Histologic evaluation of organ preservation injury and correlation with cold ischemia time in 13 intestinal grafts.

Lesions produced in the graft mucosa due to harvesting, storage, and implantation must be graduated to assess the subsequent protocolized biopsy specimens. The aim is to identify type and intensity of graft mucosal lesions observed immediately after implantation. Congestion, hemorrhage, microthrombi, neutrophilic infiltrates, shortening of villi, epithelial detachment, erosion, and crypt loss were separately evaluated by two pathologists in mucosal biopsy specimens from 13 grafts. Each change was assessed as normal, mild, moderate, or severe and by splintering the summation of points a global score was designed. Cold ischemia time was registered. Correlation between the pathologists' evaluations and between final preservation injury degree and cold ischemia time was determined using the "index of correlation rho (ρ)" (Spearman's test). The same changes were assessed in 19 biopsy specimens from day 2 to day 6 (3.6 ± 1.1) to determine their evolution. Congestion was found in 7 biopsy specimens, microthrombi in 2, hemorrhage in 4, neutrophils in 6, villous atrophy in 8, epithelial detachment in 9, erosions in 2 and/or crypt loss in 2. The maximum degree of preservation injury was expressed as intense congestion and hemorrhage associated with epithelial detachment and villous atrophy. The global preservation score was grade 3 in 2 cases, grade 2 in 5, grade 1 in 2, and grade 0 in 4. There was positive correlation (ρ = 0.915) in the evaluation between pathologists (P < .01), total agreement in 9 biopsy specimens, and partial agreement (only 1 point disagreement) in 4. Mean cold ischemia time was 327 ± 101 min. (135-480). There was positive correlation (ρ = 0.694) between preservation score and cold ischemia time (P < .01). In the follow-up biopsy procedures, histological injury decreased by at least one grade in every case. Additionally, karyorrhexis was observed in 3 grafts and very occasional apoptosis in 2 others. This scale achieves good reproducibility and allows graduate preservation injury in intestinal transplantation.

Histologic evaluation of post-implantation immediate C4d deposition in 13 intestinal grafts: correlation with cell-based crossmatching, cold ischemia time, and preservation injury.

C4d deposits are predictive of humoral rejection in kidney and heart transplantation. The aim of this study was to identify C4d deposit patterns in intestinal mucosa of the grafts on biopsy specimens obtained immediately after implantation and to detect if it could be a valuable tool to predict humoral or acute rejection. A second objective was to search for a statistically significant relationship between positive C4d deposition and other collected variables. Thirteen immediately post-transplantation mucosal graft biopsy specimens, formalin fixed, underwent immunohistochemical stain for C4d deposits. Diffuse intense staining of capillary endothelium was considered positive and absent, focal or weak stains as negative. Preservation injury grade and cold ischemia times were registered for each case. Donor-specific preformed antibodies were detected by complement dependent cytotoxicity serologic technique (crossmatching). Another 19 endoscopic follow-up biopsy specimens from days 2 to 6 were also evaluated. Statistical studies were made using the index of correlation ρ (Spearman's test). Diffuse intense C4d deposits were observed in 2 grafts, focal and weak in 5, and completely negative in 6. The mean cold ischemia time was 327 ± 101 minutes. Two cases showed diffuse positive deposits, 1 had a positive crossmatch and the cold ischemia time was 360 minutes whereas the other had not preformed antibodies and its cold ischemia time was 475 minutes. Humoral or acute rejection was not observed in follow-up mucosal biopsy specimens. There was no statistically significant relationship between the C4d deposition, cold ischemia time, crossmatching results, and preservation injury degree. In conclusion, C4d deposition was not a helpful tool for diagnosis of humoral rejection and prediction of acute rejection during the early post-transplantation period.

[Portal and mesenteric thrombosis associated with protein S deficiency]. / Trombosis portal y mesentérica asociada al déficit de la proteína S.

INTRODUCTION: liver cirrhosis is the main cause of portal thrombosis (PT), while hypercoagulability syndromes are rarely found as the etiology of PT. We report a case of portal and mesenteric thrombosis secondary to protein S deficiency. CASE REPORT: a 74-year-old woman was admitted with melena secondary to upper gastrointestinal bleeding. She reported mild, diffuse abdominal pain in the last 2 weeks. Endoscopy revealed ruptured esophageal varices. Doppler ultrasonography and CT demonstrated a heterogeneous liver, splenomegaly and ascites, and complete non-occlusive PT involving the hilum and portal branches, as well as the superior mesenteric vein, with portosystemic collaterals. At this point a complete study for cirrhosis etiologies was negative, including a liver biopsy that showed nonspecific architectural changes secondary to diminished blood flow, which suggested non-cirrhotic portal hypertension. The search for hypercoagulability states determined a deficiency of S protein, with total pS = 107% and free pS = 56%. The patient was started on anticoagulant treatment and no other thrombotic events occurred. DISCUSSION: PT usually manifests without specific symptoms. The most common presentation is upper gastrointestinal bleeding, as occurred in our patient. Liver cirrhosis is one of the most frequent cause of PT. Up to 65% of these patients present an associated prothrombotic state, including protein S deficiency. Our case reminds us of the importance of a systematic search for hipercoagulability syndromes in patients with TP, even when the etiology can be conferred to liver cirrhosis.

