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Relation of disease stage to humoral and cellular impairment of spleen reticuloendothelial system depression in a rat leukemia.

In the rat leukemia studied there is an early reversible depression of reticuloendothelial system (RES) function followed by a late-stage secondary depression, culminating in death, associated with an infiltration of leukemic cells into the bone marrow and spleen. In one set of experiments to assess RES function, isolated spleens of nonleukemic rats were perfused with blood from rats in progressively advanced stages of the leukemia. In a reciprocal set of experiments, isolated spleens of rats in comparable stages of the leukemia were perfused with blood from nonleukemic rats. The clearance of 99mTc-sulfur colloid from the blood perfusate was used as a test of RES function. In the first set, clearance was depressed in nonleukemic spleens perfused with blood collected from rats 1 hr after they had been inoculated with tumor cells, and it was more markedly depressed in a late stage of the leukemia 6 days later. Perfusion of nonleukemic spleens with blood from rats in intermediate stages of the leukemia did not depress clearance. In the reciprocal study, clearance was depressed in spleens of rats that were inoculated with tumor cells 1 hr before perfusion with nonleukemic blood. Clearance values were at the control level in spleens of rats in all other stages of the leukemia when calculated on the basis of total spleen weight. When calculated on a unit weight basis, clearance values were lower in the enlarged spleens of rats in advanced stages of the leukemia. The results indicate that impairment of RES clearance of 99mTc-sulfur colloid is associated with alternations in the humoral content of the blood of this leukemic rat. There is indirect evidence to suggest that in the terminal stage of the leukemia an impairment of splenic RES cells to clear 99mTc-sulfur colloid may develop secondarily.

Animals↗

The different migratory characteristics of lymphocyte populations from a whole spleen transplant.

Spleens from AS x BN donor rats labelled in vivo by multiple doses of [3H]thymidine were transplanted into syngeneic recipients by anastomosis to the abdominal great vessels. The recipients were killed 1-5 days after receiving the whole spleen transplants and the numbers and location of the [3H]thymidine-labelled cells which had migrated from the labelled donor spleen traced by means of autoradiographs of sections, imprints and smears of various recipient lymphoid tissues. These results were compared with the migration pattern of labelled dissociated spleen cell suspensions injected intravenously. The latter consists almost entirely of small lymphocytes which migrate to T or B areas of recipient spleen, lymph nodes and Peyer's patches. The labelled whole spleens also contained cells which migrated to the T and B areas of recipient lymphoid tissues, but in addition contained many lymphoid cells which migrated to the red pulp of the recipient spleen and to the lamina propria of the gut. These experiments showed, therefore, that the spleen contains mobile elements which have not been detected by transfer of spleen cell suspensions.

Animals↗

[Effect of Ly49A transfected mouse spleen cells on graft versus host disease and graft versus leukemia after haploidentical allogeneic bone marrow transplantation in mice].

OBJECTIVE: To observe the effect of Ly49A transfected mouse spleen cells on graft versus host disease (GVHD) and graft versus leukemia (GVL) effect after haploidentical allogeneic bone marrow transplantation in mice. METHODS: Ly49A gene was transfected into spleen cells of C57BL/6 mice by retrovirus and the expression rate of Ly49A receptor was evaluated by flow cytometry. The murine model of haploidentical allogeneic acute GVHD was established by using C57BL/6(H - 2b) mouse as donor, and (BALB/c x C57BL/6) F1(H - 2d/b) (CB(6)F(1)) mouse as the recipient which was injected EL9611 cells before transplantation. After irradiation (TBI, (60)Co 10.5 Gy), the recipient received mixed graft of spleen cells and bone marrow cells to establish a GVHD model. The effects of Ly49A transfected spleen cells on GVHD and GVL post haploidentical allogeneic bone marrow transplantation were detected with this model. RESULTS: The expression rate of Ly49A receptor was (42.20 +/- 4.87)%, (18.67 +/- 2.48)% and (18.73 +/- 3.82)% for pLXSN-Ly49A, pLXSN transfected and untransfected spleen cells respectively. Among haploidentical allo-BMT (C57BL/6(H - 2b)-->CB6F1(H - 2d/b)) groups, the survival time was (7.80 +/- 3.36) days for irradiation group; (21.70 +/- 2.87) days for cyclophosphomide therapy group; (29.40 +/- 6.43) days for mixed bone marrow cells and spleen cells transplantation group; (29.10 +/- 7.39) days for mixed bone marrow cells and pLXSN transfected spleen cells transplantation group and (45.00 +/- 12.38) days for mixed bone marrow cells and Ly49A transfected spleen cells transplantation group, which was much longer than that of any other groups (P = 0.000). CONCLUSION: The Ly49A transfected spleen cell transplantation could alleviate GVHD and retain GVL effect in the acute GVHD model post haploidentical allo-BMT.

