Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of 44-year-old woman who had shown psychiatric symptoms before and during the course of Castlemans' disease was presented. For four years, she first suffered from a paranoid-hallucinatory state and then a depressive one episodically. In the course of the latter, severe anemia developed. She was diagnosed as Castleman's disease, because the increased serum level of gamma-globulin and interleukin-6 (IL-6), and multiple lymphomata were evidenced. A paranoid-hallucinatory state relapsed about one year later from this episode. At last, some bulbar and cerebellar symptoms, and a delirium suddenly occurred. The ischemic changes at the level of the pons and midbrain were revealed by the magnetic resonance imaging (MRI) examination. It is certainly that both neurological and psychiatric symptoms were related to the lesions. This ischemic lesions may have resulted from the anoxia secondary to the severe anemia and/or hyperviscosity syndrome in the disease. On the other hand, the increased serum level of IL-6 as well as the ischemic lesions might have caused psychiatric symptoms in this case, as the interferone which is one of the analogues of IL-6, is known to induce emotional and behavioral symptoms.
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PMID:[A case of Castleman's disease with a variable neuropsychiatric symptomatology]. 128 94

A 58-year-old female was admitted to our hospital because of anemia in March 1987. Monoclonal protein (IgA, kappa) was detected and a diagnosis of multiple myeloma was made. Partial remission was obtained after VAD therapy with alpha-interferon. In December 1989, she was readmitted because of a pathological fracture of the left humerus. A white blood cell count was 4400/microliters with 30% myeloma cells and the urine protein (Bence Jones protein) was 26 g/day. Systemic chemotherapy was not effective. She developed pleural and pericardial effusions, bone mass, disturbance of consciousness and died of respiratory failure only 3 months after readmission. The pleural and pericardial fluids contained many myeloma cells. c-myc gene rearrangement was detected in myeloma cells obtained from the pleural fluid using c-myc exon1 and exon2 probes. The levels of interleukin-6 (IL-6) measured by ELISA was 107.4 pg/ml in serum, 56.2 pg/ml in pleural fluid and 780.0 pg/ml in pericardial fluid. Because of the lack of any overt infectious focus, the level of IL-6 appears to have been related to aggressive proliferation of myeloma cells. It was of interest that C-reactive protein, induced by IL-6, was a good marker reflecting disease activity.
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PMID:[A high serum level of interleukin-6 in a patient with aggressive multiple myeloma]. 175 53

A 75-year-old female was diagnosed as having multiple myeloma (IgG.lambda type. Stage IIA) with plasmacytoma of the head and back in October, 1989. She obtained partial remission by MCNU and MP therapy, but relapsed with massive ascites in January, 1991. VAD therapy was not effective and she died of multiple organ failure on February 23. Her ascites contained a large number of myeloma cells, and the phenotypic analysis and the response to interleukin-6 (IL-6) of these myeloma cells were examined. The myeloma cells were positive for CD33, CD45, CD45RA, CD63, CD71, plasma cell associated antigens such as CD38, PCA-1, BL3, and various kinds of adhesion molecules: CD11a/CD18 (LFA-1), CD29 (VLA-beta 1), CD44 (H-CAM), CD49d (VLA-4), CD54 (ICAM-1), CD56 (N-CAM), CD58 (LFA-3). IL-6 level in the ascites was increased at 91.0pg/ml. The myeloma cells showed an IL-6 dependent growth, which was inhibited by anti-IL-6 antibody (Ab) and anti-IL-6 receptor Ab in vitro. Myeloma cells appearing in ascites have rarely been reported. Our case suggested that IL-6 was a potent growth factor of myeloma cells through an autocrine mechanism in the ascites, and resulted in an aggressive myeloma.
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PMID:[Multiple myeloma with massive ascites fluid--immunophenotypic analysis of myeloma cell and its IL-6-dependent growth]. 786 16

