samples with 30 clusters of 70 children each, 1 taken in urban Abengourou and the other in rural cantons of the subprefecture of Abengourou. A standardized questionnaire was administered to all the mothers about their births within the last 3 years. Supplementary questionnaires concerning all deaths of children of the sample mothers were interpreted by 3 physicians who agreed on a probably diagnosis in each case. The survey covered 2375 infants under 1 year and 1825 aged 12-30 months. The total mortality was 103 deaths in the total sample and 70 for infants aged 0-11 months, for a rate of 29.4%. The difference between the urban rate (31.7%) and the rural rate (26.8%) was not significant. The rate varied significantly by sex for deaths due to malnutrition (11 boys, 1 girl), and pneumopathies (6 girls, 1 boy). Mortality varied significantly according to treatment received and place of death. 55% received traditional treatment and 45% modern treatment. 53% died at home, 36% at a health center, and 9% at the home of a healer. Among infants aged 0-27 days, the cause of death was tetanus for 8, prematurity for 12, neonatal distress for 5, neonatal jaundice for 5, and infection for 2. Among infants aged 1-11 months the cause of death was malaria for 10, meningitis for 7, tetanus for 2, diarrhea for 9, pneumopathy for 3, measles for 4, whooping cough for 2, and unknown for 1. Among infants aged 12-30 months the cause of death was malaria for 11, malnutrition for 12, meningitis for 3, pneumopathy for 4, measles for 1, and sickle cell anemia for 2. Malaria was the single most important cause of death followed by malnutrition for the overall sample. In urban and rural areas respectively, the proportions of infants correctly vaccinated for their age groups were 78.1% and 76.0% for those under 11 months; 92.3% and 80.6% for those 12-17 months; 78.3% and 76.6% for those 18-23 months; and 66.5% and 71.4% for those 24 months and over. Mortality rates varied very significantly by vaccination status. 70 of the children dying had not been vaccinated. Their mortality rate was 19.6%, compared to .5% for children in process of vaccination, 1.1% for children incompletely vaccinated, and .9% for children correctly vaccinated.
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PMID:[Infant mortality and its causes in a sub-district of the Ivory Coast]. 196 15

Ticlopidine inhibits platelet aggregation induced by adenosine diphosphate (ADP) and most other platelet agonists in ex vivo studies of human platelets. The drug also improves other abnormalities of platelet function seen in patients with cerebrovascular disease, peripheral arterial disease, ischaemic heart disease or other conditions involving platelet hyperaggregation. Abnormal platelet activity has been implicated in a variety of clinical conditions in which patients are at high risk of thromboembolic events, and thus the effectiveness of ticlopidine has been investigated in such patients. Since the initial review of the drug appeared in the Journal, data from several large multicentre studies have shown that ticlopidine has a substantial benefit to offer patients who have experienced transient ischaemic attacks or stroke, and in those with peripheral arterial disease or ischaemic heart disease. Ticlopidine reduces the incidence of further stroke, myocardial infarction or vascular death, and is superior to placebo and aspirin in this regard in studies of patients with recent stroke or transient ischaemic attacks, or intermittent claudication. Ticlopidine is equally effective in both men and women and also improves symptoms of claudication in patients with peripheral arterial disease, and appears to reduce anginal pain. Patients with subarachnoid haemorrhage and sickle cell disease have shown some improvement with ticlopidine administration. The drug reduces thromboembolic events and re-stenosis in patients undergoing haemodialysis and cardiac surgery, and appears to prevent the progression of nonproliferative diabetic retinopathy. Ticlopidine in large clinical trials is associated with a higher incidence of adverse effects than placebo and an overall incidence similar to aspirin. Most adverse effects do not require withdrawal of treatment. Gastrointestinal symptoms (particularly diarrhoea) are most common, occurring almost twice as frequently with ticlopidine as with aspirin. Other adverse effects associated with ticlopidine include skin rash, haemorrhagic disorders, and haematological effects; these latter effects require careful monitoring of patients during the initial weeks of therapy. In conclusion, ticlopidine is a valuable addition to the prophylactic treatments available for the management of patients with cerebrovascular disease, peripheral arterial disease or ischaemic heart disease, who present a high risk of thromboembolic events. Although tolerability may be a problem for some patients, the overall benefit conferred by the drug would appear to outweigh this potential disadvantage. Because of its antiplatelet activity, ticlopidine has a promising role in other disorders mediated by platelet dysfunction. However, the precise role of the drug in these additional therapeutic indications awaits clarification with wider clinical experience.
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PMID:Ticlopidine. An updated review of its pharmacology and therapeutic use in platelet-dependent disorders. 222 15