Animals↗

Mouse hepatitis virus infection suppresses modulation of mouse spleen T-cell activation.

Natural infection by mouse hepatitis virus (MHV) can affect interpretation of immunological studies in mice. MHV, a collective term describing a group of corona viruses, is found in natural infections in over 70% of laboratory mouse populations in the U.S.A. and Canada. Natural outbreaks of MHV in our animal colony afforded us the opportunity to study MHV-induced immunosuppression as well as the effects of MHV infection on neurotransmitter immunomodulation. Concanavalin A (Con A)-stimulated DNA synthesis by spleen T lymphocytes from MHV-infected mice was 20-50% that of non-infected mice. The MHV infection also altered neurotransmitter modulation of spleen T-lymphocyte activation. In contrast to noradrenaline ablation of Con A-activated DNA synthesis by spleen lymphocytes from non-infected mice, DNA synthesis by the infected group was not inhibited by noradrenaline or dibutyryl-cAMP. These effects of MHV infection were specific for spleen T lymphocytes since MHV infection did not alter Con A stimulation of thymocytes, lipopolysaccharide stimulation of spleen B lymphocytes, or noradrenaline inhibition of thymocyte and B-cell DNA synthesis. MHV infection also did not alter spleen T-lymphocyte subset proportions. Thus, MHV infection inhibits spleen T-lymphocyte activation and blocks in vitro catecholamine and cAMP regulation of spleen T-cell activation but does not affect activation of thymic cells or spleen B cells.

Animals↗

[Early clinical experience with postoperative monitoring of a patient after laparoscopic splenectomy combined with spleen autotransplantation. A case report].

We performed splenectomy combined with spleen autotransplantation after blunt abdominal trauma by minimally invasive technique at the County Teaching Hospital in Kecskemét. In case of advanced post traumatic spleen injury, spleen autotransplantation (Furka's spleen chips) is a well-known method to try to avoid postsplenectomy syndrome. During the operation, when in situ preservation of the spleen is not possible, chips of spleen tissue are transplanted into the omentum. Function of the transplanted spleen tissue was monitored by scintigraphy. We describe two different types of spleen scintigraphy to check the viability of spleen chips.

Humans↗

Replication of herpes simplex virus in mouse spleen cell cultures stimulated by lipopolysaccharide.

Replication of HSV was demonstrated in spleen cell cultures of D2 and several other strains of mice after prestimulation with mitogenic doses of LPS for 2 days. No viral replication occurred in unstimulated cultures or in cultures prestimulated with PHA and Con A, whereas there was some viral replication in spleen cell cultures of D2 mice after prestimulation with Poly I-C. Spleen cells of B6 mice did not support replication of HSV under any of the conditions we have tested thus far. The reasons for this defect are not clear, but it was obviously not caused by a defective lymphoproliferative response to LPS or by an active anti-viral principle elaborated by B6 spleen cells. F1 hybrids between B6 and D2 mice were capable of HSV replication to the same extent as were spleen cells of D2 mice. Several strains of both HSV-1 and HSV-2 could be replicated in D2 spleen cells cultures. Nylon column treatment of D2 spleen cells removed the ability to replicate HSV, whereas macrophage removal from the spleens by plastic adherence was without effect. Purified peritoneal exudate cells from D2 mice did not support replication of HSV. Together these data suggest that B cells activated by LPS represent the target cell of HSV replication in mouse spleen cell cultures.

