Implicaciones anestésicas del síndrome de Gorham / Anaesthetic implications of Gorham syndrome

No disponible

The 5-year results of an oxidized zirconium femoral component for TKA.

UNLABELLED: Osteolysis secondary to polyethylene wear is one of the major factors limiting long-term performance of TKA. Oxidized zirconium is a new material that combines the strength of a metal with the wear properties of a ceramic. It remains unknown whether implants with a zirconium femoral component can be used safely in TKA. To answer that question, we reviewed, at a minimum of 5 years, the clinical outcome and survivorship of a ceramic-surfaced oxidized zirconium femoral component implanted during 98 primary TKAs between April 2001 and December 2003. Survivorship was 98.7% at 7 years postoperatively. No revision was necessary and only one component failed because of aseptic loosening. Mean Knee Society score improved from 36 to 89. No adverse events were observed clinically or radiologically. These results justify pursuing the use of oxidized zirconium as an alternative bearing surface for a femoral component in TKA. LEVEL OF EVIDENCE: Level IV, therapeutic study. See Guidelines for Authors for a complete description of levels of evidence.

Toward a core nutraceutical program for cancer management.

As previously suggested, it may be feasible to impede tumorevoked angiogenesis with a nutraceutical program composed of glycine, fish oil, epigallocatechin-3-gallate, selenium, and silymarin, complemented by a low-fat vegan diet, exercise training, and, if feasible, a salicylate and the drug tetrathiomolybdate. It is now proposed that the scope of this program be expanded to address additional common needs of cancer patients: blocking the process of metastasis; boosting the cytotoxic capacity of innate immune defenses (natural killer [NK] cells); preventing cachexia, thromboembolism, and tumor-induced osteolysis; and maintaining optimal micronutrient status. Modified citrus pectin, a galectin-3 antagonist, has impressive antimetastatic potential. Mushroombeta-glucans and probiotic lactobacilli can amplify NK activity via stimulatory effects on macrophages. Selenium, beta-carotene, and glutamine can also increase the number and/or cytotoxic activity of NK cells. Cachectic loss of muscle mass can be opposed by fish oil, glutamine, and beta-hydroxy-beta-methylbutyrate. Fish oil, policosanol, and vitamin D may have potential for control of osteolysis. High-dose aspirin or salicylates, by preventing NF-B activation, can be expected to aid prevention of metastasis and cachexia while down-regulating osteolysis, but their impacts on innate immune defenses will not be entirely favorable. A nutritional insurance formula crafted for the special needs of cancer patients can be included in this regimen. To minimize patient inconvenience, this complex core nutraceutical program could be configured as an oil product, a powder, and a capsule product, with the nutritional insurance formula provided in tablets. It would be of interest to test this program in nude mouse xenograft models.

Effects of diphosphonate and x-rays on bone lesions induced in rats by prostate cancer cells.

Prostate adenocarcinoma-III (PA-III) cells deposited over the scapula of Lobund-Wistar (L-W) rats induced osteolytic and osteoplastic changes in that bone. The osteolytic process was prevented and interrupted by administrations of dichloromethylene diphosphonate (Cl2MDP); but the osteoplastic process, once initiated, continued. The latter process was interrupted by ionizing radiation. Treatments of PA-III-affected bones with Cl2MDP and x-rays immobilized both osteolytic and osteoplastic processes.

Long-term estrogen replacement therapy prevents bone loss and fractures.

Although several case-control studies have shown an inverse association between postmenopausal estrogen use and fractures, quantitation of fracture incidence has been lacking. To quantify the degree to which estrogen replacement therapy prevents postmenopausal osteoporosis, a retrospective study was done comparing the occurrence of fractures in 245 long-term estrogen users and 245 case-matched controls, followed for an average of 17.6 years. Quantitative bone mineral assessments were obtained from 18 women using estrogen replacement therapy and their controls (average age, 73 years). Osteoporotic fracture incidence in estrogen users was 50% as great as in the controls (p less than 0.01). Estrogen users showed significantly greater bone mineral: 54.2% greater spinal mineral (p less than 0.0002), 19.4% greater forearm mineral (p less than 0.0005), and 15.6% greater metacarpal cortical thickness (p less than 0.005). Long-term estrogen replacement therapy confers significant protection against bone loss and fracture.

Fluoride in the prevention of osteopenia: studies of the skeletal mass in calcium deficient rats.

Growing rats, five weeks old and weighing 80 g at the beginning of the experiment, during 30 weeks were given a normal diet and distilled water with, in one group, a fluoride supplement of 50 ppm. During this period all animals gained weight similarly. The skeletal mass of the fluoride treated animals became slightly but siginficantly larger than that of the controls. After 30 weeks half of the animals were given a calcium deficient diet for another 16 weeks. Osteopenia developed regardless of a simultaneous fluoride supplement. However, animals given fluoride during the initial 30 weeks only, did not lose bone during the subsequent period of calcium deficiency. Conceivably, fluoride could be a long-term preventative measure but should not be considered a therapeutic agent alone.