| For medical practitioners and osteopaths - Osteopathy Journal Articles Catalog. |
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| Effects of different doses of vitamin D on the nature of the osteopathy produced by calcium deficiency in the growing rat Mathieu, H., M. Laval-Jeantet, et al. (1966), Pediatrie 21(3): 351-2. |
| Effects of vitamin D on protein turnover in children with renal osteopathy Denisova, S. N., E. K. Kutafina, et al. (1996), Vopr Pitan(6): 31-4. Abstract: Amino acid analysis and investigation of nitrogen balance were done in 2 groups of the patients with renal failure and osteodystrophy on the diet and vitamin D treatment. The results of the investigations confirm vitamin D influence on free amino acid turnover. We observed significant elevations of plasma amino acids in patients treated with the diet and vitamin D in comparison with the patients without vitamin D supplementation. Vitamin D didn't influence on the retention, urinary and fecal excretion of endogenous nitrogen in patients with renal failure |
| Elimination of urinary steroids in certain forms of menopausal osteopathy. Vanek, R. (1960), Ann Endocrinol (Paris) 21: 899-908. |
| Endocrine-metabolic aspects of rarefying osteopathy of patients with cirrhosis Grandi, M., S. Pederzoli, et al. (1991), Recenti Prog Med 82(7-8): 363-6. Abstract: Hepatic diseases and particularly cholestasis are well known to affect bone metabolism and induce osteoporosis. We have studied bone metabolism in normal volunteers and in 20 patients with non alcoholic liver cirrhosis without cholestasis, classified stage "B" according to Child's classification. A reduced bone density as measured by mineralometry was observed in patients as compared to controls. Serum osteocalcin and urinary hydroxyproline levels were consistent with the "low turnover" osteoporosis type of osteopathy. The major determinants of the bony loss seem to be low blood testosterone and the consequent reduced metabolism in cirrhotics. |
| Engelmann's disease; (hyperostotic sclerosing infantile multiple osteopathy). de, S. S. and M. Grivaux (1950), Acta Physiother Rheumatol Belg 17(12): 622-31. |
| Engelmann's disease; hyperostotic and multiple sclerosing infantile osteopathy. Jammes, A., R. Serny, et al. (1953), Rev Rhum Mal Osteoartic 20(5): 406-14. |
| Evaluation and critical review published in the European literature on osteopathic studies in the clinical field and in the area of fundamental research Schwerla, F., K. Hass-Degg, et al. (1999), Forsch Komplementarmed 6(6): 302-10. Abstract: OBJECTIVE: Identification of studies of osteopathic treatment in defined countries. Evaluation of methods and results of the studies and assessment of the available evidence concerning the effectiveness of osteopathy. STUDY DESIGN: Systematic review. Assessment of the quality of the studies, with respect to the osteopathic concept and current methodological criteria according to predefined keys. DATA SOURCES: Clinical trials and fundamental studies originating from Germany, England, Austria, The Netherlands, Scandinavia +/- published or unpublished. RESULTS: Out of a total of 30 studies retrieved, 9 reached the predetermined minimum number of points to be rated into quality categories. In 2 of these studies the osteopathic treatment was more effective than the control intervention (p < 0.05). CONCLUSIONS: No definitive conclusions about the effectiveness of osteopathy can be drawn so far because of the low number of evaluated studies. It seems necessary to scrutinize the relevance of osteopathy through further methodologically adequate studies. Additionally, criteria for evaluation are proposed which correspond to the highest international standards in order to ensure a valid (and commonly accepted) evaluation of the osteopathic literature. |
| Experimental studies on the pathogenesis of osteopathy in uremia Krempien, B. and E. Ritz (1971), Verh Dtsch Ges Inn Med 77: 249-52. |
| Familial condensing osteopathy with leontiasis ossium Bernard, R., F. Giraud, et al. (1972), Arch Fr Pediatr 29(4): 447. |
| Familial striated osteopathy. Layani, F., R. Ducroquet, et al. (1954), Rev Rhum Mal Osteoartic 21(2): 154-8. |
| Fibrous osteopathy of the face. Beaux, F. and M. E. Peetermans (1955), Arch Stomatol 10(2): 75-86. |