Animals↗

Inhibition of the graft-versus-host reaction. III. Altered in vivo distribution of spleen cells pretreated with Fab fragments of antithymocyte globulin.

51Cr-labeled parental strain spleen cells were pretreated in vitro with antithymocyte globulin (ATG) or Fab fragments of ATG before i.v. injection into F1 recipients. Recipients were killed at various intervals after injection and their organs were assayed for radioactivity in order to determine the in vivo distribution pattern of pretreated cells. 51Cr spleen cells pretreated with ATG were almost totally prevented from migrating to spleens, lymph nodes, bone marrow, Peyer's patches, lungs, and peripheral blood of recipients. Pretreatment of 51Cr spleen cells with noncytotoxic Fab of ATG also inhibited localization to these organs and tissues; however, the inhibition was not as complete as that of ATG-treated cells. Localization of Fab-treated 51Cr spleen cells to recipient nodes was inhibited to a greater extent than was localization to recipient spleens. There was no significant difference in the extent of inhibition of ATG-treated 51Cr spleen cells to recipient nodes and spleen. Organ counts from recipients killed at various intervals after injection of Fab-treated 51Cr spleen cells showed that Fab-treated cells do not recover their recirculating potential in vivo.

Animals↗

Suppression in Xenopus laevis: thymus inducer, spleen effector cells.

Studies were carried out on suppressor function in the amphibian Xenopus laevis, the South African clawed toad. Suppression by the thymus of haemagglutinin (HA) production by spleen is antigen-dependent, partially specific and not MHC-restricted in this species (Ruben, Buenafe & Seivert, 1983). Three questions were considered in this study. Does the thymus effect suppression by stimulating peripheralized spleen effector cells, or do effector cells reside within the thymus? Do macrophages participate in the induction and/or expression of thymus-dependent suppressor function? Can thymus suppressor and helper functions be distinguished by using irradiation treatment? The capacity of immunized thymus to suppress HA when co-cultured with spleen fragments from immunized, cyclophosphamide (CyP)-injected animals was tested. Immunized thymus failed to suppress the high levels of HA production by spleen fragments from CyP-treated, immunized donors. Colloidal carbon injection resulted in blockade of macrophage function, and both the capacity of thymuses to suppress and of spleens to be suppressed in co-cultures. Finally, the effect of thymus exposure to gamma-irradiation in vitro was tested using autogeneic thymus/spleen combinations. This enabled the visualization of thymic helper function, which is MHC-restricted in Xenopus (Bernard et al., 1981). Four dosages of irradiation were tested after antigen challenge. The highest HA titres were produced by spleen co-cultures with thymuses which had received 1000 rads. We conclude that suppression of HA production in spleen is not the result of thymus suppressor effector cells, but that suppressor function is mediated by thymus inducer cells which stimulate suppressor effectors in spleen. Both the thymic inducers and effectors in the spleen are sensitive to CyP and macrophage blockade. Our studies further suggest that we are able to distinguish between the thymic functions of help and suppression in Xenopus by taking advantage of their differential sensitivities to irradiation. While it has been postulated, on other grounds, that suppression was one of the earliest thymic regulatory functions to have evolved (L.N. Ruben & R.H. Clothier, submitted), here we suggest the presence of sequential activities of more than one cellular subset, as early in evolution as the primitive anuran (tail-less) amphibia.

Animals↗

Production by mouse spleen cells of factors stimulating differentiation of mouse myeloid leukemic cells that differ from the colony-stimulating factor.

