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Laparoscopic splenectomy for torsion of wandering spleen associated with celiac axis occlusion.

BACKGROUND: Wandering spleen is a spleen lacking its normal ligamentous attachments, and thus subjected to free movement in the abdominal cavity, and even torsion around its pedicle. Surgical treatment includes either fixation (splenopexy) or resection (splenectomy). Both procedures can now be accomplished using the laparoscopic approach. METHODS AND RESULTS: We describe a case of a torsion of a wandering spleen, leading to recurrent episodes of abdominal pain, and eventually to splenic ischemia, necessitating splenectomy. The diagnosis was complicated by associated angiographic findings of celiac axis occlusion, possibly by median arcuate ligament compression. Laparoscopic splenectomy was successful, and led to complete resolution of symptoms. CONCLUSIONS: Although a rare condition, wandering spleen can be diagnosed accurately by imaging studies, mainly CT scan and angiography. Nowadays, the laparoscopic approach is preferred and enables the surgeon to perform either splenopexy or splenectomy, depending on the vascular status of the spleen.

Adult↗

Laparoscopic removal of retroperitoneal accessory spleen in patient with relapsing idiopathic thrombocytopenic purpura 30 years after classical splenectomy.

The clinical success of therapeutic splenectomy for idiopathic thrombocytopenic purpura depends on the complete removal of all functional splenic tissue. Among reasons for poor response to splenectomy, failure to remove accessory spleens is mentioned. We present our experience with laparoscopic removal of accessory spleen from retroperitoneal space in a patient with relapse of ITP 30 years after classical splenectomy. A 45-year-old female patient underwent in 1972 classical splenectomy for ITP. Progressive decline in thrombocyte count was observed 7 years ago. Scintigraphy, CT, and ultrasound revealed residual splenic tissue. A laparoscopic approach was proposed. Four trocars placed along left costal margin were used. After dissection of all the adhesions behind the pancreatic tail deep in the retroperitoneal space a round structure 4 cm in diameter, macroscopically resembling splenic tissue, was found. The accessory spleen was removed intact. The patient recovered well; 2 months later steroids were discontinued while the thrombocyte level was 251 x 10(9)/L. Identification of accessory spleen seems to be major intraoperative problem. We believe that accessory spleen can be safely removed laparoscopically, avoiding a major open procedure, and a satisfactory postoperative result could be expected.

Female↗

Laparoscopic splenectomy for hematologic diseases: a preliminary analysis performed on the Italian Registry of Laparoscopic Surgery of the Spleen (IRLSS).

BACKGROUND: The Italian Registry of Laparoscopic Surgery of the Spleen (IRLSS) was developed to provide at the national level an informative tool useful for performing multicenter studies in the field of spleen laparoscopic surgery. In this first study analyzing the IRLSS data, a cohort of patients with hematologic diseases was retrospectively investigated for potential predictive parameters that could affect the outcome of laparoscopic splenectomy. METHODS: A total of 309 patients who underwent laparoscopic splenectomy for hematologic diseases in 17 Italian centers (between February 1, 1993, and September 30, 2004) were entered in the IRLSS. Their records were analyzed retrospectively by the Student's t-test, chi-square, and logistic regression. RESULTS: The mean operative time was 141 min (range, 30-420 min). Conversion was necessary in 21 cases (7%), and approximately 1 accessory spleen in 25 patients (9%) was found. The mean spleen weight was 1191 g (range, 85-4,500 g). Perioperative death occurred in two cases (0.6%). No complications were experienced by 253 patients (81.9%), who had a mean hospital stay of 5.4 days (range, 2-30 days). Overall morbidity occurred in 56 patients (18.1%), mainly associated with transient fever (n = 22), pleural effusion (n = 13), and actual or suspected hemorrhage (n = 12), requiring a reintervention for 7 patients. Multivariate analysis found that body mass index (p = 0.024) and clinical indication (p = 0.004) were independent predictors for surgical conversion. The clinical indication was almost significant as an independent predictor for the occurrence of postoperative complication (p = 0.05). CONCLUSIONS: This first study analyzing the IRLSS data shows that laparoscopic splenectomy may represent the gold standard treatment for hematologic diseases with normal-size spleen. The low morbidity and mortality rate suggests that laparoscopic splenectomy can be successfully proposed also for splenomegaly in hematologic malignancies.

