Disease relevance of Cadmium Poisoning

• Results of the in vivo studies are consistent with a significant role of cadmium in the etiology of Itai-Itai disease among postmenopausal women in Japan and may in part explain the increased risk of postmenopausal osteoporosis among women who smoke [1].
• Osteomalacia of cadmium (Cd) poisoning (Itai-Itai disease) is induced by renal tubular dysfunction; however, the precise pathological changes and mechanisms have not been adequately elucidated [2].
• Studies on the women with acquired Fanconi syndrome observed in the Ichi river basin polluted by cadmium. Is this Itai-itai disease [3]?
• Retinol-binding protein in tubular proteinuria of patients with Itai-Itai disease [4].
• Relating our results to humans, women who contracted itai-itai disease (analogous to mice on the deficient, 5 ppm cadmium diet), in addition to their characteristic bone disease, could have experienced decreases in fertility and in growth of their offspring related to their dietary deficiencies [5].

High impact information on Cadmium Poisoning

• Regression analyses of data from cases of itai-itai disease suggested that an Aluminon-positive metal inhibited mineralization and that renal tubules were injured [6].
• Neither ferritin nor transferrin were visualized at mineralization fronts in itai-itai disease by immunohistochemical staining [6].
• Furthermore, proper cancellous tissue of the ribs from 24 autopsy cases of Itai-itai disease with Looser zones or with the healing bands, 27 autopsy cases of Itai-itai disease without such lesions, and 29 control cases were studied by the same method to pursue the histogenesis of Looser zones [7].
• No relationship exists between itai-itai disease and TA repeat polymorphisms of the estrogen receptor alpha gene [8].
• However, estrogen receptors have never been studied in itai-itai disease [9].

Chemical compound and disease context of Cadmium Poisoning

• Twelve Looser zones and 17 healing bands of the ribs obtained from autopsy cases of Itai-itai disease were analyzed by bone histomorphometry [7].
• To investigate whether chronic exposure of cadmium (Cd) chloride induces osteomalacic lesions similar to Itai-itai disease (IID), ovariectomized rats were injected intravenously with the cadmium at doses of 0.05 and 0.5 mg/kg/day, 5 days per week, for 50 weeks [10].
• Retinol-binding protein(RBP) was purified from fresh urine of patients suffering from Itai-Itai disease [11].
• Renal cortex in 15 cases with Itai-itai disease was morphometrically examined, i.e. the cross-size of tubuli in the renal cortex was measured using a color image analyzer (Olympus CIA-102) and the ratio of preserved urinary tubuli occupying renal cortex was calculated by means of the point-counting method [12].
• Iron (Fe) concentrations in liver and kidney of cadmium (Cd)-exposed people (11 Itai-Itai patients, 13 persons requiring observation and 4 Cd-exposed persons) were compared with those of nonexposed people [13].

Biological context of Cadmium Poisoning

• The results provide evidence that the combination of cadmium exposure and multiparity may have played a role in the etiology of Itai-Itai disease in Japan [14].
• Such results may bear on the etiology of Itai-Itai disease, a disease of the skeleton potentially related to oral cadmium exposure, with an incidence predominantly among postmenopausal women with a history of multiple childbirths [15].
• A comparison between health effects of cadmium and cadmium concentration in urine among inhabitants of the Itai-itai disease endemic district [16].
• Bone density was measured in 28 women with itai-itai disease, 92 men and 114 women with cadmium-induced renal dysfunctions and 44 men and 66 women living in the three different non-polluted areas using a microdensitometer [17].
• Biological monitoring of cadmium exposure in itai-itai disease epidemiology [18].

Anatomical context of Cadmium Poisoning

• CONCLUSION: We concluded that in Cd poisoning, a mitochondrial gene deletion in the mitochondria of the proximal tubule cells was the primary event for the pathogenesis of osteomalacia in itai-itai disease [19].

Gene context of Cadmium Poisoning

• Urinary N-acetyl-beta-D-glucosaminidase and beta 2-microglobulin in 'itai-itai' disease [20].
• Demonstration of vitamin D-binding protein (Gc-globulin) in the urine of Itai-itai disease patients [21].
• We have recently reported that the serum level of erythropoietin (EPO) remained low despite the severe anemia in patients with Itai-itai disease, the most severe form of chronic Cd intoxication [22].
• Hypoproduction of erythropoietin contributes to anemia in chronic cadmium intoxication: clinical study on Itai-itai disease in Japan [23].
• Urinary trehalase activity and leucine aminopeptidase activity were parabolically correlated with urinary beta 2-microglobulin, and these enzymes were observed to be biphasic in relation to urinary beta 2-microglobulin when the study populations included patients of Itai-itai disease and inhabitants of a cadmium-polluted area [24].

Analytical, diagnostic and therapeutic context of Cadmium Poisoning

• An animal model for itai-itai disease was produced in rats by low-dose Cd treatment, intraperitoneally for a period of 70-80 weeks [19].
• Epidemiological studies on cadmium in the environment in Japan: etiology of itai-itai disease [25].

References