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At least 19 recordsLinked to original sources
PubMed1975

Splenomegaly, macrothombocytopenia and stomatocytosis in healthy Mediterranean subjects (splenomegaly in Mediterranean macrothrombocytopenia).

Spleen size, stomatocytosis, macrothrombocytopenia, haemoglobin level, white cell count, and abdominal pain episodes were assessed in a coded study of healthy Mediterranean immigrants to Australia. Spleen size was estimated from a length measurement, L, on a standardized plain abdominal radiograph and expressed both as spleen weight and as a spleen length index, L/square root BSA; the platelet count and size parameters were determined electronically and the presence of stomatocytes was evaluated in stained blood films. In relation to 16 Northern European control women 12 of 25 Mediterranean women had radiographic splenomegaly, 10 had macrothrombocytopenia, 9 had stomatocytosis, but none had episodes of abdominal pain. The median spleen weights of the two groups were estimated as 157 and 247 g with ranges from percentile 2.3 to 97.7 of 75 to 328 and 112 to 669 g. Within the Mediterranean group splenomegaly correlated with macrothrombocytopenia (P less than 0.001) but not with stomatocytosis, haemoglobin values or white cell counts. Thus, mild splenomegaly may be expected in Mediterranean macrothrombocytopenia, Mediterranean stomatocytosis appears unrelated, and all of these apparently benign anomalies may be incidental findings in patients from the Italian and Balkan peninsulas.

Adult↗
PubMed1992

[Pathological classification of splenomegaly in portal hypertension].

The morphometric analysis was carried out for 150 cases splenomegaly pathological sections (1010 sections) after being stained with histochemical, immunohistochemical, hematoxylin and eosin methods, summarizing that the proliferation of three types of fibers, the number and distribution of T, B lymphocytes and macrophages, the changes of sections stained with HE, the ultrastructure of splenomegaly under electron microscope would be the criteria for partially preserving splenomegaly. The data of morphometry was treated by IBM/PC computer. The research was aimed to establish a pathological indication for preserving partial splenomegaly clinically. The study demonstrated that the pathological classification, based on the fibrosis degree of splenomegaly, may objectively reflect the changes of immunological function of splenomegaly, by which it was also revealed that the immunological function in pathological class II and III was markedly lowered. Because the proportion of class I splenomegaly remained only in 31% of good function, there are less splenomegaly worth preserving.

B-Lymphocytes↗
PubMed1979

Splenomegaly in murine trypanosomiasis: T cell-dependent phenomenon.

Splenomegaly resulting from Trypanosoma musculi infection was found to be dependent upon a functioning T-lymphocyte system. When both humoral and cell-mediated immune systems were suppressed by treatment with cyclophosphamide 2 days after infection, splenomegaly was inhibited for about 6 days. However, when only humoral immunity was suppressed by treatment with cyclophosphamide 3 days before infection, splenomegaly still occurred. In addition, splenomegaly was absent in congenitally athymic nude mice. Nude mice and immunologically intact heterozygote mice were also sacrificed at varying times after infection, and spleens were examined histologically. A lymphocytic hyperplasia was observed in immunologically intact mice but not in nude mice. These data indicate that splenomegaly of T. musculi infections is T cell dependent and that splenomegaly is the result of a proliferation of B and/or T lymphocytes.

Animals↗
PubMed1975

Malignant histiocytosis with massive splenomegaly in asymptomatic patients. A possible chronic form of the disease.

Four patients with malignant histiocytosis (MH) are described whose initial manifestation of the disease was massive splenomegaly without associated systemic symptoms. The diagnosis of MH was made after histologic evaluation of splenectomy specimens. Splenomegaly in an otherwise asymptomatic patient is unusual for malignant histiocytosis, but when such a clinical picture is seen, it may be confused with other diseases that often present with massive splenomegaly and that have a similar diffuse infiltrative pattern in the spleen. Although three of these patients did eventually develop systemic symptoms characteristic of MH 3, 6, and 10 months after the detection of splenomegaly, the 15-month asymptomatic survival of one patient who received no chemotherapy suggests that MH presenting with massive splenomegaly, rather than with constitutional symptoms, may have a protracted course.

Abdomen↗
PubMedDate not supplied

Diethylcarbamazine in the control of splenomegaly associated with Bancroftian filariasis in the Ok Tedi area of Papua New Guinea.