Adolescent↗

Pathogenic avian adenovirus type II induces apoptosis in turkey spleen cells.

Wild-type mammalian adenoviruses are known to inhibit programmed cells death in infected cells. This study demonstrated for the first time that an avian type II adenovirus, the hemorrhagic enteritis virus (HEV) of turkeys, induced apoptosis in turkey spleen cells at 3 and 4 days post infection. The increased apoptosis rate in spleens of HEV-infected turkeys was associated with increased virus replication. Increased apoptosis preceded extensive virus-induced cellular necrosis. At 3 days post infection, spleen cells from HEV-infected turkeys released tumor necrosis like factor and nitric oxide inducing factors after ex vivo stimulation with concanavalin A. Spleen cells from HEV-exposed turkeys also secreted an interleukin 6-like factor when cultured in vitro. These cytokines may have contributed to HEV-pathogenesis and HEV-induced apoptosis and necrosis in the spleen. Induction of apoptosis by an avian adenovirus but not by wild-type mammalian adenoviruses indicates that evolutionarily distant adenoviruses may have different pathogenic mechanisms.

Adenoviridae Infections↗

Ultrasonographic fetal spleen measurements in red blood cell-alloimmunized pregnancies.

OBJECTIVES: This study was performed to evaluate the possible relationship between fetal spleen size and fetal hemoglobin levels and to assess the predictive value of ultrasonographically measured fetal spleen size as an estimate of the severity of fetal hemolytic anemia. STUDY DESIGN: Before 85 consecutive fetal blood samples in 28 red blood cell-alloimmunized pregnancies ultrasonographic fetal spleen measurements were performed. Results were compared with our own longitudinally derived reference ranges and were correlated with fetal hemoglobin deficit. RESULTS: A significant positive correlation was found between spleen perimeter and fetal hemoglobin deficit. The ultrasonographic finding of splenomegaly correctly predicted severe fetal anemia (hemoglobin deficit > 5 SD from normal mean) in 44 of 47 cases, a positive predictive value of 94%. At first transfusion all fetuses showing splenomegaly were severely anemic. CONCLUSION: Fetal spleen measurements may be a useful adjunct to ultrasonographic evaluation in the management of severe red blood cell-alloimmunized pregnancies.

Anemia↗

Preservation of splenic function in adults and children with injured spleens.

Mounting evidence supports efforts to preserve splenic function. This evidence indicates (1) that the problem of postsplenectomy sepsis warrants splenic preservation whenever possible, and (2) that the spleen, as a whole or in part, and its function, can be preserved in cirmustances which formerly seemed to necessitate removal of the entire spleen. Nine patients with splenic injuries in whom splenic function was preserved successfully are presented. Approaches to management of the splenic injuries included (1) nonoperative management, (2) hemostasis by application of microfibrillar collagen (Avitene), (3) partial splenic resection, and (4) preservation of accessory spleen. Since reliable prevention and treatment of postsplenectomy sepsis do not seem attainable in the near future, continuing efforts to preserve function of the spleen whenever possible, in patients with injured spleens, seem justified and desirable.

Adolescent↗

Properties of acid ceramidase from human spleen.

