PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Allograft function”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources
PubMed1994

Occurrence of cancers in immunosuppressed organ transplant recipients.

The findings in this study emphasize the need for lifetime follow-up of organ transplant recipients. Although a high percentage of posttransplant tumors are low-grade malignancies that are readily amenable to treatment, cancer has become a major cause of death in patients otherwise successfully treated by transplantation (6). An Australasian study of the causes of death of patients who survived for at least 10 years with a functioning renal allograft compared to those on dialysis for at least 10 years without transplantation, or with a failed transplant, showed that the proportions of deaths caused by cancer were 26%, 1%, and 3%, respectively. Nonetheless, the future holds promise. Attempts are being made to modify the present blunderbuss attack on the immune system with more specific methods of control. Much work is currently being done to induce states of immune unresponsiveness directed specifically, and only, at the foreign antigens of the allograft. Hopefully these efforts will eliminate the need for long term or intense immunosuppressive therapy and the problem of posttransplant malignancies will be relegated to a footnote in the history of organ transplantation.

Adolescent↗
PubMed1994

A seven year experience with kidney transplantation for pediatric end stage renal disease.

Renal transplantation for pediatric end stage renal disease (ESRD) is a preferred option in dealing with these chronically ill patients. The pediatric renal transplant program at University of Missouri-Kansas City School of Medicine was begun in 1986 at St. Luke's Hospital and subsequently shifted to the Children's Mercy Hospital as experience was accumulated. To date 35 transplants have been performed in 31 recipients. Fifty-one per cent of the patients transplanted were adolescents (older than 13 years) and 91% of the patients were older than 4 years. Sixteen of the 35 transplants were from living related donors and 19 patients received their kidneys from cadaveric donors. Immunosuppression consisted of corticosteroids, azathioprine, cyclosporine and antilymphoblast globulin. No patients died following transplantation with a functioning kidney. Allograft survival with living related transplants at one year and three years was 91% and 86% respectively. Cadaveric allograft survival at one year and three years was 78% and 46% respectively. Most kidneys were lost due to either acute or chronic rejection although there were three patients who lost their kidney due to primary nonfunction, including one child age 23 months. The growth pattern of all but the youngest children (< or = 2 years) following transplantation showed no evidence of accelerated growth. Results in this early series of pediatric renal transplant patients is encouraging from the standpoint of patient and allograft survival and even though accelerated growth is not seen in the older children, it seems to offer a better quality of life for children with end stage renal disease.

Adolescent↗
PubMed1997

Evaluation of the pediatric renal transplant recipient.

Renal transplantation is the preferred therapy for children with end stage renal disease. A functioning renal allograft can dramatically improve a child's quality of life. Advances in immunosuppressive therapy and clinical practice approaches have significantly improved graft survival rates allowing children to attain near normal growth and development. Accurate assessment and appropriate nursing care enhances long-term survival of these young patients.

Child↗
PubMed1998

Pretreatment of donor stimulator cells by 16,16 dimethyl prostaglandin E2 influences the recipient immune response.

BACKGROUND: Immunosuppressive strategies have largely ignored donor-derived stimulatory cells as a target. This study examined whether lipopolysaccharide (LPS) or 16,16 dimethyl prostaglandin E2 (dmPGE2) pretreatment of stimulator cells from B10.BR mice influences effector function of responder T lymphocytes from C3H/HeJ mice in vitro or in vivo. METHODS: B10.BR spleen cells were incubated in vitro in the presence or absence of dmPGE2 or or LPS before the cells were used as stimulators in a mixed lymphocyte culture (MLC) with T cells from C3H/HeJ mice. In parallel studies, B10.BR mice were treated in vivo with dmPGE2 or LPS; spleen cells from these animals were used as stimulators in an MLC and skin was harvested for skin grafts. Cells from untreated or pretreated mice were examined for expression of intercellular adhesion molecule-1 (ICAM-1), B7-1, and B7-2 by fluorescence-activated cell sorter analysis. ICAM-1 mRNA transcripts were determined by reverse transcriptase-polymerase chain reaction. RESULTS: Stimulation of B10.BR-derived spleen cells with LPS before their use as stimulator cells in a MLC resulted in an increase in responder T-cell proliferation compared with use of unstimulated spleen cells (P < 0.05). In contrast, pretreatment of stimulator spleen cells with dmPGE2 resulted in dose-dependent inhibition of the responder T-cell proliferation, with maximum effect seen using a concentration of dmPGE2 of 10(-5) mol/L. The decreased expression of interleukin-1, tumor necrosis factor, leukotriene B4 procoagulant activity, and ICAM-1 by the dmPGE2 pretreated spleen cells correlated with their inefficient in stimulating T-cell proliferation. Spleen cells harvested from B10.BR mice previously injected with dmPGE2 similarly were inefficient as stimulator cells. Skin graft survival was delayed, but not prevented, by in vivo pretreatment of donor mice with dmPGE2. CONCLUSIONS: These data demonstrate the effect of immunomodulation of allogeneic stimulator spleen cells on subsequent responder T-lymphocyte function and allograft survival.