| Fibrous osteopathy; hyperplastic tumors and latent sclerosis of the jaws. Dechaume, M. and S. Coronel (1950), Revue Stomatol 51(4): 227-60. |
| Fluoride osteopathy induced by niflumic acid Hummel, P., R. Treves, et al. (1983), Ann Radiol (Paris) 26(8): 687-90. |
| Generalized osteopathy associated with functional disorders of the renal tubules. Hiltemann, H., F. Kuhlencordt, et al. (1952), Dtsch Arch Klin Med 199(5-6): 538-53. |
| Generalized osteopathy with pathological fractures in a patient with long-term exposure to fluorine-containing plastics Rhomberg, W., F. Bohler, et al. (1995), Schweiz Med Wochenschr 125(48): 2330-7. Abstract: In a 68-year-old man with a painful syndrome of the lower extremities which began at the age of 64 years, workup revealed a generalized osteopathy with sclerosis of the axial skeleton and osteopenia at the extremities associated with pathologic fractures. The occupational history showed exposure to several synthetics such as vinyl chloride, polyethylene, delrine and polyamides over 30 years. However, a presumptive connection between the skeletal disorder and the occupational exposure could not initially be substantiated. In a later analysis of the bone biopsies from 1991, a significant increase of fluorine in the tibia and fibula of the patient was detected and thus the diagnosis of industrial fluorosis established. The fluorine presumably originated from the workup of polytetrafluorethylene plates. A detailed analysis of the workplace is ongoing. The fluorosis may obviously appear as a variable skeletal disease. The clinical picture of fluorosis is incompletely described in most of the German textbooks. It calls for an extended description of the X-ray findings associated with fluorosis and a new definition of the disease. |
| Generalized rarefying osteopathy. Casuccio, C. (1957), Riforma Med 71(37): 1029-36. |
| Generalized scleroderma with atrophico-condensating diffuse osteopathy and arthropathy and calcinosis associated with tuberculous lymphadenitis; clinical and radiologic study. Trimarchi, E. and F. Racchiusa (1953), Marginalia Dermatol 7: 42-56. |
| Glycosuric osteopathy: so-called Fanconi syndrome in adults. Kuhlencordt, F. (1958), Ergeb Inn Med Kinderheilkd 9: 622-65. |
| Gouty osteopathy. Clinical case report of the disease with an unusual course Pacovsky, V., H. Wilczek, et al. (1985), Cas Lek Cesk 124(24): 749-51. |
| Hemochemical picture of 3 cases of Camurati-Engelmann's osteopathy. Cozzolino, A. (1960), Arch Ortop 73: 541-4. |
| Hemopathy caused by osteopathy. Pietrogrande, V. (1955), Minerva Pediatr 7(50): 1652-4. |
| Hemophilic osteopathy of the wing of the ilium Cosmacini, G. and F. De Cataldo (1966), Arch Ortop 79(4): 199-202. |
| Heparin-induced osteopathy in animal experiments--a model for osteoporosis? Influence of heparin on the concentrations of hydroxyapatite, citrate, and hydroxyproline in the bones of rats of various ages. I Hahnel, H., K. Lindenhayn, et al. (1973), Z Alternsforsch 27(1): 71-5. |
| Hepatobiliary osteopathy Mirejovsky, P. (1973), Cesk Patol 9(1): 24-30. |
| Hepatogenic osteopathy. Results of histomorphometric studies Schiwy-Bochat, K. H., H. Kuhn, et al. (1991), Pathologe 12(2): 89-93. |
| Hexa-calcium-hexa-sodium-hepta-citrate hydrate complex for prophylaxis and treatment of renal osteopathy in chronic hemodialysis Albert, F. W., U. Schmidt, et al. (1973), Med Welt 24(5): 185-7. |
| Hunger osteopathy as a sequel of dystrophy. Weber, H. J. (1958), Arch Orthop Unfallchir 49(5): 486-92. |
| Hyperostosis corticalis deformans juvenilis: unfamiliar generalized osteopathy in 2 siblings. Swoboda, W. (1958), Helv Paediatr Acta 13(4): 292-312. |
| Hypertrophic osteopathy and acropachy associated with noncirrhotic alcoholic liver disease. Apropos a case Farrus, M., G. Ortiz, et al. (1989), Aten Primaria 6(4): 246-8. Abstract: Hypertrophic osteoarthropathy (HOA) may be an idiopathic condition or may be secondary to other diseases, the most common of which is bronchogenic carcinoma. Among non neoplastic etiologies, it is commonly associated with chronic liver disease, usually cirrhosis and chronic active hepatitis. The concomitant occurrence of HOA and hepatic steatosis is another association that has recently been reported. We report here a 70-year-old male with periostitis, clubbing of the fingers and alcoholic hepatitis stenosis. We emphasize the need to perform observational studies to validate this association. |
