Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The success of a transfusion of thrombocytes is influenced by numerous factors concerning both the preparation of the platelet concentrate and the recipient. In a long-term substitution of thrombocytes on account of the appearance of immunological and unspecific consumption processes the control of the effectiveness is indicated. The determination of the thrombocyte increment and the resonance thrombography are suitable for this purpose. Fever, sepsis, splenomegaly and haemorrhage cause a diminution of the increase of thrombocytes after transfusion. Isoantibodies have the greatest influence on the shortening of the survival time of transfused thrombocytes. The corrected increase of thrombocytes (CI) 1 hour after the transfusion is lowered under 5.0 Gpt/l (m2). Directives are given for the transfusion and statement of the success of thrombocyte concentrate in patients with leukaemia and malignant tumours.
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PMID:[Thrombocyte substitution, 2: Thrombocyte preparations and determining the effectiveness of thrombocyte transfusion]. 357 56

Gaucher's disease is an autosomal recessive disorder caused by deficiency of beta glucocerebrosidase, resulting in an accumulation of glucocerebroside in the reticuloendothelial system. These patients have massive splenomegaly and bone pain, but may have normal life expectancy. Traditionally, splenectomy has been used to treat hypersplenism, but may be associated with a high incidence of postsplenectomy sepsis and accelerated hepatic and bone lipid deposition. Two children are reported who had partial splenectomy for symptoms of Gaucher's disease. Both patients had laboratory evidence of hypersplenism. A 90% splenectomy was performed, and the residual splenic fragment was wrapped in Vicryl mesh. Both patients are currently asymptomatic with normal hematologic parameters. Postoperative radionuclide scans demonstrate increase in the size of the residual splenic fragment. Partial splenectomy may benefit patients with Gaucher's disease, but long-term follow-up care is necessary.
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PMID:Partial splenectomy for Gaucher's disease. 359 12

Since April 1985, 82 patients with HCL entered a multicenter study using lymphoblastoid alpha-interferon; 51 (including 15 who failed splenectomy and 24 with substantial splenomegaly) enrolled before April 1986 are evaluated in this study. The patients were treated with 3 mega units daily subcutaneously until complete or partial response and were thereafter randomly allocated to a maintenance regime of 3 mega units/week or to observation only. Ten cases had a complete response, 18 a partial response, and 15 a minimal response. Two patients had no response, two interrupted therapy due to major toxicity (toxic hepatitis and thrombocytopenia), six died before completing 1 month of therapy of sepsis, and two died of myocardial infarction. In the two groups of splenectomized and nonsplenectomized patients the mean time to hemoglobin recovery was 8.5 and 6.5 weeks, respectively, the neutrophil count recovery was 6.5 and 9.3 weeks, and the time to platelet count recovery was 4.0 and 5.4 weeks, respectively. No significant differences in recovery time and response rate were observed between the two groups. In 31 out of 32 patients with substantial splenomegaly the spleen became either inpalpable (18) or significantly smaller (13). This study confirms the responsiveness of HCL to IFN in nonsplenectomized patients with high tumor burdens and is therefore recommended as a first-line therapy.
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PMID:Human lymphoblastoid interferon for hairy cell leukemia: results from the Italian Cooperative Group. 366 57

Sixteen dogs with lymphoma underwent splenectomy to relieve signs of massive splenomegaly including splenic rupture. The most common preoperative hematologic abnormalities, anemia and thrombocytopenia, were reversed in all dogs surviving the initial postoperative period. Within 6 weeks after surgery, 5 dogs died because of disseminated intravascular coagulation and sepsis. The remaining 11 dogs underwent chemotherapy. These 11 dogs had a complete response rate of 66% at one month after surgery; the mean and median survival times were 9.3 and 5 months, respectively. In 7 dogs evaluated until death, the mean and median survival times were 13.4 months and 14 months, respectively.
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PMID:Use of splenectomy in the management of lymphoma in dogs: 16 cases (1976-1985). 367 80

We report the clinical features and outcome of 16 patients with cryoglobulinaemia. Two patients with Type I cryoglobulinaemia both had IgG kappa monoclonal paraproteins. Nine of 10 with Type II disease had monoclonal IgM kappa and polyclonal IgG; one had monoclonal IgG kappa and polyclonal IgG in the cryoglobulin. Underlying disorders identified in 3 of the 4 Type III patients were Sjogren's syndrome, infective endocarditis, and non-A non-B hepatitis and HTLV III infection. The commonest presenting features were rash in 94 p. 100 (ulceration 25 p. 100), arthralgia in 63 p. 100 (erosive arthritis 32 p. 100), renal disease in 63 p. 100, neurological involvement in 56 p. 100, hepatomegaly in 32 p. 100 and splenomegaly in 32 p. 100. Major associated conditions were progressive bronchiectasis in one case, and severe peripheral vascular disease in another; underlying malignancy was found in 2 cases (lymphoma and malignant melanoma). Treatment was with plasma exchange (PE) and immunosuppressive drugs (ID) in 10, PE alone in 3, ID alone in 2 and antibiotics [corrected] in 1. Fourteen of 16 patients showed an initial clinical response and fall in cryoglobulin levels. Four patients have died, one each from gastro-intestinal haemorrhage, sepsis, pulmonary embolism and lymphoma. Of the remaining 12 patients, all are symptomatically controlled and 10 have persisting cryoglobulinaemia (3 on PE and ID, 2 on PE, 2 on ID and 3 on no treatment). Of the two cases in whom cryoglobulinaemia resolved, one (Type II) had received PE and ID and the other (Type III) had been treated with antibiotics and surgery for infective endocarditis.
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PMID:Cryoglobulinaemia: clinical features and response to treatment. 376 96

