Dr. T. Tóth szerk.: Studia historico-anthropologica (Anthropologia Hungarica 21. Budapest, 1990)

CLINICAL PATTERNS AND THEIR DIFFERENTIAL DIAGNOSIS IN HISTORICAL MATERIAL Clinical patterns PH may accompany a wide variety of inherited or acquired diseases and pathological conditions (Table 1). It is frequently associated with severe, congenital clinical patterns, its frequency is almost 100% with Cooley-anaemia cases, while it is 50-80% with spherocytic and sickle-cell anaemias. Acquired haemolithic anaemias, the continuous consumption of haemolithic toxins (some mycotoxins, filix maris), chronic toxic conditions usually have 5-10% of associated PH. Some hallucinogenic fungi contain fallizin, a haemolithic toxin (LÁSZLÓ 1981). These formed a regular item in the diet of shamanistic peoples. PH is rare in megaloblastic anaemias (B-j2 vitamin deficiency, folic acid deficiency) (LALLO & al. 1977, HENGEN 1971). Most iron deficiency anaemias are caused by biased diets. Iron deficiency anaemia develops with an almost 100% certainty if a mixed diet with greens and meat is not introduced at the age of 618 months. Anaemia starts in the first year of the children's life and it ends only with a basic change of diet. In the Middle Ages children were breast-fed up to the age of 2-3 years according to historical sources. Breast-feeding was occasionally supplemented by cereals (bread and pulps). Infections produce rapidly developing severe anaemia with infants and young children - as a consequence of accelerated. Then it can result in even more severe nutritional anaemia with all its skeletal manifestations. Biased diet, chronic infections and achlorhydria can lead to iron deficiency anaemia with children above 5 years of age. Iron deficiency anaemia is regularly associated with malignant tumours and chronic renal diseases. The majority of anaemias is not accompanied by PH, though the living organism attempts to compensate iron deficiency anaemia by increased red blood cell production. This lesion occurs mainly on the cranial bones of children, ft is quite rare on the skulls of adults but it is more frequent on their sternum and ribs. Uncured and therefore lasting iron deficiency and nutritional anaemias lead to the formation of cribra in 50-80% of the recent material. A similar ratio is probable for historical material, too. Though we found no references on the relationship of PH and red blood cell count (the authors mention its presence with severe anaemia at best), we attempt to provide data from our own limited recent material. A long lasting red blood cell count of about 2 million/mm

3 or the lasting 50% decrease of haemoglobin content results in porotic alterations on the sternum and very seldom on cranial bones (primarily on the parietal bone) in 1-2% of adults. From a total of several thousand autopsies only two children who died of malignant tumours were affected with PH. Their red blood cell counts were between 1.5-2 million/mm

3 with 30-45% haemoglobin contents - despite chemical and transfusion therapies. Though leukaemia also has associated anaemia and bone marrow hyperplasia, no PH was found at all in 100 autopsy cases of leukaemia. Red blood count may be as high as 6 million/mm

3 with 130-160% haemoglobin contents in congenital

, heart malformation (Fallot tetralogy, truncus arteriosus, Eisenmenger disease, transposition of great blood-vessels, etc.). Only 1-5% of the cases showed PH in spite of the increased red blood cell production. Differential diagnosis It is not difficult to establish differential diagnosis for recent cases with laboratory data available. However, the situation is quite different with PH of fossil bone material. When we try to draw conclusions on etiology on the primary disease, we must consider a number of factors, as the geographical and race frequency of diseases, all kinds of morphological and radiographic alterations of bones, and family relations.