Trombosis portal y mesentérica asociada al déficit de la proteína S / No disponible

Introducción: la causa más frecuente de trombosis portal (TP)es la cirrosis hepática, mientras que los estados hipercoagulables sonraramente identificados como etiología de la TP. Presentamos uncaso de TP y mesentérica secundaria al déficit de la proteína S (pS).Caso clínico: paciente mujer de 74 años, que debuta con dolorabdominal difuso de 2 semanas de evolución y hemorragia digestivaalta tipo melena secundaria a varices esofágicas. En el estudiose objetiva un hígado heterogéneo, esplenomegalia y ascitis,así como una trombosis portal completa no oclusiva del hilio hepáticoy de sus ramas y de la vena mesentérica superior con circulacióncolateral. El estudio etiológico de hepatopatía fue negativo,incluyendo una biopsia hepática que mostraba cambios arquitecturalessecundarios al flujo hemático disminuido compatible conhipertensión portal no cirrótica. El estudio de hipercoagulabilidadfue positivo para un déficit de proteína S. pS libre 56%, pS total107%. Desde entonces se inició tratamiento anticoagulante sinpresentar descompensaciones posteriores.Discusión: la trombosis portal suele manifestarse con síntomasinespecíficos, siendo la forma de presentación más frecuentela hemorragia digestiva alta como el caso que nos ocupa. La cirrosises una de las causas más frecuentes de trombosis portal, sinembargo existe hasta un 65% de estos pacientes que tienen unaenfermedad protrombótica asociada, como es el déficit de proteínaS. Nuestro caso remarca la importancia de realizar estudios defactores trombogénicos en pacientes con TP, incluso cuando laetiología se puede atribuir a una cirrosis

Introduction: liver cirrhosis is the main cause of portalthrombosis (PT), while hypercoagulability syndromes are rarelyfound as the etiology of PT. We report a case of portal andmesenteric thrombosis secondary to protein S deficiency.Case report: a 74-year-old woman was admitted with melenasecondary to upper gastrointestinal bleeding. She reported mild, diffuseabdominal pain in the last 2 weeks. Endoscopy revealed rupturedesophageal varices. Doppler ultrasonography and CT demonstrateda heterogeneous liver, splenomegaly and ascites, andcomplete non-occlusive PT involving the hilum and portal branches,as well as the superior mesenteric vein, with portosystemic collaterals.At this point a complete study for cirrhosis etiologies was negative,including a liver biopsy that showed nonspecific architecturalchanges secondary to diminished blood flow, which suggested noncirrhoticportal hypertension. The search for hypercoagulabilitystates determined a deficiency of S protein, with total pS = 107%and free pS = 56%. The patient was started on anticoagulant treatmentand no other thrombotic events occurred.Discussion: PT usually manifests without specific symptoms.The most common presentation is upper gastrointestinal bleeding,as occurred in our patient. Liver cirrhosis is one of the mostfrequent cause of PT. Up to 65% of these patients present an associatedprothrombotic state, including protein S deficiency. Ourcase reminds us of the importance of a systematic search forhipercoagulability syndromes in patients with TP, even when theetiology can be conferred to liver cirrhosis (AU)

Hepatic metastases from the spindle cell variant of medullary thyroid carcinoma: report of a case with diagnosis by fine needle aspiration biopsy.

BACKGROUND: The liver is a common site of neuroendocrine tumors (NTs) metastatic from primaries in the gastrointestinal tract, pancreas, biliary system and lungs. Medullary thyroid carcinoma (MTC) is also a potential source of metastases of NTs. Their metastases to the liver are frequent and can appear several years after the primitive tumor. Although a wide variety of cytomorphologic features are normally exhibited by MTC in smears, a spindle-shaped cell pattern can predominate, complicating the correct interpretation of a metastasis. CASE: A 63-year-old man presented with multiple liver nodules two years after a total thyroidectomy for MTC. Fine needle aspiration biopsy smears of the liver revealed neoplastic cells occurring in loose groupings or lying singly, most of them with a spindle shape and elongated nucleus with the characteristic "salt and pepper" chromatin pattern of a neuroendocrine tumor. Cytoplasmic dendritic processes and intranuclear inclusions were frequently seen. The cytomorphologic features of the tumor were essentially the same as those of the primary MTC. Immunoreactivity for calcitonin confirmed the diagnosis. CONCLUSION: In fine needle aspiration biopsy of liver masses, knowledge of the spindle pattern of the NT is important in order to achieve a correct diagnosis when metastases are the first manifestation of an occult primary tumor. Among neuroendocrine tumors, MTC must be included in the differential diagnosis.

Seminal vesicle epithelium as a potential pitfall in the cytodiagnosis of presacral masses. A report of two cases.