Mouse myeloid leukemic M1 cells can be induced to differentiate into macrophages and granulocytes in vitro by a protein inducer, differentiation-stimulating factor (D-factor), and by various other compounds. Mouse spleen cells produced D-factors when treated with various mitogens, such as concanavalin A, phytohemagglutinin, pokeweed mitogen, lipopolysaccharide, and synthetic double-stranded polyribonucleotide copolymer of polyinosinic and polycytidylic acids. Concanavalin A, phytohemagglutinin, and pokeweed mitogen stimulated spleen lymphocytes, but not spleen macrophages, to produce a D-factor with an apparent molecular weight of 40,000 to 50,000. On the other hand, lipopolysaccharide and copolymer of polyinosinic and polycytidylic acids stimulated both spleen lymphocytes and spleen macrophages to produce D-factors. Spleen macrophages produced D-factors with molecular weights of 40,000 to 50,000 and 20,000 to 25,000, whereas spleen lymphocytes produced only the larger molecules. In addition to D-factor, colony-stimulating factor (CSF), which stimulates growth and differentiation of normal bone marrow cells, and interferon, were detected in conditioned medium of spleen cells treated with concanavalin A or lipopolysaccharide. On gel filtration of the conditioned medium with Sephadex G-100, CSF was eluted between the larger D-factor and the smaller one. The fraction with interferon activity overlapped that of the larger D-factor. Incubation of the conditioned medium at pH 2 abolished the activity of interferon but did not affect the activity of either D-factor or CSF. The addition of cytochalasin B suppressed the production of interferon but not of D-factor or CSF by the spleen cells. These results indicate that the D-factor is a different substance from CSF or type II interferon.

Animals↗

Natural killer activity in spleens and lymph nodes from patients with Hodgkin's disease.

Natural killer (NK) activity against K-562 myeloid cell line was evaluated in 21 spleens and 14 lymph nodes from patients with Hodgkin's disease (HD). NK activity of eight HD-involved (HD+) spleens [556 lytic units (LU)] was found 5-fold higher than that of 13 HD-uninvolved (HD-) spleens (112 LU) (p less than 0.01). Moreover, NK activity of HD+ spleens was significantly different (p less than 0.05) from that of three spleens involved by non-HD lymphoma (100 LU). NK activity of four spleens from nonneoplastic patients (250 LU) was intermediate between those of HD+ and HD- spleens. Lymph node cells were about 10-fold less cytotoxic. NK activity of seven HD+ lymph nodes (43 LU) was 3-fold higher than that of three lymph nodes involved by non-HD lymphoma (8 LU). However, these differences were not statistically significant. Our data are compatible with increased NK activity in HD+ tissues as well as with depressed NK activity in HD- tissues. The observation that NK activity of peripheral blood leukocytes from nine HD patients (116 LU) (p less than 0.05 only at 100:1 effector:target cell ratio) may support the latter interpretation. Partial characterization of effector cells in HD+ and in HD- spleens indicated that, in both instances NK cells were nonadherent and almost equally distributed between the erythrocyte-negative and -positive cell fractions. Finally, NK activity of both HD+ and HD- spleen cells could be further potentiated in vitro by interferon.

Adolescent↗

Specific, transient suppression of the immune response by HGG tolerant spleen cells. II. Effector cells and target cells.

