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Query: UMLS:C0240066 (iron deficiency)
7,156 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A well-preserved mummified child from about A.D. 1200 was recovered fron Canyon de Chelly in northeastern Arizona in 1971. Striking skull changes were found and microscopic, ultrastructural, and cytochemical studies confirm the diagnosis of porotic hyperostosis that resulted in spongy bone appearance. We suggest that a possible cause for this condition could be iron deficiency of a severity seldom found in modern societies.
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PMID:Spongy bones in prehistoric America. 77 29

Porotic hyperostosis was observed in 34 percent of 539 crania excavated from sites in Arizona and New Mexico. Common causes of this cranial pathology in the Old World (thalassemia, sickel cell anemia, and malargia) do not explain its occurrence in the American Southwest, as malaria and hemoglobinopathies are not known to have existed in the New World prior to European contact. Iron deficiency anemia which may also be assoicated with porotic hyperostosis occurs on a mass level only with hookworm infestation or nutritionally-related iron deficiency. Since hookworm infestation is rare in the American southwest and has not been reported in prehistoric southwestern American Indians, the hypothesis of nutritional anemia was examined. In canyon bottom sites where the diet was heavily dependent on maize, which is low in iron and also contains an inhibitor of iron absorption, significantly more crania had porotic hyperostosis than in sage plain sites, where the diet included ample animal protein rich in easily absorbable iron (p less than .001). Furthermore, canyon bottom children, who were more susceptible to iron deficiency anemia, had a higher incidence of porotic hyperostosis lesions than adults (p less than .0001).
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PMID:The paleoepidemiology of porotic hyperostosis in the American Southwest: Radiological and ecological considerations. 110 84

The 256 skulls and 66 skull fragments of the pre-Columbian Peruvian Indians in the Hrdlicka archeologic collection were examined for a porous bone lesion known as porotic hyperostosis. The age, sex, and geographic distribution, as well as the severity and pattern of involvement of the skull bones were noted in an attempt to define the etiology and the pathogenesis of the lesion. Porotic hyperostosis of the skull was present in 20% of the specimens and was probably caused by marrow expansion on the basis of iron deficiency. The lesion was more prevalent and severe among coastal dwellers; men and women were equally affected, and the parietal and occipital bones were the most frequently involved sites. Severe cases were observed only in infants and children, presumably because of limited marrow space and a special predilection for iron deficiency in infants, and of healing of the lesion in adults. Radiographic abnormalities included thinning of the outer table of the skull, diploic space widening, and a "hair-on-end" appearance. Sixty percent of all cases and 100% of severe cases demonstrated one or more of these findings.
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PMID:On the etiology and pathogenesis of porotic hyperostosis of the skull. 638 27

The present study discusses in detail the osteological changes associated with sickle cell anemia in children and their importance in differential diagnosis. Posterior calcaneal and specific articular surface disruptive metacarpal lesions are diagnostic for sickle cell anemia. Calvarial thickening, tibial and femoral cortical bone thickening, and bowing are of more limited utility in differential diagnosis. Granular osteoporosis, pelvic demineralization and rib broadening are nonspecific. Localized calvarial "ballooning," previously not described, may have diagnostic significance. Bone marrow hyperplastic response (porotic hyperostosis) in sickle cell anemia produces minimal radiologic changes contrasted with that observed in thalassemia and blood loss/hemolytic phenomenon. Two other issues, the osteological criteria for discriminating among the anemias and the purported relationship between porotic hyperostosis and iron deficiency anemia, are also discussed. There is sufficient information to properly diagnose the four major groups of anemias, and further, to establish that iron deficiency is only indirectly associated with porotic hyperostosis. The hyperproliferative bone marrow response (manifest as porotic hyperostosis) to blood loss or hemolysis exhausts iron stores, resulting in secondary iron deficiency.
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PMID:Recognition of sickle cell anemia in skeletal remains of children. 938 28

Porosities in the outer table of the cranial vault (porotic hyperostosis) and orbital roof (cribra orbitalia) are among the most frequent pathological lesions seen in ancient human skeletal collections. Since the 1950s, chronic iron-deficiency anemia has been widely accepted as the probable cause of both conditions. Based on this proposed etiology, bioarchaeologists use the prevalence of these conditions to infer living conditions conducive to dietary iron deficiency, iron malabsorption, and iron loss from both diarrheal disease and intestinal parasites in earlier human populations. This iron-deficiency-anemia hypothesis is inconsistent with recent hematological research that shows iron deficiency per se cannot sustain the massive red blood cell production that causes the marrow expansion responsible for these lesions. Several lines of evidence suggest that the accelerated loss and compensatory over-production of red blood cells seen in hemolytic and megaloblastic anemias is the most likely proximate cause of porotic hyperostosis. Although cranial vault and orbital roof porosities are sometimes conflated under the term porotic hyperostosis, paleopathological and clinical evidence suggests they often have different etiologies. Reconsidering the etiology of these skeletal conditions has important implications for current interpretations of malnutrition and infectious disease in earlier human populations.
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PMID:The causes of porotic hyperostosis and cribra orbitalia: a reappraisal of the iron-deficiency-anemia hypothesis. 1928 Jun 75