BACKGROUND: Whenever abdominoperineal resection is performed because of a rectal adenocarcinoma, the prostate and seminal vesicles may be displaced backward to the presacral space, giving rise to a false radiologic image of a presacral tumor. Due to cytologic atypia associated with the epithelium of seminal vesicles, there is a real possibility, in fine needle aspiration biopsy (FNAB), of erroneously giving a malignant diagnosis. CASES: Two men, aged 53 and 57 years, presented with presacral masses three months and six years, respectively, after abdominoperineal resection for rectal adenocarcinoma. In both cases, FNAB smears showed some groups and single cells with large and irregular nuclei. These cells suggested a recurrence of carcinoma. The presence of cytoplasmic coarse pigment and a background with spermatozoa and blobs of inspissated secretory product were sufficient to determine that these presacral masses represented the seminal vesicles. CONCLUSION: Awareness that seminal vesicles may give rise to a radiologic impression of presacral tumor after abdominoperineal resection of the rectum will avoid unnecessary FNAB and a cytologic false positive diagnosis of colorectal adenocarcinoma.

Pérdida del injerto en trasplante hepático. Estudio anatomoclínico de 131 injertos fracasados en la primera década (1986-1996) del programa del hospital 12 de octubre / Graft loss in liver transplantation: pathological and clinical study of 131 graft failures during the first decade (1986-1996) of the liver transplant program at Hospital 12 de Octubre

Introducción. Existen diversas complicaciones que pueden conducir a la pérdida del injerto hepático (por retrasplante o fallecimiento). Los objetivos del presente trabajo son conocer las complicaciones morfológicas que se desarrollan en estos injertos fracasados y determinar cuáles son las causas de fracaso más relevantes en esta terapéutica. Pacientes y métodos. En el Hospital 12 de Octubre (Madrid) se realizaron 494 trasplantes hepáticos entre 1986 y 1996. Su indicación más frecuente fue la cirrosis (criptogénica, alcohólica y por hepatitis C). En 61 pacientes se indicó retrasplante. En 22 se realizó un segundo retrasplante y en dos un tercer retrasplante. En 56 pacientes fallecidos (40 por ciento de los fallecimientos del programa) se realizó autopsia. Un total de 131 injertos fracasados (75 obtenidos en el retrasplante y 56 tras autopsia) fueron estudiados morfológicamente de forma protocolizada. Las causas de fracaso fueron establecidas tras la oportuna correlación anatomoclínica. Resultados. En 109 injertos las lesiones hepáticas explicaban su fracaso. El rechazo crónico (31 por ciento), las alteraciones circulatorias (31 por ciento) y el fallo primario (16 por ciento) fueron las causas hepáticas de fracaso más frecuentes. Las alteraciones circulatorias fueron infartos, necrosis isquémicas parenquimatosas zonales y/o colangitis isquémicas, no siempre asociadas a lesiones vasculares del injerto. En los injertos con fallo primario se observaron lesiones isquémicas parenquimatosas con algunas características similares a las de los injertos con alteraciones circulatorias. La causa más común de muerte fue la sepsis (46 por ciento), frecuentemente asociada a alteraciones circulatorias. La causa más frecuente de retrasplante fue el rechazo crónico (40 por ciento; 75 = 100 por ciento), seguido de las alteraciones circulatorias (27 por ciento) y del fallo primario (21 por ciento). Sin embargo, la incidencia de rechazo crónico decreció de manera muy notable en el segundo lustro de la década estudiada, cediendo su puesto a las alteraciones circulatorias como primera causa de fracaso. Conclusiones. Tras el descenso del rechazo crónico del injerto como causa de su fracaso, se requiere mejorar el control de los factores favorecedores de cualquier forma de isquemia en el injerto para continuar reduciendo el número de injertos fracasados (AU)

Simultaneous occurrence of Hodgkin's disease, nodal Langerhans' cell histiocytosis and multiple myeloma IgA(kappa).

A 35-year-old man suffered simultaneously from nodular sclerosis Hodgkin's disease (HD), Langerhans' cell histiocytosis and multiple myeloma (MM). There was no prior history of irradiation or chemotherapy, and clinically the lymphoma was confined to cervical lymph nodes. Immunohistochemically, neoplastic lymphoma cells reacted with CD15 and CD30 markers. The patient's bone marrow exhibited a diffuse infiltration by rather atypical plasma cells showing kappa immunoglobulin light-chain restriction. At 14 months after the diagnosis, after autologous bone marrow transplantation, the clinical evolution is favourable with complete remission of the diseases. This is the first time that the coexistence of these three haematological disorders has been discussed, and only the fourth documented case of simultaneous HD and MM. Speculations about the significance of this finding are discussed.

Torsion of a Meckel's diverticulum: sonographic findings.

There are few reports of the sonographic appearance of Meckel's diverticulum. We present a case of torsion of a Meckel's diverticulum that was suggested by sonography and confirmed pathologically. We discuss the sonographic differential diagnosis, which includes acute appendicitis, enteric duplication cyst and intestinal volvulus.