We describe 20 adult patients with malignant lymphoma with primary presentation in the spleen. The most common presenting symptoms were fever, malaise, and weight loss. Physical examination revealed prominent splenomegaly without palpable lymphadenopathy. Small lymphocytic lymphoma was the most frequent histologic type (11/20), followed by large cell lymphoma and mixed cell lymphoma (3/20 each). Bone marrow involvement was found in ten of 17 patients. At laparotomy, lymph node involvement, usually retroperitoneal, was found in six of 13 patients. There was liver involvement in seven of 15 patients. Follow-up has been relatively short, with an average of 24 months (range, one to 48 months). Four patients died as a result of progressive disease, one died of sepsis after splenectomy, and one died two years after diagnosis of a stroke. The prognosis in primary splenic lymphoma appears to be similar to that in nodal lymphoma.
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PMID:Malignant lymphoma with primary presentation in the spleen. A study of 20 patients. 384 Sep 80

The technique, and short and long term results, of splenectomy for massive splenomegaly are presented. The latter was defined as a spleen weighing in excess of 1.5 kg. Thirty-five of the 38 patients had a serious haematological disorder as the indication for the operation, usually non-Hodgkin's lymphoma or myelofibrosis. All operations were carried out through abdominal incisions. Accessible splenic attachments were divided, and the splenic artery was ligated in continuity, prior to posterior mobilization. Two patients (5.3%) died as a result of the operation, both deaths being due to sepsis. Septic and thrombo-embolic complications were common, and occurred both early and late after the operation. Overall, eight of the 12 deaths during the first postoperative year were due to the primary disease, whereas all of the five deaths after that time were due to causes other than the primary disease. Twenty-four patients lived at least 1 year, and 10 patients are alive for more than 5 years.
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PMID:Splenectomy for massive splenomegaly. 386 13

The immune status of patients in Harare modifies their response to acute P.falciparum infection. Malnourished children were the group at greatest risk and fits were a feature of malaria in this age group. Fever and headache were the commonest symptoms overall, but 12,5% of patients were never pyrexial. Splenomegaly was common in young children but uncommon in adults. A leukocytosis, thrombocytopenia and normochromic normocytic anemia were common features of acute P. falciparum malaria as were hyponatremia and hypokalemia. The leukocytosis and hypokalemia are not well documented features of acute malaria and genetic differences may account for varying responses. The diagnosis was proven in only 26% of cases thought clinically to have malaria. In several cases malaria was not considered in the differential diagnosis. More than 1/2 the patients with positive blood slides received antibiotics as well as chloroquine. Bacteria were isolated from blood cultures in 8 patients. Septicemia may be an uncommonly recognized complication of acute P. falciparum malaria.
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PMID:The clinical features and laboratory findings in acute Plasmodium falciparum malaria in Harare, Zimbabwe. 391 Feb 59

A 54 year old man, hospitalised for thoraco-abdominal pain resulting from a septicemia which gives positive hemocultures for streptococcus D Bovis, is diagnosed to have a splenic abscess which will require splenectomy. At the same time, an endocarditis develops and gets worse, with auriculo-ventricular blockade and, especially, major aortic insufficiency, which is the cause of death by a brutal and massive pulmonary oedema. In the progression of an endocarditis, the occurrence of a splenic abscess, primary localisation of the initial septicemia or the secondary of an arterial septic embolism, is a rare contingency compared to the frequency of splenomegaly or splenic infarction: less than 2 percent of the cases in the literature. This very atypical and exceptional case serves as a reminder, on the one hand, of the diagnostic inadequacy of echocardiography which cannot visualise vegetation in the course of progressive endocarditis, and, on the other, of the prognostic importance of auriculoventricular blockade in septal and aortic endocardial lesions.
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PMID:[Splenic abscess disclosing endocarditis]. 393 91

Hereditary spherocytosis is a clinically heterogeneous, genetically determined red blood cell membrane disorder resulting in hemolytic anemia. A deficiency of spectrin, the largest and most abundant structural protein of the erythrocyte membrane skeleton, results in the formation of spherocytes which lack the strength, durability, and flexibility to withstand the stresses of the circulation. Clinical manifestations of the disease are primarily dependent on the severity of hemolysis, which additionally results in an increased incidence of pigment gallstones. The likelihood of cholelithiasis is directly related to patient age and is uncommon before 10 years of age. Splenectomy is indicated in virtually every patient. When the disease is diagnosed in early childhood, the risk of overwhelming postsplenectomy sepsis makes it advisable to delay splenectomy until after 6 years of age if possible. At the time of splenectomy, it is important to identify and remove any accessory spleens. If gallstones are present, cholecystectomy should be performed. Although spherocytosis persists following splenectomy, hemolysis is alleviated and clinical cure of the anemia is achieved for most patients. Patients with recessively inherited spherocytosis are exceptions. Although they are significantly benefited by splenectomy, their anemia is not completely corrected. Splenectomy reduces hemolysis in all patients and thereby decreases the risk for development of pigment gallstones. Excision of an enlarged spleen removes the danger of traumatic rupture.
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PMID:Hereditary spherocytosis. Recent experience and current concepts of pathophysiology. 394 20


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