Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0243026 (sepsis)
 52,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathology of lymphoid organs in 38 low birth weight (LBW) human infants has been evaluated by morphological and morphometric features. The gestational ages of infants ranged from 22 to 32 wks and their age at death varied from 1 hr to 153 days post partum. Infants were divided into 3 groups: 1) without antigenic effects, 2) with mild (bronchopneumonia), and 3) with severe antigenic effects, mainly sepsis. In mildly affected LBW infants, the fetal type of the immune reaction was found. It continued during the period studied (till 5 mths) and was manifested in the reaction of macrophages and the transformation of lymphocytes to lymphoblasts. Reactive centres of follicles and mature plasmocytes were not found. During the first months of postnatal development, an increase in the amount of lymphocytes in the lymphoid organs and in the rate of proliferation of reticular epithelium and a decrease in the area of the cortex in the thymus were found in all infants. In severely affected infants, the number and the size of follicles in the spleen decreased significantly and the total number of cells decreased more than 3 times. Similar changes were found in lymph nodes. These changes as well as the weak reaction of the thymus are the main features of the insufficiency and fast devastation of the lymphoid system. A compensatory increase in the number of neutrophils and eosinophils in the red pulp of the spleen and lymph nodes was found after the second week.
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PMID:Pathology of lymphoid organs in low birth weight infants subjected to antigen-related diseases: a morphological and morphometric study. 756 36

Intravascular lymphomatosis (IL), previously called "malignant angioendotheliomatosis", is a rare neoplastic disease in which mononuclear cells, of demonstrated lymphoid origin, proliferate in small blood vessels lumen. Any organ may be involved, standing out general status affectation, skin and central nervous system (CNS) because their frequency. A case of this disease is reported, who presented general impairment with prolonged fever, abdominal pain and cutaneous arborescent telangiectasias as the most significant clinical data. It become fatal in a short time. It was clinically considered to be a sepsis and diagnosis was only obtained in post-mortem study. This study revealed multiple organ infiltration by this neoplasm, with the notable exception of CNS. Immunohistochemical study confirmed the lymphoid origin of neoplastic cells. The main characteristics of IL are reviewed.
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PMID:[Intravascular lymphomatosis. Report of a case and brief review of the disease]. 766 79

Splenic regeneration represents an interesting phenomenon both in relation to its role as a model system (to study the development of the complex three-dimensional architecture of an immunological organ) and because of the clinical application, namely autotransplantation of spleen. The latter is one of the attempts to restore splenic functions after splenectomy, which is known to increase a life-long risk of fatal sepsis. However, splenic functions of autotransplanted splenic tissue are known to be highly dependent on the recovery of the complex microenvironment and immunoarchitecture of the splenic compartments during the regeneration processes, but the elements inducing splenic reorganization are still unknown. Therefore, the present work investigates whether splenic stroma depleted of cells is able to induce regenerative processes after implantation. In addition, we tried to recombine stromal tissue with selected cell populations to study their influence. Cell-free stromal tissue induced angiogenesis and to a lesser extent also attracted the immigration of lymphocytes during the first 60 days of regeneration. However, after this period of regeneration, the transplants began to degenerate and were resorbed. The recombination of stromal tissue with mitogen-stimulated spleen cells only resulted in intensifying the degenerative processes, and all implants were resorbed after 120 days. Except that in the first 30 days there were some accumulations of lymphocytes that resembled primitive follicles, no splenic compartments such as red pulp, periarteriolar lymphoid sheath, or marginal zone could be detected in any of the transplants. From these results it can be concluded that splenic stroma can induce the primary events of splenic regeneration (like angiogenesis), but is not able to provide an appropriate microenvironment and immunoarchitecture for a correct repopulation and differentiation of cells. Furthermore, the recombination experiments point to a minor role of T-cells and possibly an important role for accessory cells in splenic regeneration.
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PMID:Regeneration of splenic stromal elements. 780 Sep 31