We have characterised ceramidase activity in extracts of human spleen from control subjects and from patients with Gaucher disease. In Triton X-100 extracts of control spleens, a broad pH optimum of pH 3.5-5.0 was found; no ceramidase activity was detectable at neutral or alkaline pH. About 45-60% of acid ceramidase could be extracted from spleen without detergents, but for complete extraction, Triton X-100 was required. For the radiolabelled substrate oleoylsphingosine, a Km of 0.22 +/- 0.09 mM and a Vmax of 57 +/- 11 nmol/h per mg protein was calculated in spleen from a control subject. Flat-bed isoelectric focussing in the presence of Triton X-100 revealed a pI of 6.0-7.0 for acid ceramidase; similar values were found for sphingomyelinase and glucerebrosidase. HPLC-gel filtration indicated that in the presence of Triton X-100, acid ceramidase has an Mr of about 100 kDa. In the absence of detergents, the enzyme forms high-molecular-weight aggregates. Similar aggregation behaviour was observed for sphingomyelinase, while the elution of beta-hexosaminidase was not affected by detergents. The elution profile of glucocerebrosidase was only slightly altered by Triton X-100. There was no difference in the properties of acid ceramidase present in spleen from control subjects and from patients with type I Gaucher disease.

Acid Ceramidase↗

Translational regulation of ferritin synthesis in rat spleen: effects of iron and inflammation.

Translational control of ferritin synthesis was studied in rat spleen, and compared with that for liver, heart and brain, in response to iron and inflammation. Spleen concentrations of total RNA in the ribonucleoprotein (mRNP) fraction was comparable to that for liver, while polyribosomal RNA was less. Both fractions were ten-fold lower in heart and brain. In untreated animals, the mRNP fraction of all tissues had the largest portion of the ferritin mRNA, as determined by slot blot hybridization with 32P-labeled cDNA for the L subunit. Acute treatment with ferric ammonium citrate shifted the spleen ferritin mRNA to the polyribosome fraction. This was also so in liver but not in the heart and brain which took up much less iron. The findings were confirmed by hybridization studies of mRNPs and polyribosomes separated in sucrose gradients. Turpentine-induced inflammation also caused a shift in ferritin mRNA from the mRNP to the polyribosome fraction of spleen and liver, over 12 h. We conclude that as in liver, spleen ferritin synthesis is under translational control by iron, and that both tissues also respond to inflammation by shifting of ferritin mRNA to the polyribosomes.

Animals↗

Kappa opioid receptor agonists inhibit sigma-1 (sigma 1) receptor binding in guinea-pig brain, liver and spleen: autoradiographical evidence.

The present study examined whether the kappa-opioid agonists U50,488H (trans-(+/-)-3,4-dichloro-N-methyl-N[-2-(1-pyrrolidinyl)- cyclohexyl]-benzeacetamide methane sulphonate), bremazocine, spiradoline and ICI 197067 bind to sigma sites in guinea-pig tissues using in vitro, semi-quantitative receptor autoradiography and receptor binding, and compared the binding profile so obtained with those for several selective sigma ligands. Guinea-pigs were killed and their brians, livers and spleens were removed, tissue sections cut and processed for sigma binding site autoradiography using (+)-[3H]-3-(3-hydroxyphenyl)-N-(1-propyl)piperidine ((+)-[3H]-3-PPP), or tissue was wiped and determined by liquid scintillation. Serial slide-mounted sections were incubated with 9-10 concentrations (1 nM-10 microM) of kappa opioids and their potency to inhibit (+)-[3H]-3-PPP binding compared with that of the sigma ligands haloperidol, DTG (1,3 di(o)-tolylguanidine), (+)-3-PPP, (+) and (-)pentazocine, SR 31742A and rimcazole (n = 3, duplicate determinations). Binding of (+)-[3H]-3-PPP to untreated, matched serial tissue sections was used as control. Kd values were estimated in brain, liver and spleen using quantitative, saturation binding analysis, IC50 values were determined from the binding data obtained by slide wiping experiments for each drug, and Ki values were calculated using the Cheng-Prussoff equation. All four kappa opioids inhibited (+)-[3H]-3-PPP binding to sigma 1-receptors with order of potency: brain: U50,488H = spiradoline > bremazocine > ICI 197067; liver: spiradoline > U50,488H > ICI 197067 > bremazocine; spleen: U50,488H > spiradoline > ICI 197067 > bremazocine. By comparison, the sigma ligands inhibited (+)-[3H]-3-PPP binding to matched, serial slide-mounted brain tissue sections (similar results in liver and spleen) with order of potency: SR 31742A > haloperidol > (+)pentazocine > (+)-3-PPP > DTG > (-)pentazocine > rimcazole. (+)-[3H]-3-PPP autoradiography confirmed these binding data. It is concluded that the kappa opioids tested moderately inhibit (+)-[3H]-3-PPP binding to sigma 1-receptors in guinea-pig brain, liver and spleen tissue with Ki values comparable to some selective sigma ligands and therefore are not opioid selective.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Size and frequency characteristics of alpha beta and gamma delta T cells in the spleens of normal and cyclophosphamide-suppressed virus-infected chickens.