16,16-Dimethylprostaglandin E2↗
PubMed1998

Coronary arteriosclerosis after T-cell-mediated injury in transplanted mouse hearts: role of interferon-gamma.

This study evaluated the contribution of acute parenchymal rejection and interferon (IFN)-gamma to the development of graft arterial disease (GAD) in totally allogeneic murine cardiac transplants. BALB/c (H-2d) hearts were transplanted into wild-type C57BL/6 (B6, H-2b) or B6 IFN-gamma-deficient (GKO) recipient mice. Assessing the role of acute parenchymal rejection in the GAD process involved two different immunosuppression protocols using anti-CD4 and -CD8 monoclonal antibodies (MAbs): virtually complete long-term immunosuppression (denoted as complete immunosuppression) was achieved by administering both MAbs 6, 3, and 1 day before transplantation and weekly thereafter; in contradistinction, a single, early, transient episode of rejection (transient rejection) was attained by administering MAbs beginning 4 days after transplant and then at weekly intervals. The extent and duration of T cell depletion under these two regimens were evaluated using flow cytometric analysis of peripheral blood lymphocytes. After a single injection of MAbs, peripheral blood CD4+ and CD8+ T cell depletion was approximately 98% at 1 week and approximately 88% at 2 weeks. After three injections (analogous to days 6, 3, and 1 before transplant), peripheral blood CD4+ and CD8+ T cell depletion was >98% at 2 weeks and approximately 87% at 4 weeks. Functioning cardiac allografts were removed at 8 and 12 weeks after transplant and analyzed by hematoxylin and eosin, elastic tissue, and immunohistochemical stains, and the severity of parenchymal rejection versus GAD was scored. With complete immunosuppression (antibody before and after transplant), BALB/c allografts showed little parenchymal rejection or GAD, suggesting that persistent depletion of T cells blocked subsequent development of GAD. However, even a single transient acute rejection episode allowed the subsequent development of GAD accompanied by augmented major histocompatibility complex (MHC) class II, VCAM-1, and ICAM-1 expression at 12 weeks; these allografts showed no residual CD4+ or CD8+ T cells. In comparison, allografts undergoing transient rejection in GKO recipients did not develop GAD, despite persistent macrophage and natural killer cell (NK) infiltrates comparable to those seen in wild-type recipients. Moreover, the arterioles of hearts transplanted into GKO recipients showed no or minimal increases in MHC class II, ICAM-1, and VCAM-1 relative to baseline expression. In conclusion, a single episode of allogeneic injury mediated by T cells suffices to evoke subsequent graft arteriosclerosis, even in the absence of additional T-cell-mediated injury, and the process appears to depend on IFN-gamma.

Animals↗
PubMed2006

Cardiac functional and morphologic changes of renal allograft recipients in the early posttransplant period.