Bancroftian filariasis is highly endemic in the Ok Tedi region of Papua New Guinea, with a reported mean rate of 39% before the implementation of a single-dose diethylcarbamazine (DEC) treatment programme in 1986. This was followed by a 72% decline in the rate of detectable microfilaraemia and a 40% reduction in pre- and post-treatment splenomegaly. No significant difference was observed when spleen enlargement was compared to the presence of patent malaria. A significant difference in splenomegaly was observed between DEC-treated villagers and their untreated counterparts. Significant differences were reported in the rate of detectable microfilariae of Wuchereria bancrofti, but not of malaria, between the two groups. The number of DEC administrations and the period of time since the first treatment played a significant role immunologically. Significant differences were observed in immunoglobulin (Ig) M and IgG levels and in the extent of splenomegaly between DEC-treated and untreated areas. Filarial infection associated with malaria resulted in higher spleen rates and size. W. bancrofti is a major contributor to splenomegaly in the Ok Tedi region, and splenomegaly associated with bancroftian filariasis can be reduced or controlled by low, well-spaced doses of DEC.

Animals↗
PubMed1992

Massive splenomegaly in sarcoidosis.

We have presented a case of massive splenomegaly. Our patient was initially thought to have lymphoma, but at operation she was found to have sarcoidosis with splenic involvement. At 2250 g, the spleen was one of the largest recorded in the literature on sarcoidosis. Although the spleen is frequently involved in sarcoidosis, a review of 6074 cases showed that the incidence of actual splenomegaly is only 10%. In 628 of these cases the authors described various degrees of splenomegaly, but the incidence of massive splenomegaly was only 3%. We conclude that sarcoidosis must be considered in the differential diagnosis of splenomegaly.

Adult↗
PubMed1976

Experimental models for prevention of graft-versus-host reaction in bone marrow transfusion. I. Selective suppression and augmentation of splenomegaly and cytotoxicity.

Induction and suppression of splenomegaly and cytotoxicity against C57BL/L cells were studied in (AKR X C57BL/6) F1 hybrid adult mice after the transfer of AKR lymphoid and bone marrow cells. 1) Splenomegaly and cytotoxicity were dissociated in the developmental stages of the graft-versus-host reaction. When lymphoid and bone marrow cells of normal AKR mice were injected into F1 recipients, splenomegaly was prominent on days 5 and 7, but cytotoxicity of spleen cells was not detected. Splenomegaly became less prominent but the cytotoxicity became detectable on day 14 after the injection. 2) Cytotoxic activity of spleen cells of F1 recipients was suppressed by the treatment of AKR donors with C57BL/6 lymphoid cells in Freund's complete adjuvant. Splenomegaly, however, was substantially enhanced by such a treatment of the donors. On the other hand, induction of the cytotoxic activity was facilitated by the treatment of donors with C57BL/6 skin grafts. 3) F1 hybrid mice could be protected from the graft-versus-host reaction by the injection of AKR anti-C57BL/6 serum or pretreatment of AKR donors with sonicated cellular antigens of C57BL/6.

Animals↗
PubMed1977

Inverse relationship between splenomegaly and stem cell compartment size in mice treated with nitrogen mustard.

Following the administration of similar doses of nitrogen mustard (4 mg/kg) to different strains of mice, wide variations in the subsequent degree of splenomegaly were observed, implying strain differences in the role of the spleen in the compensatory erythropoietic response to haematopoietic stress. This investigation was undertaken to determine whether or not these differences were related to the size of the haematopoietic stem cell compartment size in the various strains of mice. Groups of 4 different strains of mice (Swiss Webster, A/J, C57BL/6J and CS1/ASH) were injected i.v. with nitrogen mustard (4 mg/kg body weight) and autopsied at regular intervals up to 20 d post-injection. At autopsy, the wet weight of the spleen was determined. Subsequently, groups of the same 4 strains of mice were exposed to single doses of wholebody gamma-irradiation in the range of 500-900 rads. 9 d after gamma-irradiation the mice were autopsied, their spleens removed, and the number of endogenous spleen colonies determined. The greatest degree of splenomegaly was observed in the C57BL/6J mice. The Swiss Webster mice showed no splenomegaly during the time period studied. There existed a linear inverse relationship between the maximum degree of splenomegaly observed and the dose of wholebody gamma-irradiation required to completely eliminate endogenous spleen colonies. This data is in accord with the hypothesis that there exists an inverse relationship between the extent of splenomegaly observed following haematopoietic stress and the haematopoietic stem cell compartment size.

Animals↗
PubMedDate not supplied

Serum immunoglobulin concentrations, malarial and schistosomal antibodies in patients with massive splenomegaly in Malawi.