The characteristics of avian lymphocytes expressing surface CD8 (CT8) and T cell receptor (TCR) glycoproteins have been monitored by two-color flow microfluorimetry. Exposure of 1-month-old birds to a lethal influenza A virus, which is known to be lympholytic, significantly decreased the frequency of both the alpha beta TCR2+CT8+ and gamma delta TCR1+CT8- subsets in spleen. However, all categories of T cells showed evidence of greater mean cell size, indicating that they are responding. Inoculation of baby chicks with fowl pox virus induced a response more typical of specific immunity in the TCR2+CT8+ set, in that the lymphocytes increased in both frequency and mean cell size. Greater numbers of lymphoblasts were also found for the TCR2+CT8-, TCR1+CT8+, and TCR1+CT8- subsets, but the total cell counts for the minority TCR1+CT8- cells in spleen were consistently decreased. Immunosuppression with cyclophosphamide prior to infection eliminated 90% of the white blood cells from spleen, with the greatest effect being on the TCR1+ populations. The CT8+ alpha beta T cell response in chick spleen following exposure to a poxvirus is thus comparable to the situation observed for this subset of lymphocytes in mice infected with other viruses. However, although the gamma delta T cells increase in size, their frequency in spleen either does not change (CT8+) or is significantly decreased (CT8-).

Animals↗

Macromolecular covalent binding of [14C]nitrobenzene in the erythrocyte and spleen of rats and mice.

Nitrobenzene exposure is known to produce red blood cell damage as well as engorgement and sinusoidal congestion of the spleen in male Fischer-344 (F-344) rats but not in male B6C3F1 mice. These studies were conducted to investigate the species differences in the covalent binding of [14C]nitrobenzene in the erythrocyte and spleen and to assess the contribution of nitrobenzene-induced erythrocytic damage to the splenic effects. Total and covalently bound 14C concentrations in erythrocytes of rats were 6-13 times greater than those of mice following a single oral dose of 75, 150, 200 or 300 mg/kg [14C]nitrobenzene, suggesting that species differences in nitrobenzene-induced red blood cell toxicity may be related to differences in erythrocytic accumulation of nitrobenzene and its metabolites. Covalently bound 14C in erythrocytes of rats peaked 24 h following administration of 200 mg [14C]nitrobenzene/kg; in contrast, bound radiolabel in erythrocytes from mice plateaued at 10 h. Splenic engorgement increased in a time-related manner in treated rats but not in mice. Species specificity was also observed in the accumulation of bound radiolabel in the spleen. Gel filtration and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) of lysed, dialyzed erythrocytes from treated rats revealed that hemoglobin was the primary, if not the exclusive, site of macromolecular covalent binding following nitrobenzene treatment. SDS-PAGE of dialyzed rat spleens revealed that 82% of total bound 14C migrated identically to hemoglobin. These data indicate that covalent binding of [14C]nitrobenzene and its metabolites in the spleen is primarily derived from bound 14C from scavenged erythrocytes. Therefore, the species differences in splenic engorgement and accumulation of [14C]nitrobenzene may be related to differences in susceptibility to nitrobenzene-induced red blood cell damage.

Animals↗

Release of prostaglandins evoked by neurohormonal stimuli in the isolated spleen of rabbit.