We describe a 60-year-old woman who developed mixed connective tissue disease (MCTD) associated with multicentric Castleman's disease (MCD) and Crow-Fukase syndrome (CFS). She showed HLA DR-4 antigen and an abnormal X chromosome (47,XXX). The serum interleukin-6 (IL-6) level was markedly increased and IL-6 mRNA was detected in enlarged lymph node cells. After prednisolone was administered, her IL-6 level decreased and the symptoms of MCTD, MCD, and CFS all improved. Thus, IL-6 may be involved in the modification of the pathologic condition in this patient.
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PMID:Mixed connective tissue disease associated with multicentric Castleman's disease. 809 Nov 49

A 71-year-old woman remained under the rubble of her house for 4 hours after an accidental gas explosion. She suffered from a crush syndrome associating fractures, minor skin burns (< 10% body surface area), inhalation lung injury and moderate hypothermia (34 degrees C). In addition to local signs of compression of the lower limbs, the patient presented with hypovolemic shock and developed acute renal failure on day 3. We describe here the variations in hemodynamic and oxymetric parameters and cytokine response during the first post-injury week. A vasoplegic state resulting from low systemic vascular resistances with progressively increasing cardiac index, oxygen delivery and oxygen consumption closely followed the brief hypovolemic shock. Tumor necrosis factor-alpha remained below normal levels while interleukin-6 increased markedly with a major peak on day 2, in parallel with the drop in systemic vascular resistances. Interleukin-6 is a mediator of impairment in cell membrane function and a vasoconstriction inhibitor. Isolated increased interleukin-6 has been previously reported in severely burned patients suggesting a pathophysiological and hemodynamic similarity between crush syndrome and burn injury.
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PMID:[Hemodynamic profile and serum cytokines in crush syndrome. Analogy with severe burns]. 868 94

A 57-year-old female was admitted to Uji hospital for the further evaluation of nodular shadow on her right lung. During the period of admission, she developed cervical lymph node swelling. She was diagnosed as having malignant lymphoma (diffuse, small cleaved cell) by lymph node biopsy. She received combined chemotherapy and obtained partial remission for seven months until she developed fever and pancytopenia. Laboratory data showed increased number of large granular lymphocytes (LGLs) in blood. Bone marrow revealed increased number of LGLs with hemophagocytosis by macrophage. Surface marker analysis revealed LGLs were positive for CD2 CD16, and CD56 and negative for CD3, CD4, CD8, and CD20. T-cell receptor genes beta and gamma were in germ line configuration. Analysis of Epstein-Barr virus genome using termini probe indicated a monoclonal proliferation of LGLs. Reexamination of the biopsy specimen of lymph node revealed LGLs which was negative for CD3 and CD20. The patient was diagnosed as a leukemic phase of natural killer (NK) cell lymphoma complicated with hemophagocytic syndrome (HPS). Serum levels of interferon-gamma, macrophage colony-stimulating factor, granulocyte colony-stimulating factor, and interleukin-6 increased, which might be related to HPS.
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PMID:[Natural killer cell lymphoma having a nodular shadow in the lung as an initial finding, developed to leukemia complicated with hemophagocytic syndrome at the time of relapse]. 882 78

The present study examined stressor interactions with genotype and light/dark cycle. Male Brown Norway (BN), Fischer 344 (F344), Lewis (from two different vendors: Lew/CR and Lew/H) and Sprague Dawley (SD) rats were exposed to footshock either in the early light or early dark circadian phase. Immediately after footshock, the spleen and whole blood proliferation to PHA and Con A was assessed. To provide endocrine indices of stress, serum was measured for corticosterone and interleukin-6 (IL-6). All rats showed significant increases in serum corticosterone and IL-6 following footshock either in the light or the dark. Rat strain differences were noted in the IL-6 response, while the corticosterone response was strong for all strains. The criterion for 'suppression' of lymphocyte proliferation was p < .05 (as determined by ANOVA) compared to non-shocked controls. Spleen: with the exception of BN rats, the other strains showed suppressed spleen cell proliferation to PHA and Con A both in the light and the dark. BN rats failed to show suppression of mitogenic activity to PHA when footshock was given in the light. Peripheral blood lymphocytes: suppression in Lew rats from either vendor, and in F344 and BN rats, did not vary with time of day nor with the type of mitogen tested. SD rats did not show suppression to PHA if shocked in the light. These results highlight the generality of stressor-induced mitogenic lymphocyte proliferation during the early diurnal and nocturnal periods of the day.
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PMID:Suppression of lymphocyte mitogenesis in different rat strains exposed to footshock during early diurnal and nocturnal time periods. 883 90