Serum immunoglobulin concentrations, malarial antibodies and schistosomal antibodies were measured in 33 patients with a provisional diagnosis of schistosomal splenomegaly, 16 with TSS of presumed malarial aetiology and in 52 controls. IgG and IgM were higher in both splenomegaly groups than in the controls and IgG was significantly higher in patients with schistosomal splenomegaly than in TSS. Although a very high IgM was found more often in the TSS group, there was no significant difference between the mean IgM levels in the two splenomegaly groups. The mean antischistosomal antibody titres were significantly higher in the schistosomal group than in those with TSS but there was no difference in the antimalarial antibody titres. These results emphasise the problems of diagnosis of gross splenomegaly in areas where schistosomiasis and malaria coexist.

Adolescent↗
PubMed1976

Platelet storage in the spleen in idiopathic thrombocytopenic purpura and congestive splenomegaly.

The kinetics of 51Cr-tagged platelets was studied in 10 patients with idiopathic thrombocytopenic purpura and in 8 patients with congestive splenomegaly. The surgically removed spleens were examined for their platelet content and for their microscopic structure. In idiopathic thrombocytopenic purpura the life-span of platelets was reduced, the number of platelets washed out from the spleen averaged 4.36 X 10(10)/100 g splenic tissue (intrasplenic platelet reserve). The index platelets per g splenic tissue/platelets per ml whole blood reflecting the tendency of platelets to concentrate in the spleen was 8.06. Microscopically, extensive phagocytosis of platelets by macrophages and a preserved lienal architecture were seen. In the group of congestive splenomegaly the life-span of platelets was not significantly shortened and the intrasplenic platelet reserve agreed with the figure found in idiopathic thrombocytopenic purpura. The spleen was characterized by fibroid degeneration and endothelial hypertrophy causing partial obstruction of the sinusoids. It is concluded that while the intrasplenic platelet reserve is nearly the same in idiopathic thrombocytopenic purpura and congestive splenomegaly, in idiopathic thrombocytopenic purpura hypersequestration while in congestive splenomegaly platelet storage predominates.

Adolescent↗
PubMed1979

Splenectomy for undiagnosed splenomegaly.

During the 9-year period 1968-76 116 splenectomies were performed at the General Hospital, Nottingham. Of these, 13 (11 per cent) were undertaken for unexplained splenomegaly. In 6 patients a diagnosis was established by the operative procedure (2 with sarcoidosis, 2 splenic cysts, 1 Gaucher's disease and 1 haemangiosarcoma). Histological examination of the excised spleens in the remaining 7 patients showed no specific features. Two of these patients benefited considerably from removal of very large spleens. Another patient died from lymphosarcoma which was diagnosed 21 months after splenectomy. In the remaining 4 patients with mild to moderate splenomegaly, there were no real diagnostic or therapeutic advantages. It is concluded that splenectomy should always be considered in patients with unexplained moderate or gross splenomegaly but it may not be helpful in the patient whose spleen is only midly enlarged.

Adolescent↗
PubMed1979

Splenomegaly and splenectomy in sarcoidosis.

The natural history of 30 patients with sarcoidosis who showed histological evidence of granulomatous involvement of the spleen has been studied; 24 patients had splenomegaly, 16 of whom had splenectomy. The main indication for splenectomy was splenomegaly and resultant discomfort. Corticosteroids reduced spleen size but reduction or withdrawal of the relatively high dosage required resulted in rebound splenomegaly within a period of three months to three years. Haematological abnormalities were controlled by splenectomy in all patients so affected, but the natural history of their sarcoidosis remained unaltered.

Adolescent↗
PubMed1976

Splenomegaly in Northern Nigeria.

Seventy five patients with large spleens were investigated in order to establish the causes of splenomegaly in Northern Nigeria, to define further the diagnostic criteria of tropical splenomegaly syndrome (TSS), and to study its pathogenesis. Investigations included examination of liver biopsy, bone marrow cytology, lymphocyte response to phytohaemagglutinin (PHA), serum immunoglobulins and complement, and the presence of immunoglobulin and complement fixed in Kupffer cells. Thirty patients had TSS, five chronic lymphatic leukaemia (CLL), four a syndrome of gross lymphoid hyperplasia (GLH) distinct from TSS, CLL and the lymphomas, and twenty three miscellaneous conventional diseases. In thirteen cases no definite diagnosis could be established. TSS was found to be predominantly a disease of female Fulani cattle herders. Its essential characteristics were splenomegaly in the presence of acquired immunity to malaria, a grossly raised serum IgM, a lowered serum complement, and the presence of IgM fixed in Kupffer cells. There was lymphoid hyperplasia in bone marrow, hepatic sinusoids and often blood which may be indistinguishable from that in CLL. Lymphocytes undergo normal blastogenesis to PHA. There was clinical and haematological response to proguanil therapy. Reticuloendothelial phagocytosis of IgM, probably as a complex, seems to be the essential feature of the condition. As it was impossible to identify early cases of TSS it is unclear whether IgM overproduction or phagocytosis of IgM complexes is the first stage of the disease. The precise nature of the association with malaria remains obscure. The diagnosis of CLL demanded the demonstration of an abnormally low immunoglobulin level and impaired lymphocyte responsiveness to PHA by blast transformation or 3H-thymidine incorporation, in addition to the usual haematological findings. The syndrome GLH occurred in multiparous Hausa women. It was characterised by intense lymphocytosis with active, PHA-responsive cells, and normal immunoglobulin levels. Patients responded to proguanil therapy. It is suggested that these patients have a depressed immune response to malaria, perhaps through repeated pregnancies, and to a leukaemogenic agent, both of which stimulate lymphocytosis. Antimalarial treatment at this stage may prevent the development of frank leukaemia or lymphoma. The usefulness of the various investigative procedures and the problem of managing the large number of undiagnosed cases are discussed.