In a previous report, it was shown that spleen cells from mice made tolerant to human gamma-globulin (HGG)5 could specifically inhibit the immune response of normal spleen cells after adoptive transfer to lethally irradiated recipients. However, that report also showed that the suppressive activity was only transiently associated with tolerant spleen cell populations. It was concluded from those experiments that while suppressive activity could be demonstrated in tolerant spleen cells under certain conditions, such activity was not obligatory for the maintainance of the tolerant state. The experiments presented here were performed to determine the nature of the effector cell(s) and the target cell(s) involved in this system of suppression of the immune response. Treatment of cells from tolerant animals with anti-thymocyte serum and complement to remove thymus-derived (T) cells completely abrogated suppresive activity. Removal of adherent cells from tolerant spleen cells by passage over glass wool columns resulted in partial loss of the suppression. The inhibitory activity of the suppressor cells was resistant to 900 R irradiation regardless of whether the tolerant spleen cells were irradiated before or after adoptive transfer. The cellular target(s) for the supprssor cells was examined by using lipopolysaccharide (LPS) as an alternative source of helper activity for the response to HGG. LPS, injected at the time of the initial antigenic challenge of mice that had been reconstituted with tolerant and normal spleen cells, prevented the expression of suppression against bone marrow-derived (B) cells. However, when LPS was presented only at the time of secondary antigenic challenge, it was unable to overcome suppression of the immune response of reconstituted recipients. Thus, LPS could produce a state where the B cells were resistant to suppression, but LPS could not rescue the responsiveness of B cells once the cells in the reconstituted recipient had been suppressed. In addition, the immune response to both the hapten dinitrophenol (DNP) and the carrier (HGG) were suppressed when recipients of tolerant and normal spleen cells were challenged with DNP6HGG. This indicates that T helper cells are also a target for suppression. The results presented in this paper are discussed in relation to a possible mechanism of suppression which proposes that suppressive activity represents the induction of tolerance in immunologically competent cells by HCG which is closely associated with the tolerant spleen cells.

Animals↗

Interleukin 2 deficiency in murine Leishmaniasis donovani and its relationship to depressed spleen cell responses to phytohemagglutinin.

This study examined the kinetics and mechanisms of depressed spleen cell responses to phytohemagglutinin (PHA) that occur during Leishmania donovani infection of BALB/c mice. In co-culture experiments, neither spleen cells from infected animals nor parasite-infected macrophages suppressed PHA responses of normal spleen cells. In addition, parasite-mediated suppression of PHA-stimulated spleen cell proliferation could not be demonstrated. Mice with 2 wk of infection did manifest an impairment in spleen cell production of interleukin 2 (IL 2) and by 8 wk IL 2 activity in supernatants from these cells was reduced by approximately 95%. This finding was not explained by an alteration in the kinetics of IL 2 production. Furthermore, diminished IL 2 activity in supernatants of PHA-activated spleen cells from infected animals was not caused by suppressive factors in these fluids as shown by their inability to suppress IL 2 stimulation of IL 2-dependent T cells. When spleen cells from mice with 8 wk of infection were cultured with PHA and supplemented with exogenous IL 2, there was an approximately 48% increase in mitogenesis. These data indicate that abnormal PHA-induced spleen cell activation in BALB/c mice with L. donovani infection is associated with impaired production of IL 2. In addition, the observation that supplementation of spleen cells from infected mice with IL 2 resulted in partial reconstitution of the PHA response is consistent with a defect in IL 2 responsiveness.

Animals↗

Effect of cyclophosphamide on spleen cell suppressor activity and tumour growth in mice.

Following a single injection of cyclophosphamide (Cy) a biphasic spleen reaction occurred. During the first week the spleen size as well as the proliferative activity of the spleen cells were markedly reduced. However, during the next week a compensatory reaction developed with spleen enlargement and cellular proliferation far above normal. In the period of increasing spleen size, days 7-12 after Cy injection, the mitogenic response of the spleen cells was reduced and simultaneously they developed a suppressor activity which was able to inhibit the mitogen response of normal spleen cells. This suppressor activity could be reduced if the mice were reconstituted by an injection of normal spleen cells after Cy injection. Injection of Cy one day before tumour transplantation resulted in reduced tumour growth in syngeneic recipients compared with non-treated controls. However, this inhibition of tumour growth was abolished when normal spleen cells were injected after Cy treatment.

Animals↗

Modulation of F1 cytotoxic potentials by GvHR. Host- and donor-derived cytotoxic lymphocytes arise in the unirradiated F1 host spleens under the condition of GvHR-associated immunosuppression.