We reported a 59-year-old woman who received a diagnosis of psoriasis vulgaris at the age of 35 and had been under medical treatment. She was admitted to our department on August 16, 1993 because of lymphadenopathy, arthralgia and neuralgia. We observed cervical and axillar lymphadenopathy 1-3 cm in diameter, anemia and leukothrombocytosis. Elevated levels of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and immunoglobulin G (IgG), but not M-protein were observed by immunological analysis of the serum. Bone marrow aspiration biopsy revealed hypercellularity with myeloid hyperplasia and slight increase in plasma cells. Elevated levels of serum interleukin-6 (IL-6) and granulocyte colony-stimulating factor (G-CSF) were detected; IL-6 was 62.1 pg/ml and G-CSF was 66 pg/ml, but IL-1 alpha, IL-1 beta and TNF-alpha were within the normal range. Idiopathic plasmacytic lymphadenopathy (IPL) with polyclonal hyperimmunoglobulinemia was diagnosed by lymph-node biopsy and the patient received following treatment with prednisolone and hydroxyurea. Leukocytes, platelets and skin eruptions increased again when the steroid dose was tapered, so we changed treatments to MP (melphalan, prednisolone) therapy. In addition, various neurological abnormalities such as convulsions, loss of consciousness and peripheral polyneuritis were observed. Despite treatment her condition deteriorated and she finally died. Very few reports show these neurological abnormalities in IPL or Castleman's disease therefore we think this is a very rare case.
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PMID:[Idiopathic plasmacytic lymphadenopathy with polyclonal hyperimmunoglobulinemia in a patient who died of progressive peripheral polyneuritis and cerebral dysfunction]. 905 65

A diffuse macular erythroderma and subsequent desquamation after 1 to 2 weeks are two of the five major diagnostic criteria of toxic shock syndrome (TSS). We present the case of a 15-month-old girl with TSS, but without erythroderma or desquamation. She was admitted with high fever, shock, and multiorgan involvement. Minimal or no cutaneous signs were present. Initially the diagnosis of the syndrome of hemorrhagic shock and encephalopathy was made. After 7 days, a TSS toxin 1-producing strain of Staphylococcus aureus was cultured from an inguinal lymph node, where inflammation had already been noticed on admission. Moreover, the girl had no antibodies against this toxin. The serum cytokine profile during the acute phase of her illness showed high levels of tumor necrosis factor-alpha, interleukin-6 and interferon-gamma, as is seen during activation of the immune system by TSS toxin 1. Other possible causes for the patient's illness were excluded. We conclude that the patient had TSS without rash. Without the evidence implicating a TSS toxin 1-producing strain of S. aureus as the cause of her disease, a diagnosis of syndrome of hemorrhagic shock and encephalopathy would have been made. It is possible that some cases of syndrome of hemorrhagic shock and encephalopathy represent a variant of TSS in small children.
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PMID:Toxic shock syndrome without rash in a young child: link with syndrome of hemorrhagic shock and encephalopathy? 967 39

We report the unusual case of an 87-year-old woman with cardiac myxoma and adenomatous goiter. She exhibited slight elevations of serum interleukin-6 (IL-6), but levels of thyroid hormones such as T3, free T3 and free T4 were all abnormally low. Interleukin-6 may potentiate the alteration of thyroid metabolism.
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PMID:Reduced serum T3 level in a patient with nodular goiter and cardiac myxoma. 960 90


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