Adolescent↗
PubMed1976

Mechanism of dilutional anemia in massive splenomegaly.

Twenty patients with anemia and massive splenomegaly were studied in order to elucidate the mechanism by which splenomegaly results in plasma volume expansion. In 18 patients, increased plasma volume accounted for most of the anemia. Fourteen patients had an exaggerated renin response to standing, mean 1967 +/- 613 (SE) ng angiotensin ll/100 ml plasma (p less than 0.05). The mean resting forearm blood flow was increased 3.47 +/- 0.32 (SE) ml/100 ml forearm tissue (p less than 0.001). The venous capacitance was normal, as contrasted to a marked decrease in venous capacitance in patients with anemia of comparable degree without splenomegaly. Cardiac indices were increased in 10 of 11 patients (range 4.1-8.1 liters/min/sq m). In nine of ten patients oxygen consumption was increased (range 147-231 ml/min/sq m). Splenectomy was performed on 14 patients. Splenic blood flow was elevated in four of four patients (range 750-2000 ml/min). Splenic A-V oxygen difference was exaggerated in seven of seven patients and in three of three patients splenic indocyanine-green dye dilution curve failed to show an early peak suggestive of A-V shunting in the spleen. Free portal pressure was elevated in 12 of 12 patients and decreased immediately after splenectomy. The intravascular albumin mass decreased in ten patients, was unchanged in three at 2-4 mo after splenectomy, and was accompanied by a rise in the plasma albumin concentration in nine. These data suggest that a flow-induced portal hypertension with expansion of the portal vascular space is an important early hemodynamic change. This finding, together with a decreased peripheral resistance, probably results in a decrease in effective intravascular volume, resulting in stimulation of the renin-angiotensin-aldosterone system and other renal hemodynamic changes necessary for salt and water retention. Splenectomy usually accomplishes a complete reversal of these abnormalities and correction of the anemia.

Anemia↗
PubMed1992

[Rapid aggravation of splenomegaly by administration of erythropoietin in a case of myelodysplastic syndrome].

In myeloproliferative disorders, aggravation of splenomegaly was reported as an adverse effect of erythropoietin (EPO). Recently, we experienced the adverse effect of EPO in myelodysplastic syndrome (MDS). A 65-year-old male was admitted to our hospital for scrutiny of pancytopenia in July 8, 1991. He was diagnosed as having MDS (refractory anemia: RA). After discharge, daily subcutaneous administration of EPO (3,000U) was started on August 1 because his Hb concentration had decreased to 9.2 g/dl. After the daily dose of EPO was increased up to 6,000U in August 15, left hypochondralgia gradually developed. EPO administration was haltedon August 22. His splenomegaly was aggravated from 2 finger breadths below the left costal margin before EPO administration to 4.5 finger breadths. Bone marrow examination revealed a change to extremely hypercellular marrow from slightly hypocellular marrow before EPO administration. The peripheral blood cell count was not altered. We concluded that he was a rare case of MDS in which aggravation of splenomegaly was observed, probably as a result of extramedullary hematopoiesis induced by administration of EPO.

Aged↗
PubMed1979

Chemical properties of the principle in C. parvum that produces splenomegaly in mice.

Suspensions of Wellcome C. parvum strain 6134 produce splenomegaly in mice when injected i.p. in amounts as low as 20 microgram. This lymphoreticular stimulatory activity is extremely sensitive to cell breakage and is abolished by heating for 4 h at 100 degrees. Periodate oxidation of the bacteria destroys their capacity to produce splenomegaly and abrogates the agglutination of intact C. parvum by Con A. Mild HCl hydrolysis also abolished the splenomegaly but phenol:chloroform:ether and chloroform:methanol extractions did not. These results suggest that the relevant stimulatory principle in C. parvum is of carbohydrate nature, and most probably present on the surface of the bacterium.

Animals↗