UNLABELLED: After renal transplantation there is a substantial alteration in cardiac morphology and functions. This prospective study was undertaken to observe changes in different cardiac parameters in early months after transplantation. PATIENTS AND METHODS: Twenty-two allograft recipients (primary disease glomerulonephritis) were evaluated in the immediate pretransplant period (0 month) and 1 and 3 months after transplantation by clinical and echocardiographic (M mode, 2D) evaluations. RESULTS: Pretransplant echocardiogram showed left ventricular hypertrophy (LVH) in 100% subjects, LV dilation in 52%, and systolic dysfunction in 18%. By the third month, significant differences in systolic blood pressure (SBP-161 +/- 16 to 133 +/- 26 mm Hg, P < .002); diastolic BP (DBP-101 +/- 9 to 86 +/- 11 mm Hg, P < .006), and hemoglobin level (Hgb-7.3 +/- 1.6 to 11.2 +/- 3.9 g/dL, P < .006) were evident. Echocardiography showed decreased left atrial diameter (LADd-41 +/- 5 to 35 +/- 3 mm, P < .001); left ventricular internal diameter (LVIDd-54 +/- 6 to 47 +/- 6 mm, P < .02); left ventricular muscle mass index (LVMI-379 +/- 114 to 248 +/- 58 g/m(2), P < .001); and left ventricular end diastolic volume index (LVEDVI-96 +/- 28 to 64 +/- 17 ml/m2, P < .002). Bivariate correlations showed positive associations of mean blood pressure (MBP) and serum creatinine with LVMI, LVEDVI, and negative association of hemoglobin with MBP, serum creatinine, LVMI, and LVEDVI. CONCLUSION: From these observations, we concluded that cardiac morphological parameters start improving in the early posttransplant period. Improvements in renal function, anemia status, and lower blood pressure showed strong associations with these changes.

Adolescent↗
PubMed1994

Successful islet allotransplantation in diabetic rats immunosuppressed with FK506: a functional and immunological study.

The effect of a novel immunosuppressive agent, FK506, on fresh islet allografts was evaluated in diabetic rats across major histocompatibility complex (MHC) barriers with respect to the transplantation (TR) site, islet source, treatment regimen, and antidonor antibody (Ab) titers of the recipients after TR. The functional periods of Wistar (Wi) islets transplanted under kidney capsule (KC) or intraportally (IPo) and of a mixture of Wi and Lewis (Le) islets under KC or IPo in nonimmunosuppressed ACI rat recipients were 6.9 +/- 0.4 (n = 7), 6.4 +/- 0.5 (n = 7), 5.6 +/- 0.4 (n = 7), and 6.2 +/- 0.4 (n = 5) days, respectively. FK506 treatment at 1 mg/kg/d intramuscularly (IM) for 2 weeks (protocol I) following islet TR under KC and IPo significantly prolonged the allograft function to more than 71.8 +/- 11.3 (n = 10) and 161.7 +/- 18.6 (n = 11) days, respectively. Additional treatment with FK506 at 1 mg/kg/wk (protocol II) further increased the islet survival under KC to more than 212.6 +/- 22.3 (n = 8) days. With this FK506 treatment protocol, the Wi + Le mixed-islet allograft function was extended to more than 106.1 +/- 10.5 (n = 7) and 167.9 +/- 28.6 (n = 7) days under KC and IPo, respectively. Nephrectomy in 8/8 ACI rats with long-term-functioning Wi (n = 6) and Wi + Le (n = 2) islet allografts resulted in their return to hyperglycemia. Immunohistochemical staining showed abundant insulin-positive cells at the graft site, with small numbers of CD4- and CD8-positive cells present in the vicinity of the normal-appearing islets. Macrophages were not detected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Inhibition of inducible nitric oxide synthase ameliorates functional and histological changes of acute lung allograft rejection.

BACKGROUND: We recently demonstrated that inhibition of inducible nitric oxide synthase (iNOS) ameliorated severe acute lung allograft rejection. This study used a rat lung transplant model to determine (1) the time course and cellular localization of iNOS expression during the histological progression of unmodified acute rejection and (2) whether inhibition of iNOS prevented impaired gas exchange function of the allograft lung and/or ameliorated the histological changes of acute rejection. METHODS AND RESULTS: iNOS mRNA and enzyme activity were expressed in allograft lungs during mild, moderate, and severe acute rejection, but not in normal, isograft, or allograft lungs before histological changes of mild acute rejection. iNOS expression in allografts resulted in elevated serum nitrite/nitrate levels, indicative of increased in vivo nitric oxide (NO) production. In situ hybridization demonstrated iNOS mRNA expression in infiltrating inflammatory cells, but not in allograft parenchymal cells. Allografts had significantly impaired gas exchange, which was prevented with the selective iNOS inhibitor aminoguanidine (PaO2 of 566+/-19, 76+/-22, and 504+/-105 mmHg for isograft, allograft, and aminoguanidine-treated allograft, respectively; P<0.0002). Aminoguanidine also significantly improved the histological rejection scores. CONCLUSIONS: (1) iNOS expression and increased NO production occurred during the early stages of acute rejection, persisted throughout the unmodified rejection process, and localized to infiltrating inflammatory cells, but not allograft parenchymal cells; (2) aminoguanidine ameliorated the histological and functional changes of acute rejection; and (3) increased NO production, detected by the presence of iNOS mRNA, protein, or noninvasively by measuring serum nitrite/nitrate levels, may serve as an early marker of acute allograft rejection.

