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PubMed1996

[Thrombotic complication in the course of aplastic anemia-paroxysmal nocturnal hemoglobinuria syndrome; possible involvement of dysplasminogenemia (plasminogen Tochigi) in the pathogenesis of thrombosis].

A 44-year-old Japanese man having aplastic anemia (AA)-paroxyamal nocturnal hemoglobinuria (PNH) syndrome was referred to our hospital because of purpuras due to thrombocytopenia in July 1994. He suffered from pneumonia after admission, complicated with cerebral, splenic, and left renal infarction. Pulmonary infaction was also confirmed by perfusion lung scan. He had a plasma plasminogen (PLG) functional activity of 54.4% with a normal level of PLG antigen. The gel isoelectrofocusing pattern of the plasminogen derived from the patient showed 10 normal bands and 10 additional doublet bands with slightly higher isoelectric points than the normal components. Abnormal PLG is converted by urokinase to an inactive two-chain plasmin molecule. These findings were similar to those of a case with dysplasminogenemia (PLG Tochigi) reported by Aoki et al. He was given warfarin for the prevention of thrombosis in December 1994. As of October 1995, these was no recurrence of thrombosis. The cause of thrombosis in the present case have been the association with PNH, predisposition to PLG Tochigi, or the complication of pneumonia. This is the first report of AA/PNH syndrome associated with dysplasminogenemia.

Adult↗
PubMed1997

Chronic expression of murine flt3 ligand in mice results in increased circulating white blood cell levels and abnormal cellular infiltrates associated with splenic fibrosis.

The effect of chronic expression of flt3 ligand (FL) on in vivo hematopoiesis was studied. Retroviral vector-mediated gene transfer was used in a mouse model of bone marrow transplantation to enforce expression of mouse FL cDNA in hematopoietic tissues. As early as 2 weeks posttransplantation, peripheral blood white blood cell counts in FL-overexpressing recipients were significantly elevated compared with controls. With the exception of eosinophils, all nucleated cell lineages studied were similarly affected in these animals. Experimental animals also exhibited severe anemia and progressive loss of marrow-derived erythropoiesis. All of the FL-overexpressing animals, but none of the controls, died between 10 and 13 weeks posttransplantation. Upon histological examination, severe splenomegaly was noted, with progressive fibrosis and infiltration by abnormal lymphoreticular cells. Abnormal cell infiltration also occurred in other organ systems, including bone marrow and liver. In situ immunocytochemistry on liver sections showed that the cellular infiltrate was CD3+/NLDC145+/CD11c+, but B220- and F4/80-, suggestive of a mixed infiltrate of dendritic cells and activated T lymphocytes. Infiltration of splenic blood vessel perivascular spaces resulted in vascular compression and eventual occlusion, leading to splenic necrosis consistent with infarction. These results show that FL can affect both myeloid and lymphoid cell lineages in vivo and further demonstrate the potential toxicity of in vivo treatment with FL.

Animals↗
PubMed1986

Small intestinal transplantation using cyclosporine. Report of a case.

A case of small intestinal allotransplantation is described. Cyclosporine and Solumedrol were used for immunosuppression. A hemolytic episode occurred, caused by anti-A antibodies derived from graft lymphocytes. Sudden severe encephalopathy developed on the ninth postoperative day, followed by intractable hypotension and death. Hepatic and splenic microinfarcts were identified on postmortem examination. Allograft rejection was identified by serial stomal biopsies and correlated with a rise in monocyte procoagulant activity, a potentially useful serologic marker of rejection. The absence of an anatomic circuit for recycling of cyclosporine did not alter serum radioimmunoassay/high-performance liquid chromatography ratios.

Adult↗
PubMed2005

Pathology of Berkeley sickle cell mice: similarities and differences with human sickle cell disease.

Because Berkeley sickle cell mice are used as an animal model for human sickle cell disease, we investigated the progression of the histopathology in these animals over 6 months and compared these findings to those published in humans with sickle cell disease. The murine study groups were composed of wild-type mixed C57Bl/6-SV129 (control) mice and sickle cell (SS) mice (alpha-/-, beta-/-, transgene +) of both sexes and between 1 and 6 months of age. SS mice were similar to humans with sickle cell disease in having erythrocytic sickling, vascular ectasia, intravascular hemolysis, exuberant hematopoiesis, cardiomegaly, glomerulosclerosis, visceral congestion, hemorrhages, multiorgan infarcts, pyknotic neurons, and progressive siderosis. Cerebral perfusion studies demonstrated increased blood-brain barrier permeability in SS mice. SS mice differed from humans with sickle cell disease in having splenomegaly, splenic hematopoiesis, more severe hepatic infarcts, less severe pulmonary manifestations, no significant vascular intimal hyperplasia, and only a trend toward vascular medial hypertrophy. Early retinal degeneration caused by a homozygous mutation (rd1) independent from that causing sickle hemoglobin was an incidental finding in some Berkeley mice. While our study reinforces the fundamental strength of this model, the notable differences warrant careful consideration when drawing parallels to human sickle cell disease.