In the isolated spleen of rabbit perfused with Tyrode solution, sympathetic nerve stimulation (NS) and administration of either noradrenaline (NA), 50--75 ng, or bradykinin (BK), 50 ng, released a material into the venous effluent that caused contraction of rat stomach strip (RSS), rat colon (RC), chick rectum (CR) and bovine coronary artery (BCA). The musculotropic activity of the material released from the spleen was not diminished when it was allowed to stand at either 37 degrees C or at room temperature. The release of this musculotropic material evoked by neurohormonla stimuli was abolished during the infusion of the prostaglandin (PG) synthesis inhibitor, indomethacin, 1 microgram/ml. Application of authentic PGE2 directly on the assay organs caused contraction, whereas PGI2 contracted RSS, RC, and CR but relaxed BCA. In the spleen labeled with [14C]AA, NS, NA or BK released radiolabeled products having the chromatographic characteristics of PGE2 and, to a lesser extent, of PGF2 alpha. Indomethacin abolished the release of these radiolabeled products from the spleen. These observations taken together with the musculotropic characteristics of the material in the venous effluent, suggest that PGE2 is the major product of cyclo-oxygenase relased by NS, NA and by BK from the isolated perfused spleen of rabbit.

Animals↗

Antigen dependent release of interleukin 5 in vitro from spleen cells of mice infected with Angiostrongylus cantonensis.

The kinetics of eosinophil growth and/or survival stimulating factors (Eo-stimulating factors) released by spleen cells from A. cantonensis-infected mice were assessed by in vitro marrow cultures. When spleen cells from C57BL/6 mice 8 to 20 days p.i. were cultured with young adult A. cantonensis worm antigen or Con A, almost equal amounts of Eo-stimulating factors were detected in the conditioned media obtained from both stimulations. No Eo-stimulating factor activity was detected in cultures from spleen cells without stimulation or from normal spleen cells with stimulation. Production of Eo-stimulating factors was inhibited by the pretreatment of the spleen cells with anti-Thy1.2 or anti-L3T4 antibodies plus complement but not with anti-Lyt2.2 antibody. In the presence of anti-mouse IL-5 monoclonal antibody, the activity of Eo-stimulating factors was inhibited by up to 99%. IL-5, therefore, appears to play a principal role in induction of eosinophilia in mice infected with A. cantonensis.

Angiostrongylus cantonensis↗

The splenic snood: an improved approach for the management of the wandering spleen.

A wandering spleen is in constant danger of torsion and infarction. Splenectomy, the traditional treatment, leaves children in danger of postsplenectomy sepsis. Three children with wandering spleens were treated by a new splenopexy technique, the splenic snood. After detorsion, the spleens were wrapped in polyglycolic mesh and anchored by the mesh subdiaphragmatically in the left upper quadrant. All have retained their spleens which have remained where anchored up to a 4-year follow-up. The simplicity and technical ease of the splenic snood operation recommend it as an improved method to avoid splenectomy and safely normalize intraabdominal anatomy in the management of the wandering spleen.

Child↗

Long-term venous access using endogenous splenic tissue: the 'spleen-o-port'.

The authors sought to determine whether endogenous splenic tissue placed in a subcutaneous pouch ("spleen-o-port") could function as a viable alternative to central venous catheters/ports for long-term venous access. A small transverse incision was made in the left upper quadrant of each puppy (n = 6) under general anesthesia. Using a stapler, the authors divided the splenic parenchyma. The superior portion was returned to its native location, and a subcutaneous pocket was created to house the inferior pole with its attached vascular supply. The fascial and muscular layers were closed with care to avoid compressing the blood supply to the spleen-o-port. Postoperatively the dogs resumed normal activity. There have been no deaths, infectious complications, splenic ruptures, or thromboses over a 6-month period. Under fluoroscopy, the dogs were imaged from postoperative day (POD) 10 to 177. Contrast agent entering the splenic parenchyma was promptly visualized in the splenic vein and then filled the portal vein. Electrolyte measurements from spleen-o-port blood samples were identical to those from peripheral venous samples. After gentamicin (mixed in a crystalloid solution) was infused through the spleen-o-port, the peak serum level corresponded to the therapeutic levels observed after standard intravenous administration. The spleen-o-port permits rapid infusion of drugs and crystalloid, and allows repetitive blood sampling while eliminating the foreign body that can promote septicemia in the immunocompromised patient.