As an approach to dissect complex cellular events that lead to GvHR-associated immune disorders, we followed cytotoxic activities, including NK cytotoxicity, in the spleens of unirradiated F1 hosts undergoing GvHR induced by parental spleen cells. Spleen cells of (B10 X DBA/2)F1 or (B10 X AKR/J)F1 hosts undergoing GvHR induced by parental B10 spleen cells displayed a prompt and marked increase in NK cell activity within 36 hr, and the heightened activity lasted until day 8. The activity then declined abruptly and disappeared on day 12 of GvHR. Inversely, donor B10-derived CTL specifically directed to the opposite parental alloantigens of the F1 hosts emerged in these F1 host spleens on day 8, and the CTL activity reached a peak on day 12 when the host NK cell activity disappeared. During the period that the donor-derived anti-host CTL were present, these F1 host spleen cells lost not only NK cell activity but also the ability to mount in vitro CTL responses. In contrast, the respective F1 strain mice undergoing GvHR induced by the parental DBA/2 or AKR/J spleen cells showed only transient but marked increases in NK cell activity during the initial 36 hr, and then the activity decreased gradually to return to the normal level on day 10. In such GvHR F1 host spleens, donor-derived CTL could never be detected, and the spleen cells showed normal in vitro CTL responsiveness during the entire observation period of 16 days. These results are discussed from the viewpoint of genetically defined cellular events that lead to the GvHR-associated immune disorders.

Animals↗

Laparoscopic splenopexy for wandering (pelvic) spleen.

Wandering spleen is a rare clinical diagnosis with a high incidence of splenic torsion and infarction. The preferred treatment for this condition currently is splenopexy to reposition and fixate the spleen in the left upper quadrant of the abdomen to preserve splenic function. We recently performed the first splenopexy for a wandering spleen using laparoscopic techniques. The patient was a 19-year-old woman who had an asymptomatic lower abdominal/pelvic mass found on physical examination. Diagnostic evaluation (ultrasound, computed tomography scan, and liver-spleen scan) showed an absent spleen in the upper abdomen, normal uterus and ovaries, and an 11 x 7-cm pelvic spleen. Laparoscopic splenopexy was performed using Vicryl mesh to suspend and fixate the spleen in the left upper quadrant of the abdomen. Total operative time was 175 min, there were no intra- or postoperative complications, and the patient was discharged on the 1st postoperative day. Follow-up at 2 and 7 months indicated that she was asymptomatic with a nonpalpable spleen. The results suggest that a laparoscopic approach to splenopexy should be considered for the treatment of patients with a wandering spleen.

Adult↗

Color Doppler sonographic findings in focal spleen lesions.

UNLABELLED: Since focal lesions of the spleen are rare (0.2%), there is little data concerning color Doppler images of focal lesions of the spleen. OBJECTIVE: The aim of this study is to describe the color Doppler images of 98 etiologically proved focal spleen lesions. METHODS: In about 110,000 consecutive abdominal ultrasound examinations, which included the spleen, 600 patients with focal lesions of the spleen were identified. In 98 of these patients a color Doppler scan of the lesion was performed and documented. These scans were analysed retrospectively and classified as avascular, hypovascular, isovascular, hypervascular and arterio-venous "high flow", using the surrounding spleen tissue as an in vivo reference. RESULTS: In color Doppler sonography (CDS) 68.4% (n=67) of the focal spleen lesions showed no flow. 15.3% (n=15) appeared hypovascular, 8.2% (n=8) isovascular, 5.1% (n=5) hypervascular, and in 3.1% (n=3) an arterio-venous "high flow"-pattern was found. CONCLUSIONS: In CDS about two thirds (68%) of focal spleen lesions appear to be avascular. Except from diagnosis of intra-splenic pseudo-aneurysm, the practical utility of CDS in diagnosing focal spleen lesions has to be estimated as low.

Adolescent↗

Nitric oxide production by murine spleen cells stimulated with lipopolysaccharide from Actinobacillus actinomycetemcomitans.