Anemia, Sickle Cell↗
PubMed2004

Histiocytic sarcoma with fatal duodenal ulcers.

Histiocytic sarcoma is an uncommon neoplasm of mature histiocytes with very poor outcome. We report an autopsy case of a true histiocytic sarcoma with characteristic symptoms of so-called "malignant histiocytosis of the intestine". The liver and spleen were enlarged, with remarkable tumor cell infiltration in the hepatic sinusoids and splenic sinuses. Tumor cells aggregated to form sporadic nodular lesions in the liver, which often showed coagulative necrosis. Infarcted lesions also occurred at the splenic subcapsular area. In addition, tumor cell infiltration was noted in the sinuses of bone marrow and lymph node. Tumor cells often demonstrated moderate pleomorphism with multinucleated giant cells. They were positive for CD68 and negative for T- and B-cell lineage markers, megakaryocytic markers, and CD30. Various examinations were done to rule out infection-associated hemophagocytic syndrome, and the absence of infectious diseases was revealed. Thus, the diagnosis of histiocytic sarcoma was made. Apart from these lesions, multiple ulcerations, some with fatal perforation, were found in the esophagus and duodenum. They showed only non-specific inflammatory changes without tumor cell involvement. The ulcers probably derived from ischemic condition through an embolic process caused by tumor cell infiltration elsewhere in the blood vessels at the periphery of the ulcers.

Antigens, CD↗
PubMed1999

Phagocytic activity of platelets in patients with myocardial infarction.

The aim of our present study was to analyse the dynamics of changes in the phagocytic activity of platelets with myocardial infarction according to the treatment applied. Twenty patients with acute myocardial infarction and thirty healthy subjects were examined. Platelet count, phagocytic activity of platelets and the phagocytic index were determined. We observed reduced phagocytic activity of platelets in the first 24 hours of infarction, which may be due to exhaustion of most active platelets in a thrombus and microaggregates. A transitory increase in the phagocytosis activity of platelets observed on the third day of infarction may be caused by the release of large, more active platelets from splenic pool. On the eight day of infarction, the phagocytic activity of platelets became normalized in both experimental groups. Our study indicates that together with platelet activation the phagocytic activity gets reduced being a likely response to the thrombocytopenic factor. This can be confirmed by the increased number of platelets on the 8th day. Our results suggest a slightly attenuated phagocytic ability of platelets, irrespective of the treatment applied. The reduction seems to result from the effect of platelets exhaustion on the procoagulative activity in patients with myocardial infarction.

Adult↗
PubMed1975

Defective phagocytosis due to deficiencies involving the tetrapeptide tuftsin.

A description of the symptoms and causes of tuftsin deficiency is presented. Two major causes which give rise to a deficiency of the tetrapeptide (thr-lys-pro-arg) are discussed. One is familial tuftsin deficiency syndrome that results from an inherited mutation involving the tetrapeptide. All patients give a history of repeated infection with variable severity. One parent, father or mother, is deficient and occasionally other siblings may have the disease. The other type of deficiency is the result of loss of splenic function whether it is due to surgical removal of the spleen and to infarction or infiltration of the organ. A method for the assay of tuftsin activity is described.

Adolescent↗
PubMed1982

Torsion of the wandering spleen: splenectomy or splenopexy.

Torsion of the wandering spleen is a rare condition usually unsuspected preoperatively. In previously reported cases in the past, attempts at splenopexy have failed and splenectomy has been regarded as the treatment of choice. We are presenting two children with splenic torsion. In one complete infarction of the spleen had occurred and so splenectomy could not be avoided. In the second, the spleen was viable and splenopexy was successfully performed. The clinical presentation, etiology, diagnostic procedures and management are discussed, and a surgical technique for splenopexy is described.

Child↗
PubMed1996

Splenic pathology after traumatic injury.

Little is known concerning the pathology of spleens removed for traumatic injury. The authors studied the gross and microscopic features of 44 spleens removed for trauma and received at the Surgical Pathology Division of Parkland Memorial Hospital and 10 normal control spleens from the Medical Examiner's Office, Dallas County, Texas. The mean age of patients undergoing post-traumatic splenectomy was 29.6 years with a male:female ratio of 6:1. The most common procedure done for traumatic splenic rupture was splenectomy (39 of 44 cases); wedge resection or partial splenectomy was done in 5 cases. The mean weight of the spleens was 167 g (181 g in males, 93 g in females, P = .056). Capsular laceration or rupture were noted in 86% of post-trauma spleens, usually involving the superior pole and/or hilum. Subcapsular neutrophilic infiltrates were seen in 7%. Gross evidence of parenchymal hemorrhage was seen in 25%, and microscopic evidence in 68%. Control spleens showed none of these findings. Germinal centers were present in 77% of spleens with germinal center hyperplasia in 55% (including patients 16-59 years old), numerous primary follicles in 45%, mantle zone hyperplasia in 10%, and marginal zone hyperplasia in 41% of patient spleens. Control spleens showed few or none of these findings. No patient spleens had histologic features suggestive of Epstein-Barr virus (EBV) or other infection, granulomas (other than lipogranulomas), or infarct. The findings suggest that splenic rupture after trauma may be related to prior immunologic stimulation of the spleen, and that spleens removed for trauma are not equivalent to normal controls.