Acute Disease↗
PubMed1979

Relationship of donor-specific mixed lymphocyte culture reactivity to graft function in recipients of cadaveric renal allografts.

The response of twelve cadaveric renal allograft recipients was serially studied in one-way MLC using the specific donor spleen lymphocytes as stimulating cells. The stimulation index (SI) progressively decreased between the second and the eighteenth post-transplantation week in the presence of normal plasma. The appearance of MLC non-reactivity (SI of less than 2.3) correlated well with the achievement of excellent graft function. In nine recipients allograft rejections have not occurred once the non-reactive state in cultures with normal plasma was established. In two of the recipients reactivity reappeared after an interval of non-reactive phase. In both instances rejection followed such reactivity and non-reactivity followed successful management of rejection. In one patient severe irreversible allograft rejection occurred in spite of the appearance of an early MLC non-reactive phase. This patient developed donor-specific lymphocytotoxic antibodies and his rejection was perhaps of antibody mediated type. Donor-specific MLC reactivity may represent cellular immune response of host to an allograft and predict cellular allograft rejection.

Adolescent↗
PubMed1995

Clinical profile and course and outcome of late acute rejection episodes in living-related-donor renal allograft recipients.

We prospectively monitored clinical data and renal function at monthly intervals in 165 patients who had received living-related-donor renal allografts in our institution between January 1981 and December 1991 and had a functioning allograft for 1 year or longer. During a mean follow-up period of 47.2 (range 13-155) months, 32 patients (17.2%) developed late acute rejections, of which 14 (43.7%) were asymptomatic. Amongst the symptomatic late acute rejections, worsening of hypertension was the commonest finding, being present in 11 (61.1%) patients, followed by oliguria in 8 (44.4%) and weight gain in 7 (38.8%) patients. Of these 32 late acute rejections, as many as 28 (87.5%) showed a response to antirejection therapy with high-dose steroids: 5 (15.6%) a complete response and 23 (71.9%) a partial response. The response rate was 100% if it was the first acute rejection (20% complete and 80% partial), 78.6% if it was the second (14.3% complete and 64.3% partial), and no or only a partial response to treatment if it was the third acute rejection episode. On long-term follow-up, patients who had responded to to antirejection treatment had a significantly better graft survival as compared with nonresponding patients: 76 and 27%, respectively. Our observations suggest that routine monitoring of the renal function at frequent intervals is essential for early diagnosis and treatment of acute rejections, even during the late posttransplant period. The chances of a response to antirejection therapy are higher during the first episode of late acute transplant rejection as compared with second or a third late rejection event.

Acute Disease↗
PubMed2002

Acute pyelonephritis causing acute renal allograft dysfunction.

In renal transplant recipients, acute pyelonephritis may cause acute deterioration of renal function. We report a case with acute allograft failure due to acute pyelonephritis, which was confirmed by graft biopsy. After appropriate antimicrobial therapy, allograft function recovered.

Acute Disease↗
PubMed1985

Experimental pancreas allograft rejection: correlation between histologic and functional rejection and the efficacy of antirejection therapy.