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc, thus the prevalence of zinc deficiency is likely to be high in the population subsisting on cereal proteins mainly. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE, and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues. Zinc atoms in some of the enzyme molecules participate in catalysis and also appear to be essential for maintenance of structure of apoenzymes. Zinc also plays a role in stabilization of biomembrane structure and polynucleotide confirmation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and biochemical manifestation zinc deficiency in human subjects. 241 3

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in the population subsisting mainly on cereal proteins. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE (acrodermatitis enteropathica), and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy, and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances, and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical and biochemical manifestations of zinc deficiency in human subjects. 258 Aug 77

To study the etiology of chronic childhood diarrhea among Nigerian children, 142 patients, aged 6 months to 5 years, with diarrhea for at least 1 month, were evaluated; the study took place during January-December 1983 at the Ahmadu Bello University Teaching Hospital, Zaria, Northern Nigeria. Enteropathogenic agents were identified in stools of 90 (63%) patients. Giardia lamblia and Entamoeba histolytica were most commonly detected, representing 41% and 23%, respectively, of all parasitic pathogens. In children with negative stool microscopy, chronic diarrhea was associated with primary lactose intolerance (2 cases), abdominal tuberculosis (2 cases), hyponatremia, low serum albumin, anemia due to sickle cell disease, or Staphylococcus aureus infection. In contrast with chronic diarrhea etiologies reported among children in Europe and North America, infections were the major cause of chronic childhood diarrhea among these children. In general, it is accepted that intestinal infection usually produces acute diarrhea--and that, if the host fails to mount a competent immune response, if there is repeated exposure to infectious agents, or if severe infection damages a substantial proportion of absorptive cells, then severe, protracted diarrhea may result. The high case fatality rate of 9% in this series was associated with specific infectious complications of septicemia, bronchopneumonia, lobar pneumonia and measles. Severe malnutrition also worsened the prognosis in chronic diarrhea. The results indicate that early detection and treatment of amebiasis and giardiasis is a useful approach in the treatment of chronic diarrhea cases among children.
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PMID:Chronic diarrhoea in Nigerian children. 383 11

The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal diseases, following uses of certain drugs such as penicillamine for Wilson's disease and diuretics in some cases, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. In pregnancy and during periods of growth the requirement of zinc is increased. The clinical manifestations in severe cases of zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males; it is fatal if unrecognized and untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss, and hyperammonemia. Zinc is a growth factor. Its deficiency adversely affects growth in many animal species and humans. Inasmuch as zinc is needed for protein and DNA synthesis and for cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis. Whether or not zinc is required for the metabolism of somatomedin needs to be investigated in the future. Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level; the hypothalamic-pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in cell division, its deficiency may adversely affect testicular size and thus affect its functions. Zinc is required for the functions of several enzymes and whether or not it has an enzymatic role in steroidogenesis is not known at present. Thymopoeitin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent. Zinc deficiency affects T-cell functions and chemotaxis adversely. Disorders of cell-mediated immune functions are commonly observed in patients with zinc deficiency. Zinc is beneficial for wound healing in zinc-deficient subjects. In certain zinc-deficient subjects, abnormal taste and abnormal dark adaptation have been noted to reverse with zinc supplementation.
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PMID:Clinical manifestations of zinc deficiency. 389 71

The essentiality of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, chronic renal disease, certain diuretics, the use of chelating agents such as penicillamine for Wilson's disease, and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during the growing age period. The clinical manifestations in severe cases of zinc deficiency included bullous-pustular dermatitis, alopecia, diarrhoea, emotional disorder, weight loss, intercurrent infections, hypogonadism in males and it is fatal if untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss and hyperammonaemia. Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and in man. Inasmuch as zinc is needed for protein and DNA synthesis and cell division, it is believed that the growth effect of zinc is related to its effect on protein synthesis. Testicular functions are affected adversely as a result of zinc deficiency in both humans and experimental animals. This effect of zinc is at the end organ level and the hypothalamic--pituitary axis is intact in zinc-deficient subjects. Inasmuch as zinc is intimately involved in a cell division, its deficiency may adversely affect testicular size and thus its function. In mice, the incidence of degenerate oocytes, and hypohaploidy and hyperhaploidy in metaphase II oocytes were increased due to zinc deficiency. Zinc at physiological concentrations reduced prolactin secretion from the pituitary in vitro and it has been suggested that this trace element may have a role in the in vivo regulation of prolactin release. Thymopoietin, a hormone needed for T-cell maturation, has also been shown to be zinc dependent. It is clear that zinc may have several roles in biochemical and hormonal functions of various endocrine organs. Future research in this area is very much needed.
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PMID:Clinical, endocrinological and biochemical effects of zinc deficiency. 390 80