Animals↗

Conversion of progesterone to deoxycorticosterone in guinea pig spleen: an animal model for the study of steroid 21-hydroxylase activity in extra adrenal sites.

Steroid 21-hydroxylase activity has been demonstrated, previously, in microsome-enriched fractions prepared from a number of human fetal tissues. The finding that this enzyme activity was present in thymus and spleen is suggestive of the possibility that deoxycorticosterone is important in regulation of immunological processes. In the present investigation, we characterized steroid 21-hydroxylase activity in microsome-enriched preparations of guinea pig spleen. The activity of the enzyme was linear with time for 40 min and with protein concentrations up to 4.8 mg X ml-1 incubation mixture. The apparent Km of the enzyme for progesterone was 0.405 microM. Thus, the potential exists for the biosynthesis of DOC from progesterone in the spleen of the guinea pig as well as in the spleen of the human fetus. Therefore, the guinea pig may be an appropriate animal model for the study of the regulation of steroid 21-hydroxylase activity in the spleen as well as a model for the study of the role of this enzyme in immunologic processes.

Animals↗

The use of spleen transplantation and cyclosporine treatment to induce unresponsiveness to pancreatic islet transplantation in rats.

One way of achieving permanent survival of allografted islets in the rat has been to first transplant a kidney of the same strain as the islets and induce acceptance of the kidney using cyclosporin A treatment. Rats bearing long-surviving renal allografts will then accept islets of the same strain without further immunosuppression. Such an approach may be effective for combined renal and islet grafting, but transplantation of the kidney as well as islets may not always be desirable, and the question arises as to whether another organ could be used to achieve the same effect. Auxiliary spleen transplants were performed from LEW to DA rats, followed by cyclosporine 10 mg/kg for 14 days. Twelve rats with long-surviving grafts were then made diabetic with streptozotocin and given LEW islets placed under the kidney capsule, 6 rats being given a further course of cyclosporine 10 mg/kg for 7 days after islet transplantation. Rats that did not reject their islets then underwent removal of the spleen transplant, and if this did not result in rejection islet function was proven by removal of the kidney bearing the islets. The results show that spleen allograft rejection can be prevented by cyclosporine treatment and that 50% of animals with long-surviving spleen allografts will accept subsequent islet allografts from rats of the same donor strain. The acceptance of islet allografts can be increased to 100% by a further short course of cyclosporine treatment. It is concluded that spleen allografts can be used to produce unresponsiveness to islets in rats.

Animals↗

Characterization of postsynaptic beta-adrenergic receptors and presynaptic muscarinic cholinergic receptors in the rat spleen.

The beta-adrenergic and muscarinic cholinergic receptors in the splenic homogenates of control and 6-hydroxydopamine (6-OHDA) treated rats were characterized. The specific binding of [3H]dihydroalprenolol (DHA) and [3H]quinuclidinyl benzilate (QNB) in the rat spleen were saturable and of high affinity and showed pharmacological specificity of splenic beta-adrenergic and muscarinic cholinergic receptors. Following 6-OHDA treatment, the Bmax value for specific [3H](-)DHA binding to the rat spleen was significantly increased by 26 percent and 22 percent compared to control at 2 and 3 weeks without a change in the Kd. In contrast, there was a 38 percent decrease in the Bmax for [3H](-)QNB in the 6-Ohda treated rat spleen at 2 and 3 weeks respectively without a change in the Kd. The Bmax value at 5 weeks was significantly greater than that at 2 or 3 weeks. The splenic norepinephrine (NE) concentration was markedly reduced by the 6-OHDA treatment at 1 to 3 weeks, while there was a significant recovery in the splenic NE concentration at 5 weeks. Thus, our results strongly suggest that we are biochemically localizing muscarinic cholinergic receptors on the sympathetic nerves of the rat spleen and that the beta-adrenergic receptors of the spleen are localized postsynaptically.

Alprenolol↗