Adolescent↗
PubMed2001

Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation.

Mesenteric vein thrombosis is generally difficult to diagnose and can be fatal. A case of extensive thrombosis of the mesenteric and portal veins was diagnosed early and successfully treated in a 26-year-old man with Down syndrome who was admitted to hospital because of abdominal pain, severe nausea and high fever. Ultrasonography revealed moderate ascites, and there was minimal flow in the portal vein (PV) on the Doppler examination. Computed tomography (CT) showed remarkable thickening of the walls of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, combined thrombolysis and anticoagulation therapy without surgical treatment was chosen. Urokinase was administered intravenously and later through a catheter in the superior mesenteric artery. Heparin and antibiotics were given concomitantly. The patient's symptoms and clinical data improved gradually. After 10 days, CT revealed that collateral veins had developed and the thrombi in the distal portions of the mesenteric veins had dissolved, although the main trunk of the PV had not recanalized. The only risk factor of thrombosis that was detected was decreased protein S activity.

Adult↗
PubMedDate not supplied

CT features of abdominal manifestations of primary antiphospholipid syndrome.

PURPOSE: The purpose of this work was to evaluate the CT features of the abdominal manifestations of primary antiphospholipid syndrome (PAPS). METHOD: Of the 32 patients who were confirmed to have PAPS among 751 patients with elevated antiphospholipid antibodies during a 2 year period, we retrospectively reviewed the 14 patients who underwent abdominal CT. The clinical indications for abdominal CT included abdominal pain, abdominal distension, or lower leg swelling. CT findings were analyzed with regard to the abdominal vascular system and abdominal organ involvement patterns as well as ancillary findings. RESULTS: Of the 14 patients with PAPS, 10 had involvement of the venous system (72%), 2 of the arterial system (14%), and 2 of both systems (14%). Of the 12 patients who had venous system involvement, 4 had thrombosis in the inferior vena cava (IVC), 2 in both the IVC and the hepatic vein, 1 in the IVC and splenic and portal veins, 1 in the IVC and hepatic and adrenal veins, 1 in the hepatic, portal, and renal veins, and 3 in the portal and superior mesenteric veins. Budd-Chiari syndrome developed in five of the nine patients who had thrombosis of the IVC or hepatic vein. Arterial thrombosis was noted in four patients, hepatic artery in two, aorta in one, renal artery in one, pancreatic arcade in one, and splenic artery in one, with infarct of multiple organs including the liver, jejunum, colon, kidney, and adrenal gland. Seven of the 14 patients (50%) manifested thrombosis or infarct of multiple extra-abdominal organs. CONCLUSION: PAPS should be included in the differential diagnosis when CT demonstrates infarcts in multiple organs or patients have recurrent episodes of venous or arterial thrombosis.

Adolescent↗
PubMed2000

Laparoscopic splenopexy for adult wandering spleen: sandwich method with two sheets of absorbable knitted mesh.

Wandering spleen is a rare entity with a constant danger of splenic torsion leading to splenomegaly and infarction, which requires surgery. The authors describe a 30-year-old woman with intermittent left hypochondralgia and back pain with wandering spleen, who was successfully treated with a new method of laparoscopic splenopexy. In this procedure, two sheets of absorbable knitted mesh were used to sandwich the detorsed spleen. The procedure is feasible and less invasive, without impaired splenic function, and is applicable even for adult splenomegalic wandering spleen.

Absorbable Implants↗
PubMed1993

Spontaneous splenic rupture complicating anticoagulant or thrombolytic therapy.

PURPOSE: To characterize the clinical course and outcomes of reported cases of splenic hemorrhage during thrombolytic or anticoagulant therapy. METHODS: The Medline, EMBASE (Excerpta Medica), BIOSIS, and SCISEARCH databases for English and foreign literature between 1966 and 1991 were searched. All reports of patients with documented splenic hemorrhage during anticoagulant therapy or thrombolytic therapy were reviewed. Foreign language manuscripts were translated into English. RESULTS: Seventeen cases of splenic hemorrhage associated with anticoagulant or thrombolytic therapy were found. In one case, there was minor antecedent trauma; in the remaining cases, hemorrhage was spontaneous. Mortality overall was 24% and was more likely in patients with splenic hemorrhage after thrombolytic therapy (50%) than in patients receiving long-term anticoagulants (9%). Splenectomy was performed in 12 of 13 survivors. CONCLUSIONS: Splenic hemorrhage associated with anticoagulant or thrombolytic therapy is a rare entity. It may be lethal, especially when associated with lytic therapy. Reversal of the anticoagulated or lytic state and emergent splenectomy are the treatment of choice. Splenic hemorrhage can mimic acute myocardial infarction and cardiogenic shock and must be considered when the condition of cardiac patients receiving lytic or anticoagulant drugs suddenly deteriorates.

Anticoagulants↗