In the randomized autopsy material of 161 patients with rheumatoid arthritis (RA), a letal, generalized septic infection (GSI) was observed in 22 cases (13.66%). The GSI was accompanied by a pyarthros in 12 (7.45%) and no pyarthros in 10 (6.21%) cases. The clinical parameters of 22 septic RA patients were compared with 139 age and sex matched RA patients without GSI. The average age of septic patients decreased (p < 0.02), with low serum electrophoretic b-globulin level (p < 0.04), and high Waaler-Rose (p < 0.02) and Latex level (p < 0.004). The clinical parameters of 22 septic patients were compared with 76 age and sex matched RA patients without sepsis, vasculitis, or generalized secondary amyloidosis (GSA), and/or miliary epitheloid granulomas of tuberculous type (mT). The differences between the two groups of patients were the same, with a statistically more pronounced age difference (p < 0.005). 29 out of 161 patients (18.01 %) suffered from a clinically manifest diabetes mellitus (in 6 patients accompanied by sepsis), and 11 (6.83 %) from a clinically latent diabetes mellitus (in 2 patients accompanied by sepsis). There was no significant relationship between sepsis and manifest diabetes mellitus. The controlled and treated diabetes mellitus does not influence the frequency of lethal sepsis. Significant correlations were found between sepsis and latent diabetes mellitus (based on the histological detection of amyloid deposition localized to the islets of Langerhans (p < 0.02). 34 out of 161 patients (21.12%) suffered from a generalized secondary amyloidosis (in 3 patients accompanied by sepsis). There was no significant relationship between sepsis and generalized secondary amyloidosis. The thickness of adrenal cortex represents the effect of steroid therapy. Critical random check, using the Mann-Whitney tests, supports significance relationship between the adrenal cortex atrophy and fatal sepsis (p < 0.010). The follicular lymphoid depletion in the spleen represents the effect of immunosuppressive therapy. The size of lympho-follicles decreased significantly in sepsis (p < 0.004). The long term corticosteroid therapy and immunosuppressive represent a potential danger for sepsis.
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PMID:[Generalized septic infections in rheumatoid arthritis. Study of autopsy material]. 782 86

Intercellular adhesion molecule-1 (ICAM-1) induction on hepatocytes was investigated in relation to acute liver allograft rejection, CMV infection, and systemic bacterial infections. Twenty-four liver transplant recipients underwent an episode of acute rejection, 13 developed a symptomatic clinical CMV infection, and 7 had bacterial sepsis. Seven recipients without rejection or infection complications were used as controls. All rejection episodes monitored by frequent FNABs were reversible, and lymphocyte and lymphoid blast-dominated with a with peak of inflammation (7.2 +/- 3.9 corrected increment units [CIU]). The rejections were treated with high-dose steroids, and the inflammation subsided within one week. ICAM-1 was demonstrated from fine needle aspiration biopsy (FNAB) preparations by a monoclonal antibody and immunoperoxidase staining. ICAM-1 was not detected on the hepatocytes immediately after transplantation or in control patients, but was always seen during rejection. ICAM-1 appeared 1-5 days before the onset of inflammation in FNAB. The intensity of ICAM-1 expression increased toward the peak of inflammation and subsided together with inflammation. During CMV infection a mild immune activation was seen in FNAB (peak 2.5 +/- 0.8 CIU) and in blood. An intense ICAM-1 induction also preceded the immune activation caused by CMV, and subsided slowly with successful antiviral treatment. In addition, a slight ICAM-1 induction on the hepatocytes was recorded during bacterial sepsis. ICAM-1 induction on hepatocytes appears to be linked with an early phase of immune response, and it even precedes the lymphoid activation of rejection. However, several infections, such as CMV and bacterial infections, raise an immune response and may also induce ICAM-1. In conclusion, ICAM-1 induction on hepatocytes can be considered an early, though unspecific, marker for acute liver allograft rejection.
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PMID:ICAM-1 induction on hepatocytes as a marker for immune activation of acute liver allograft rejection. 790 90