In this study the sequence of histologic changes in rejecting pancreatic allografts was correlated with the recurrence of hyperglycemia to evaluate the usefulness of serum glucose monitoring in pancreas transplantation. In addition, various immunosuppressive agents were evaluated for their efficacy in reversing rejection. Diabetic (streptozocin) Lewis rats were recipients of histoincompatible Lewis X Brown Norway F1 pancreatic grafts, which uniformly resulted in a fall in serum glucose levels from greater than 400 mg/dl to less than 150 mg/dl. Specimens were examined daily from the time of transplantation to determine the time of earliest histologic rejection. Functional rejection was defined as a rise in serum glucose levels to greater than 200 mg/dl and occurred at 8.5 +/- 0.8 days in the control group. Histologic evidence for rejection was present by day 3 as a perivascular lymphoid infiltrate while islets remained normal. Extensive cellular rejection of the exocrine tissue occurred by day 6 when most recipients were still normoglycemic. Complete pancreatic destruction was present by day 9. Antirejection therapy with methylprednisolone (MP), antithymocyte serum (ATS), or cyclosporine (CS) started at the time of recurrent hyperglycemia (days 8 or 9) and was uniformly unsuccessful in prolonging graft survival, with mean survival times of 8.3 +/- 0.8 (MP), 9.0 +/- 0.7 (ATS), and 9.3 +/- 0.4 (CS). In contrast, either ATS or CS but not MP begun on day 3, when histologic rejection was first observed, significantly prolonged graft survival to greater than 11 days in most recipients. We conclude that islet destruction is irreversible by the time that marked elevation in serum glucose levels occurs and therefore a more sensitive measure of pancreas rejection is needed. Furthermore, ATS and CS are more effective than are corticosteroids in reversing early rejection.

Animals↗
PubMed2003

Significance of endothelial cell survival programs for renal transplantation.

Initial and longer term kidney transplant function is determined in part by the renal allograft microcirculation because it provides a thromboresistant surface, regulates cellular infiltration, and elaborates paracrine and autocrine growth and survival factors. Loss of endothelial-derived signaling mediators accelerates vascular injury and endothelial cell (EC) death. EC apoptosis is implicated in accelerated allograft vasculopathy and premature loss of organ function. Renal allograft EC injury and replacement by recipient-derived repair mechanisms has long been proposed to influence allograft acceptance and function. Repair of cellular injury in allografts is linked with cell-survival mechanisms, but few precise indicators exist to predict recovery and repair in organ transplants. The significance of the growth phenotype of the microvascular endothelium for acute and longer term renal allograft survival is presented.

Apoptosis↗
PubMed1979

The use of bactericidal concentrations of antibiotics in hypothermic pulsatile perfusion and the effects on canine renal autograft function.

Although cadaver allograft contamination occurs frequently, the potential danger to the transplant recipient varies. Usually the results of culture from the donor and kidney perfusates are not available at the time of transplantation. A positive culture result often necessitates the use of prophylactic antibiotics. The antibiotic may be potentially nephrotoxic, and in the setting of minimal or changing renal function this effect may be potentiated. If significant contamination with virulent organisms is found prior to transplantation, clinical judgment often dictates that the graft be discarded. Perfusion and storage with solutions containing broad-spectrum antibiotics would substantially reduce the incidence of contamination in perfused kidneys. This would in turn reduce the requirement for potentially nephrotoxic antimicrobial therapy in the transplant recipient. Since the antibiotics tested are effective against a wide range of contaminants and apparently cause no detrimental effects, it would seem reasonable to add them routinely to the perfusate solution.

Animals↗
PubMed1991

Perinatal outcome in renal allograft recipients: prognostic significance of hypertension and renal function before and during pregnancy.

With more renal allograft recipients becoming pregnant, it is important to refine existing pre-pregnancy assessment criteria and to identify other factors influencing perinatal outcome. We analyzed gestational renal response and acute or chronic hypertension in relation to perinatal outcome for 22 pregnancies that continued beyond 28 weeks' gestation in 17 allograft recipients (mean age 27 years, range 20-40) transplanted between 1967-1987. Before pregnancy, all had plasma creatinine of 1.62 mg/dL or less and 24-hour creatinine clearance of 39 mL/minute or greater. Six pregnancies were to four women on antihypertensive therapy. Mean arterial pressure (MAP), antihypertensive therapy, plasma creatinine, and 24-hour creatinine clearance were recorded before and during pregnancy. Perinatal outcome was adverse in ten pregnancies: five stillbirths, four growth-retarded infants, and one neonatal death, whereas 12 pregnancies had satisfactory perinatal outcome. Early-pregnancy increments and late-pregnancy decrements in renal function were identical in both groups. Mean arterial pressure was significantly higher at 16-28 weeks in women having adverse outcomes. Hypertension (MAP above 107 mmHg) occurred in 16 pregnancies (73%); it appeared before 28 weeks in seven and was invariably associated with adverse outcome. Hypertension appeared after 28 weeks in nine women and was associated with adverse outcome in only two cases. Five of six pregnancies in women who were on pre-pregnancy antihypertensive therapy ended in adverse outcome. It can be concluded that renal function was identical in pregnancies having adverse or satisfactory perinatal outcome, whereas hypertension before or during early pregnancy, albeit apparently satisfactorily controlled, appeared to be associated with adverse perinatal outcome.