The aim of this study was to determine whether Actinobacillus actinomycetemcomitans lipopolysaccharide (LPS-A. actinomycetemcomitans) could induce murine spleen cells to produce nitric oxide (NO). Spleen cells derived from Balb/c mice were stimulated with LPS-A. actinomycetemcomitans or LPS from Escherichia coli for 4 days. The effects of N(G)-monomethyl-L-arginine (NMMA), polymyxin B, and cytokines (IFN-gamma and IL-4) on the production of NO were also assessed. The NO production from the carrageenan-treated spleen cells stimulated with LPS-A. actinomycetemcomitans or both LPS-A. actinomycetemcomitans and IFN-gamma was determined. The carrageenan-treated mice were transferred with splenic macrophages and the NO production was assessed from the spleen cells stimulated with LPS-A. actinomycetemcomitans or LPS-A. actinomycetemcomitans and IFN-gamma. The results showed that NO production was detectable in the cultures of spleen cells stimulated with LPS-A. actinomycetemcomitans in a dose-dependent fashion, but was lower than in the cells stimulated with LPS from E. coli. The NO production was blocked by NMMA and polymyxin B. IFN-gamma up-regulated but IL-4 suppressed the production of NO by the spleen cells stimulated with LPS-A. actinomycetemcomitans. The carrageenan-treated spleen cells failed to produce NO after stimulation with LPS-A. actinomycetemcomitans or both LPS-A. actinomycetemcomitans and IFN-gamma. Adoptive transfer of splenic macrophages to the carrageenan-treated mice could restore the ability of the spleen cells to produce NO. The results of the present study suggest that LPS-A. actinomycetemcomitans under the regulatory control of cytokines induces murine spleen cells to produce NO and that splenic macrophages are the cellular source of the NO production. Therefore, these results may support the view that NO production by LPS-A. actinomycetemcomitans-stimulated macrophages may play a role in the course of periodontal diseases.

Journal Article↗

Angiosarcoma of the spleen: imaging characteristics in 12 patients.

PURPOSE: To retrospectively review clinical, pathologic, and imaging features of angiosarcoma of the spleen in 12 patients. MATERIALS AND METHODS: Institutional review board approval was obtained, and informed consent was not required. Records of 12 cases of proved angiosarcoma of the spleen were accessed from the files of the Armed Forces Institute of Pathology. Clinical, pathologic, and imaging findings were reviewed. Presenting signs and symptoms were recorded, and the pathologist confirmed the diagnosis and determined gross and microscopic morphologic findings in each spleen. Radiologists reviewed available images to determine the size of the spleen and mass, amount of splenic involvement by the tumor (if enhanced at computed tomography [CT] and magnetic resonance [MR] imaging), and amount of nonviable tumor determined as decreased echogenicity at ultrasonography (US) and lack of enhancement at CT and MR imaging. Imaging and pathologic findings were compared. Five US, 10 CT, three MR, and two angiographic images were reviewed by two experienced abdominal radiologists. RESULTS: There were seven men and five women (age range, 36-86 years; mean, 55 years). The most common symptom was upper abdominal pain in eight (67%) patients: Pain was acute for 24 hours prior to admission in one patient and chronic (range, 1-6 months) in seven patients. At imaging, the spleen was enlarged (>12 cm in length) in nine patients. The most common finding, seen in seven (58%) patients, was a complex mass or masses in an enlarged spleen. Four of these patients had evidence of metastases and one had intraperitoneal hemorrhage. Two patients had solitary hypervascular tumors and liver metastases. One patient had a normal-sized spleen with multiple lesions that ranged 2-3 cm in size, as well as metastases to the spine. The 11th patient had two small lesions, with small calcifications in the periphery of one lesion. The 12th patient had intraabdominal hemorrhage around the spleen and no obvious mass at CT. Tumor necrosis was confirmed at histologic evaluation in nine patients. CONCLUSION: The most common clinical finding was upper abdominal pain. Angiosarcoma of the spleen could be suggested in the majority of cases (83%) by using the imaging features of splenic mass with evidence of metastatic disease.

Adult↗