Fifteen patients (nine male, six female) with severe aplastic anemia (SAA) undergoing HLA-identical allogeneic bone marrow transplantation (BMT) received preparative regimens consisting of cyclophosphamide and total lymphoid irradiation. Patients were aged from eight to 26 years (median 15 years). Prophylaxis of graft versus host disease (GVHD) including cyclosporine and short course methotrexate was administered. One early death occurred at day 8 post BMT. Among the other 14 patients, one died of sepsis at day 53 with no evidence of engraftment, 13 were engrafted despite the number of donors exposed in transfusions of previous blood components. Eleven patients have survived from six to 100 months (median, 54 months), post BMT. The remaining two patients died of acute GVHD-related infections on days 44 and 63. Acute GVHD occurred among eight of 13 engrafted patients, five of whom were grades II-IV clinically. Chronic GVHD developed among five patients, three of whom were clinically progressive and extensive. Two of three patients with extensive chronic GVHD had received transfusion of donor's buffy coat after BMT. Our data indicate an engraftment rate of 87% (13/15). The projected probability of disease-free survival was 73% (11/15) at 9.3 years after BMT according to the Kaplan-Meier model. Further efforts must be made to eliminate GVHD and to control fatal infections.
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PMID:Bone marrow transplantation for severe aplastic anemia. 791 56

We review the clinical manifestations and long-term outlook of patients with chronic natural killer (NK) cell lymphocytosis. After reviewing more than 1,500 peripheral blood lymphoid flow cytometry reports and molecular genetics data from patients with suspected large granular lymphocyte (LGL) proliferation, we identified 10 patients (median age at diagnosis, 60 years; range, 35 to 76 years; male:female ratio, 3:2) with persistent (greater than 6 months) increase in phenotypically determined NK cells (CD3-CD16+). Southern blot analysis performed on 9 patients showed no clonal T-cell receptor gene rearrangements. Disease duration was measured from time of initial recognition of LGL or NK cell excess (greater than 40% of the lymphocyte fraction). Clinical data from these 10 patients were compared with those from 68 patients with T-cell LGL (T-LGL) leukemia. Currently, all patients are alive (median disease duration, 5 years; range, 0.8 to 8 years). Associated disease manifestations included pure red blood cell aplasia, recurrent neutropenia, recurrent neutropenic sepsis, and vasculitic syndromes, all of which were responsive to immunosuppressive therapy. No patient had palpable lymphadenopathy or splenomegaly. Compared with the patients with T-LGL leukemia, patients with chronic NK cell leukemia has similar lymphocyte counts, associated conditions, treatment responses, and survival but had less neutropenia and anemia.
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PMID:Chronic natural killer cell lymphocytosis: a descriptive clinical study. 791 84

Immune and endocrine organs of 259 children and adults who had died of sepsis, local purulent-inflammatory affections were studied morphologically and morphometrically. It is established, that compensatory morphological changes in the lymphoid tissue and endocrine organs are integrated into a united system the structural basis of which are numerous inter- and intra-organ correlations. A systemic interaction between the lymphoid and endocrine organs at early age is pronounced much weaker than in the adults. A progressive destruction of this systemic interaction takes place in sepsis and results in an increase of informational entropy and the coefficient of the system disintegration. Inability of the body to fight bacteremia and to localize the infection is secondary to the system destruction this being due to high frequency of previous immuno-endocrinopathies.
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PMID:[Systematic study of the morphology of the immune and endocrine organs during the infectious process]. 798 47