Acute Disease↗
PubMed2003

Expression of growth arrest-specific gene 6 and its receptors in dysfunctional human renal allografts.

Growth arrest-specific gene 6 (Gas6) and its receptors Rse, Axl and Mer have recently been found to be involved in a rat model of chronic allograft nephropathy (CAN). Thus, in this study we investigated the function of Gas6 and its receptors in human renal allograft dysfunction. Expression of Gas6 and its receptors was detected by immunohistochemical staining. Gas6 and its receptors were widely expressed in glomeruli, tubules and vessels of renal allografts. Gas6 expression was detected in normal-functioning allografts and was increased in acute rejection ( P<0.05), acute tubular necrosis ( P<0.05) and CAN ( P<0.01). Gas6 receptors were not upregulated in any of the allograft groups, except for the Axl receptor, which increased only in acute tubular necrosis ( P<0.01). Gas6 expression was also found to correspond with the expression of alpha-smooth muscle actin, a general marker of CAN ( r(2)=0.21, P<0.01). These findings suggest that Gas6, acting as a growth factor, is increased in the process of kidney allograft dysfunction and in CAN.

Actins↗
PubMed2000

[Proximal femoral reconstruction with megaprosthesis versus allograft prosthesis composite. A comparative study of functional results, complications and longevity in 41 cases].

PURPOSE OF THE STUDY: To compare femoral reconstruction using megaprosthesis versus allograft prosthesis composite. MATERIAL AND METHODS: Forty-one consecutive proximal femoral reconstructions with an allograft-prosthesis composite (21 cases) or a megaprosthesis (20 cases) after tumor resection were reviewed in a retrospective study. The following criteria were considered: functional outcome; long term survival; complications. Chi-square test and Wilcox tests were used to compare groups. The medium and long-term survival curves for these reconstructions were made using the Kaplan-Meier standard methods. The failure of prosthesis was defined as revision for mechanical failure (either aseptic loosening or dislocation), for infection or local recurrence. The comparison of the curves was performed using the Log-Rank test. RESULTS: Infection (10 p. 100) and instability, in both groups, and loosening, in the megaprosthesis group, were the common causes of failure. There was difference between functional results in the two groups (limping and crutches using was more lower in allograft-prosthesis composite group). Survival analysis showed a 5 and 10-year survival of 77 +/- 12 p. 100 for the patients with composites. Five and ten - year survival were 73 +/- 11 p. 100 and 0 p 100 respectevely for those with megaprostheses. No significant difference was noted between survival of these two groups but a tendancy (p =0.09). Radiological allograft resorption was noted for more than 50 p. 100 of allograft composite prosthesis without modification of functional result or symptomatic loosening. DISCUSSION: The functional results seem better in the composite group when compared to the megaprosthesis group. Reconstruction of the abductor mechanism is essential to stabilize the prosthesis and to decrease the limp. When the great trochanter cannot be preserved, we used suture of gluteus medius tendon to tensor of fascia lata, which is re-enforced using a piece of biceps femoris. The dislocation rate was approximately the same in our two groups. Several authors reported a lower dislocation rate with composite reconstructions than massive prosthesis. The rate of infection is similar to other reported series. In our study it has been possible to show a tendancy for superior survival of the composite reconstruction. When the review was later than 5 years the radiological appearance of the graft in our series was often concerning with resorption or fragmentation present in six of the eight cases. This radiological appearance is not as yet responsible for any revision or any change in the functional result however it does remain a worry. CONCLUSION: Composite reconstructions probably allow a better functional result when considering proximal reconstruction of the femur. The radiological appearance of these allografts in the long term is however worry some without any evidence so far of worsening functional level or any evidence of prosthetic loosening. It would seem to us that the current level of knowledge would advocate the use of massive allografts together with prosthesis. This does seem still to remain the best choice for proximal femoral reconstruction.

Adult↗