The requirement of zinc for humans was recognized in the early 1960s. The causes of zinc deficiency include malnutrition, alcoholism, malabsorption, extensive burns, chronic debilitating disorders, and chronic renal diseases; use of certain drugs such as penicillamine and, in some cases, diuretics; and genetic disorders such as acrodermatitis enteropathica and sickle cell disease. The requirement of zinc is increased in pregnancy and during growth. The clinical manifestations of severe zinc deficiency include bullous-pustular dermatitis, alopecia, diarrhea, emotional disorder, weight loss, intercurrent infections, and hypogonadism in males; zinc deficiency can be fatal if unrecognized and untreated. A moderate deficiency of zinc is characterized by growth retardation and delayed puberty in adolescents, hypogonadism in males, rough skin, poor appetite, mental lethargy, delayed wound healing, taste abnormalities, and abnormal dark adaptation. In mild cases of zinc deficiency in human subjects, we have observed oligospermia, slight weight loss, and hyperammonemia. Zinc is a growth factor. As a result of its deficiency, growth is affected adversely in many animal species and humans, probably because zinc is needed for protein and DNA synthesis and cell division. The effects of zinc and growth hormone on growth appear to be independent of each other in experimental animals. Whether zinc is required for the metabolism of somatomedin needs further investigation. Thyroid and adrenal functions do not appear to change as a result of zinc deficiency. Glucocorticoids may have an effect on zinc metabolism, although the clinical relevance of this effect is not known at present. In contrast, testicular function is affected adversely as a result of zinc deficiency in both humans and experimental animals. The effect appears to be a direct one since the hypothalamic-pituitary axis is intact, and may relate to the reduction in testicular size as a result of the need for zinc in cell division. In addition, zinc is required for the function of several testicular enzymes, although a specific role in steroidogenesis has not been identified. Zinc appears to have a role in the modulation of prolactin secretion, in the secretion and action of insulin, and in the production and biologic effects of thymic hormones. It is clear that the endocrine consequences of zinc deficiency are multiple, and that continued investigation should provide additional pathophysiologic and therapeutic insights.
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PMID:Clinical, endocrinologic, and biochemical effects of zinc deficiency. 391 98

Dactylitis commonly occurs in patients with homozygous hemoglobin S disease (sickle cell anemia), sickle cell-hemoglobin C disease or sickle cell-beta-thalassemia. A case is reported of dactylitis associated with sickle cell trait, a very rare occurrence. It may be that in this patient the disorder was secondary to severe diarrhea and dehydration.
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PMID:Dactylitis in a child with sickle cell trait. 397 4

Between January 1976 and December 1978, the Microbiology Department of University College Hospital (UCH) Ibadan, isolated Salmonella typhi from the blood cultures of 93 children aged 0-14 years, who were admitted to the paediatric wards. Clinical case notes were retrieved and reviewed in 64 (68.8%) of them. Fifteen (23%) of the 64 children were less than one year of age while 22 (34%) were under the age of five years. The commonest presenting symptoms were fever, anorexia, diarrhoea and vomiting. A febrile convulsion was the presenting symptom in 13 (20%) of the patients, all of whom were under the age of five years. Hepatomegaly was almost twice as frequently observed as splenomegaly. Intestinal perforation was present in five of the patients. There was a high proportion of SS children who presented with fever, pallor, jaundice, generalized aches and pains and other clinical features of sickle cell disease and it is possible that such children are specially susceptible to typhoid fever. A clinical diagnosis of typhoid fever on admission was made in only 14 of the 64 children. Reasons are given for the low index of suspicion and it is suggested that any child with unremitting fever after adequate anti-malarial chemotherapy should be treated for enteric fever.
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PMID:Problems in the clinical diagnosis of typhoid fever in children in the tropics. 618 69


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