Preparative regimens containing busulfan (BU) followed by allogeneic bone marrow transplantation (BMT) were used in 27 consecutive patients with myelodysplastic syndromes (MDS). The median age was 33 years (range, 4 to 54). Ten were female and 17 male. Sixteen patients had primary MDS, 11 other patients had antecedent hematologic diseases or developed MDS after cytotoxic and/or radiation therapy. Six patients had leukemic transformation and received antileukemic therapy before BMT. Pre-BMT cytogenetic studies showed complex chromosomal abnormalities in 13 patients, a simple abnormality in 5 patients, and normal chromosome in 8 patients. Three BU-based preparative regimens were used: 1 patient received BU 4 mg/kg orally (PO) daily for 4 days and cyclophosphamide (CY) 50 mg/kg intravenously (IV) daily for 4 days (BUCY-4); 24 patients received BU 4 mg/kg PO daily for 4 days, cytosine arabinoside (ara-C) 2 g/m2 IV every 12 hours for 4 doses, and CY 60 mg/kg IV daily for 2 days (BAC); and 2 patients with preceding Fanconi anemia received BU 2 mg/kg PO daily for 4 days followed by total lymphoid irradiation of 5 Gy. Seventeen of 27 patients are alive with no evidence of disease. Ten patients have died: 2 from hepatic veno-occlusive disease, 3 from sepsis, 1 from a cerebral bleed, 1 from a massive gastrointestinal (GI) bleed associated with acute graft-versus-host disease, 1 from hemolytic uremic syndrome with adult respiratory distress syndrome, 1 from bronchiolitis obliterans, and the only patient who did not engraft died from acute myeloid leukemia. Regimen-related toxicities (RRT) include GI tract (diarrhea, 14; stomatitis, 11), liver (9), cardiac (1), and skin (5). Patients who received a genotypically matched marrow graft had a significantly better disease-free survival (DFS) than patients who received a nongenotypic marrow graft (P = .02). The Kaplan-Meier analysis projects an overall DFS of 56% +/- 13% and 78% +/- 10% for patients who received a genotypically matched marrow graft. With the exception of a child who did not engraft, there was no relapse of MDS or leukemia. Excellent DFS, acceptable RRT, and the ease of administration are advantages of this regimen.
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PMID:Busulfan-based regimens and allogeneic bone marrow transplantation in patients with myelodysplastic syndromes. 847 79

We developed a canine model for autologous bone marrow transplantation (AuBMT) with long-term marrow culture (LTMC) cells. Marrow was harvested from nine normal dogs. Harvests from dogs 2-7 were placed into 21 day LTMC. Cells in LTMC from dogs 4-7 were labelled with the neomycin phosphotransferase gene neo. Dogs were given 60Co total body irradiation (TBI) and then infused with LTMC cells: dog 1 received 500 cGy TBI and 2.08 x 10(8)/kg uncultured marrow cells. Dogs 2-7 received 600-800 cGy TBI and 0.07-0.45 x 10(8)/kg LTMC cells. Dogs 8 and 9 received 600 and 800 cGy TBI, respectively, but no infusion of marrow or LTMC cells. For all dogs, profound myelosuppression developed during week 1 and pyrexia developed during week 2. Enrofloxacin was given from one day before TBI until a peripheral neutrophil count > 1.0 x 10(9)/L was achieved, which eliminated Escherichia coli from feces. Dogs 1, 2 and 5-9 also received gentamicin and/or combination beta-lactam antibiotics. Numerous platelet transfusions were needed to control hemorrhages in all dogs except dog 1. Dog 1 achieved neutrophils > 1.0 x 10(9)/L on day 15, while dogs 2 and 5-9 achieved this count on days 33-48. Dogs 3 and 4 died on days 17 and 18, respectively, of beta-hemolytic streptococcal sepsis and hemorrhage, with no evidence of hematopoiesis at necropsy. The marker gene, neo, was documented in lymphoid and myeloid cells of dogs 5-7 up to 21 months post-AuBMT. Our studies indicate that dogs can recover following supralethal TBI and can survive the delayed engraftment associated with AuBMT using LTMC cells, if they receive intensive platelet and antimicrobial therapy. Used prophylactically for such therapy, enrofloxacin achieved selective intestinal decontamination, but did not prevent sepsis when used as the sole antimicrobial agent during myelosuppression. Furthermore, our studies indicate that infused LTMC cells, at the above doses, can contribute to hematopoietic recovery, but are not essential for recovery following TBI, and do not shorten the period of prolonged profound myelosuppression induced by TBI.
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PMID:Clinical and pathological findings in dogs following supralethal total body irradiation with and without infusion of autologous long-term marrow culture cells. 849 Aug 11


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