| Hypertrophic osteopathy and thyroid cancer Dexemple, P., J. P. Leleu, et al. (1984), Rev Rhum Mal Osteoartic 51(2): 105-7. |
| Hypertrophic osteopathy in alcoholic males Szanto, D. (1989), Orv Hetil 130(12): 625-7. Abstract: Hypertrophic osteopathy was observed in 5 alcohol addict men. Periosteal newbone formation on the femur, tibia, fibula, radius and ulna appeared symmetrical. The short tubular and flat bones of hands and feet did not suffer impairment. Liver biopsy confirmed in each case portal cirrhosis. Hypertrophic osteopathy is a late complication of alcohol disease. Its development may be due to individual predisposition influenced by nutritional, hormonal, genetic, pancreatohepatic and biomechanical factors. |
| Hypertrophic pulmonary osteopathy. Brauner, R., D. Grigorescu, et al. (1957), Med Interna (Bucur) 9(1): 131-7. |
| Hypertrophic toxic osteopathy associated with metastatic pulmonary myxochondrosarcoma; description of a case. De Lima, F. D. (1955), Mem Inst Oswaldo Cruz 53(2-4): 573-87. |
| Hypophosphatasia. New osteopathic syndrome. Saggese, M. (1960), Pediatria (Napoli) 68: 746-51. |
| Iatrogenic aluminum osteopathy in a uremic infant Koch, H., H. Reich, et al. (1986), Monatsschr Kinderheilkd 134(5): 279-81. Abstract: An infant with uremia due to congenital renal hypoplasia was treated with oral aluminum hydroxide for 9 months in an attempt to reduce hyperphosphatemia. An increasingly painful osteopathy with pathological fractures ensued with loss of thoracic wall stability and respiratory failure. Increased serum aluminium levels and histochemically proved deposits of aluminium at the mineralisation front between calcified and noncalcified osteoid were demonstrated. In the context of recent findings concerning aluminium bone toxicity it is beyond doubt that this phosphate binding agent was detrimental for this child. Though a low phosphate diet normalized hyperphosphatemia after aluminium hydroxide treatment had been stopped, no effect on the progressive osteopathy was observed. Since aluminium hydroxide as a phosphate binder can be replaced by calcium carbonate or a low phosphate diet at least in young children, it should not be further recommended in this age group. This seems especially important in nondialyzed patients. |
| Incidence and origin of calcipenic osteopathy. Pahlke, G. and K. H. Drogula (1959), Munch Med Wochenschr 101(8): 325-8 passim. |
| Incidence, degree of severity and type of renal osteopathy during chronic home dialysis treatment Henning, H. V., G. Delling, et al. (1977), Verh Dtsch Ges Inn Med 83: 1299-302. |
| Influence of diphosphonate on experimental heparin-osteopathy Hahnel, H., R. Muhlbach, et al. (1973), Z Alternsforsch 27(3): 289-92. |
| Informative value of ultrasonic diagnosis in recognizing metabolic osteopathy in children with enzymopathy of the small intestine Abduzhabbarova, Z. M. and F. M. Gaffarova (2002), Lik Sprava(3-4): 76-9. Abstract: Metabolic osteopathy has been ascertained in all patients presenting with grave forms of enzymopathy of the small intestine. Revealed in studying of mineral metabolism and calcium-regulating hormones was the osteomalacia syndrome. Ultrasound echoosteometry is an informative non-invasive mode of diagnosis of secondary osteopathy in patients with enzymopathy of the small intestine. |
| Inhibition of prednisolone osteopathy by diphosphonate (EHDP) in an animal experiment Trzenschik, K., K. Lindenhayn, et al. (1989), Beitr Orthop Traumatol 36(3): 81-91. Abstract: The application of a low dose of prednisolone (0.4 mg per kg body weigh and day) in young hamsters leads to a loss of bone mass. This effect is inhibited by the administration of the diphosphonate EHDP (6.2 mg per kg body weight and day). The total volume of the limb bones is increased. The application of a high dose of prednisolone (40 mg per kg body weight and day) induces a severe osteopathy. These pathological bone changes couldn't be prevented by EHDP, but there was a significant shift of the investigated parameters into the direction of normalization. |