Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study is to analyze the morphologic and functional change of human bone defect after its grafting with mixture of platelet gel and autologous cancellous bone. For one year, we have prospectively studied nine consecutive pa- tients, aged 25-73 y, with pseudoarthrosis of long bones, after unsuccessful initial surgeries. We have harvested can- cellous bone from patients' iliac crests and mixed with the ABO compatible allogeneic platelet rich plasma (PRP) gel. That mixture has been inserted in the bone defect, and surgically fixated. Radiologically, the defects achieved the bone morphology (the appearance of hazy callus) between 6th and 24th week. The time of functional recovery was varied, be- tween 12 and 40 weeks for partial weight bearing, and between 16 and 48 weeks for free limb mobility and full function of the limb. The overall healing of bone defect was 16 to 36 weeks. Two patients had complications of poor graft ingrowth and one with a reversible postsurgical nerve paresis. On the X-ray scans, solid and fast restoration of bone structure was notable, with excellent bone ingrowth, suitable for full weight bearing. The allogeneic platelet gel had no adverse effects. This method can be used for treating of long bone defects, because of its strong influence on restoration of normal bone morphology. Further investigation is required to establish efficiency relative to other methods.
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PMID:The influence of allogeneic platelet gel on the morphology of human long bones. 2542 Mar 67

We report the case of a 53-year-old-man who developed human T-cell leukemia virus type-1-associated myelopathy (HAM) after ABO-incompatible liver transplantation for alcoholic liver cirrhosis. The living donor was seropositive for human T-cell leukemia virus type-1 (HTLV-1) and the recipient was seronegative for HTLV-1 before transplantation. After transplantation, the recipient developed steroid-resistant acute cellular rejection, which was successfully treated using anti-thymocyte globulin, and he was eventually discharged. He underwent spinal surgery twice after the transplantation for the treatment of cervical spondylosis that had been present for a period of 9 months before the transplantation. The surgery improved his gait impairment temporarily. However, his gait impairment progressed, and magnetic resonance imaging revealed multiple sites of myelopathy. He was diagnosed with HAM 16 months after the transplantation. Pulse steroid therapy (1000mg) was administered over a period of 3 days, and his limb paresis improved. Presently, steroid therapy is being continued, with a plan to eventually taper the dose, and he is being carefully followed up at our institution. Our case suggests that liver transplantation involving an HTLV-1-positive living donor carries the risk of virus transmission and short-term development of HAM after transplantation.
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PMID:Myelopathy due to human T-cell leukemia virus type-1 from the donor after ABO-incompatible liver transplantation. 3102 62