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| − | == 3 If you play on pri ==
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These criteria are based on the original grading schemes and have not dramatically changed in three decades For the surgical pathologist however many of the pathological features of acute graft-versus-host disease are nonspecific In the colon ‘exploding crypt cells’ and apoptoses at crypt bases are found and used for grading of graft-versus-host disease but are not always pathological In general biopsies performed within 10–20 days of allogeneic chemotherapeutic conditioning regimens also show apoptotic epithelial cells and render a diagnosis of acute pathology difficult unless other pathological changes or clinical data are presentBiopsies of patients in our series commonly transpired within the first 20 days following myeloablation when severe diarrhea started Grading using standard criteria developed for graft-versus-host disease following allogeneic transplantation is suboptimal at this early time point but the severity of clinical symptoms in our cases warranted colonoscopic investigation In addition the pathological changes of biopsies showed a spectrum of findings not limited to apoptotic epithelial cells commonly the only findings described in patients without significant symptomatology within the first 20 days following conditioning More than half of the patients in our series (9/17) had colonic pathology corresponding to grade 3 or 4 graft-versus-host disease including crypt dropout and de-epithelialization pathology that would not be attributable to subtle changes induced by the conditioning regimen The recovery of peripheral cell counts in our patient population at least days before the onset of gastrointestinal symptoms also argues against direct myeloablative toxicity Thus it would be unlikely that effects related to myeloablation would account for the constellation of clinical and pathological features If temporally associated delayed effects of chemotherapy are clearly difficult to tease away from pathological changes induced by autologous graft-versus-host disease As many patients in our case series had recently received chemotherapy and there are no specific pathological changes to differentiate these two entities the clinical scenario and response to treatment was then used to dictate the ultimate diagnosisOther non-chemotherapeutic drug effects are also known to mimic graft-versus-host disease-like changes but require a compatible clinical history In the setting of autologous or syngeneic (twin-to-twin) hematopoietic stem cell transplantation immunosuppressive drugs may induce graft-versus-host disease-like pathology such as mycophenolate mofetil Characteristic shared findings with both allogeneic and autologous graft-versus-host disease include crypt cell apoptosis with crypt atrophy and dropout Crypt distortion and regenerative changes including dilated damaged crypts are more typical of mycophenolate-related injury However these immunosuppressive agents are not used for prophylaxis of graft-versus-host disease in autologous stem cell recipients because there is no lack of genetic disparity that would induce an alloresponse Drugs known to cause increased apoptosis such as non-steroidal anti-inflammatory drugs and laxatives are also not used in the peritransplant period Medications that are used include prophylactic antimicrobials and anti-emetics for nausea which are not known to induce histological change mimicking graft-versus-host diseaseFor the surgical pathologist excluding potential etiologies in autologous stem cell recipients can be impossible without an adequate clinical history Many possible infectious agents must be eliminated from routine laboratory and microbiological studies including C difficile and other common bacterial infections Fortunately pathological characteristics do not overlap with changes related to graft-versus-host disease Acute self-limited colitis and specific or characteristic features such as pseudomembranes and granulomas are not typical of graft-versus-host disease On the other hand viral infections such as cytomegalovirus can display a vast array of pathological changes including those mimicking graft-versus-host disease: apoptotic enterocytes and crypt atrophy/loss Typical viral inclusions are occasionally absent or rare from routinely prepared sections Owing to the spectrum of changes in viral infections lack of sensitive microbiological studies and the possibility of coexisting viral infection with graft-versus-host disease we recommend immunohistochemistry or in situ hybridization for CMV in all biopsies showing pathology consistent with autologous graft-versus-host disease This is our institutional practice whether allogeneic or autologous transplant biopsies are interpreted Depending on the clinical index of suspicion and incidence herpes simplex virus and adenovirus immunostaining should also be considered Other more unusual infectious etiologies require consideration on a case-by-case basis especially when other causes are more likely As a case in point: in one example from our series despite an exhaustive investigation for infectious agents (patient 2)—including multiple send-out tests and electron microscopy—no causative organism was identifiedTransfusion-associated graft-versus-host disease could also theoretically induce pathology identical to that seen in autologous graft-versus-host disease However our patient population universally received 2500 rad irradiated blood products in the peritransplant period These doses should be sufficient to reduce any transfused lymphocytes that may be capable of inducing a graft-versus-host response In addition transfusion-associated graft-versus-host disease is typically accompanied by concurrent decreases in peripheral blood cell counts and marrow aplasia due to transfused lymphocytes targeting hematopoietic cells In our patient series cell counts recovered during engraftment before or concurrent with the development of graft-versus-host diseaseUpon excluding alternative causes for gastrointestinal pathology perhaps the most convincing clinical evidence of immune-related gastrointestinal pathology rather than infections or another etiology is the early response to immunosuppressive therapy Despite marked pathological changes in the biopsies associated with severe clinical symptoms from patients in our case series there were dramatic responses to steroid and immunosuppressive regimens when initiated early guided by the information provided by pathological examination Patients described earliest in our series (patients 1–5) had more variable outcomes without prompt immunosuppressive therapy Many patients not initially treated with steroids did not improve clinically With our institutional experience however prompt early treatment has resulted in dramatically improved clinical outcomesTheories vary regarding the pathogenesis of autologous graft-versus-host disease but center around the loss of tolerance to ‘self’ that develops in a disrupted immune system which could have multiple causes Previous chemotherapy may deleteriously alter the content of regulatory T cells in the stem cell graft Perhaps endogenous cells that survive conditioning and assist in post-transplant maintenance of self-tolerance are affected Microchimerism due to maternal cells transmitted during fetal development and persisting throughout adult life has also been postulated as a cause That observed cases of autologous graft-versus-host disease have occurred in the last 6 years suggests a possible link between new therapeutics such as lenalidomide and bortezomib which have emerged as part of standard pretransplant chemotherapy during the rapid evolution of myeloma treatment Potentially they alter regulatory T cell content in graft recipients or otherwise explain autologous graft-versus-host diseaseTo our knowledge this represents the largest series of autologous graft-versus-host disease in hematopoietic stem cell transplantation recipients Other 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The distinct pattern of allelic loss identified in this chromosomal region appears to be an attractive candidate marker for further evaluation with regard to the discrimination between primary and secondary glioblastomas Based on our data one might hypothesize that loss of a purtative TSG on MCRD/S is more likely associated with progression to secondary glioblastoma rather than with primary glioblastomaThe novel MCRD/S was not precisely recognized by three preceding studies LOH on 22q is not a genome-wide event however and its extremely confined localization to MCRD/S may explain the discrepancy in frequency between our study and the previous ones Using only three flanking markers -(D22S280 and D22S283 at 22q123 and D22S282 at 22q132—Ino et al mapped a common region of allelic loss between the D22S280 and D22S282 loci but their series exhibited LOH predominantly in the more telomeric regions spanning 10Mb of chromosome 22 Compared with the microsatellite markers used previously markers used in this study were located at different sites at both ends of the D22S280 locus and LOH was found to be restricted to a more centromeric marker Both of the other related studies performed in nonselected glioblastoma failed to find evidence for the MCRD/S,burberry uk, We also saw a higher frequency of hypermethylation in secondary glioblastoma than in primary glioblastoma. 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