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Biomedical subjects

M Tomonaga

Publications and source records attributed to M Tomonaga.

At least 109 records · Page 6Linked to original sources
PubMed1999

Infectious complications during remission induction therapy in 577 patients with acute myeloid leukemia in the Japan Adult Leukemia Study Group studies between 1987 and 1991.

The Japan Adult Leukemia Study Group analyzed infectious episodes in 577 patients with acute myeloid leukemia during remission induction therapy between 1987 and 1991. 542 patients (93.9%) experienced at least one infectious episode, 121 (21.0%) had microbiologically documented infection; there was clinically documented infection in 184 (31.9%) and unexplained fever in 237 (41.1%). Among 121 microbiologically documented infections, bacteremia/fungemia was observed in 68, pneumonia in 33, and other types of infections in 20. Among the bacteremia/fungemia, gram-negative bacteria accounted for 41.2% (Pseudomonas aeruginosa was the most common), gram-positive bacteria for 39.7%, fungi for 16.2% (Candida spp. being most frequent), and polymicrobial for 2.9%. The most frequent isolates among pneumonia were Pseudomonas aeruginosa and Aspergillus. A total of 70 patients (12.1%) died during remission induction. Mortality of 68 patients with bacteremia/fungemia was 26.5%; in these patients, mortality with concomitant pneumonia increased to 41.4%; without pneumonia, mortality was 15.4% (P < 0.05). Mortality according to the isolated microbes was 17.2% for gram-negative bacteria, 25% for gram-positive bacteria, and 54.5% for fungi. Mortality of 113 patients with pneumonia (33 microbiologically documented and 80 clinically documented), 20 with other microbiologically documented infections, 104 with other clinically documented infections, and 237 with unexplained fever was 25.7%, 5.0%, 5.8%, and 5.1%, respectively.

Acute Disease↗
PubMed1999

[Phase II clinical study of SH L 573 (fludarabine phosphate) in patients with chronic lymphocytic leukemia].

We conducted a multicenter phase II clinical study of fludarabine phosphate, a new purine nucleotide analogue, in patients with chronic lymphocytic leukemia (CLL). Fludarabine phosphate was administered at a dose of 20 mg/m2/day intravenously for 5 days every 4 weeks as one course. Six courses as a maximum were repeated. The response rate was 38.5% (95% confidence intervals: 20.2% to 59.4%), with 1 complete remission and 9 partial remissions out of 26 treated patients. Major drug-related adverse reactions were fever, nausea, weakness, and paresthesia of the fingers; as a grade-3 reaction, varicella was also reported. Neutropenia and thrombocytopenia were observed as manifestations of hematologic toxicity. Clinical laboratory test results revealed abnormalities in hepatic function, including increased GPT, but none of these was rated grade 3 or 4.

Adolescent↗
PubMed1999

Cerebral acetylcholine levels and long-term spatial cognitive impairment following middle cerebral artery occlusion in rats.

The behavioral and neurochemical changes in the chronic phase of permanent occlusion of the right middle cerebral artery (MCA) in rats were investigated. Nineteen MCA-occluded rats failed to solve the 8-arm radial maze task (cognitively impaired rats), while 11 MCA-occluded rats could complete it (cognitively unimpaired rats). When a delay of 60 min was imposed in the task, however, 5 cognitively unimpaired rats failed to complete the task. The rats that underwent behavioral testing were studied for any changes in ACh levels in various brain regions using HPLC with electrochemical detection. The ACh levels in the infarcted areas decreased considerably in all MCA-occluded rats, but no region of the infarcted areas correlated with the spatial cognitive deficit. The ACh levels tended to decrease in the frontal cortex of the cognitively impaired rats and greatly increased in both ipsilateral and contralateral parietal cortex of the cognitively unimpaired rats. A significant correlation was observed between the ACh levels and spatial cognitive deficit in the contralateral frontal cortex, and ipsilateral and contralateral parietal cortex. These results suggest that the cholinergic function of the frontal and parietal cortices might play a role in acquiring spatial cognition in MCA-occluded rats.

Acetylcholine↗
PubMed1999

[Relationship between hippocampal arachidonic acid content and induction of LTP in aged rats].

There are several lines of evidence indicating that membrane AA correlates with the ability of aged rats to sustain LTP. The age-related decrease in membrane AA seems to be triggered by increased lipid peroxidation, which is involved with the decline of LTP. The chronic treatment of DHA could decrease membrane AA without an increase in lipid peroxidation. We have thus investigated the effect of chronic treatment of DHA on hippocampal LTP to assess whether the decrease in membrane AA could directly affect the induction of LTP. The effects of daily supplementation of DHA for 3 months on membrane AA, LTP, and Ca2+ response were evaluated using hippocampal slices from 26-month-old Wistar rats. Chronic treatment of DHA reduced the hippocampal AA significantly, but did not change the amplitude of LTP. Neither 30 mM K+ nor 500 microM NMDA-induced Ca2+ response was affected by chronic treatment of DHA, while the 500 microM carbachol-induced Ca2+ response was reduced. From these results, the reduction of membrane AA might suppress the carbachol-induced Ca2+ response by inhibiting the muscarinic receptor function, IP3 formation and/or Ca2+ release from Ca2+ stores by IP3. However, the reduction of membrane AA is not likely to be a main causal factor of the decline of LTP.

Aging↗
PubMed1998

Allelotype analysis of adult T-cell leukemia.

Allelotype analysis of adult T-cell leukemia (ATL) was undertaken for the first time to identify chromosomal loci relevant to the development of acute/lymphomatous ATL. Loss of heterozygosity (LOH) was screened using 94 highly polymorphic microsatellite markers, distributed among all nonacrocentric, autosomal chromosomes. In each of the 22 cases, DNA obtained from their leukemic cells in acute/lymphomatous phase was compared with their constitutional DNA from mononuclear cells in chronic or remission phase. Allelic losses of at least on one chromosome arm occurred in 91% of the cases (20 individuals). Among 39 chromosome arms, allelic losses were observed on 31 arms at least for one sample. A high frequency of allelic loss (>30%) was seen on chromosome arms 6q (41%) and 17p (48%). The mean fractional allelic loss (FAL) was 0.109. These findings suggest that a novel tumor suppressor gene on chromosome arm 6q, as well as the p53 gene on chromosome arm 17p, probably have an important role in the development of acute/lymphomatous ATL.

Adult↗
PubMed1998

Interleukin-15 (IL-15) can replace the IL-2 signal in IL-2-dependent adult T-cell leukemia (ATL) cell lines: expression of IL-15 receptor alpha on ATL cells.

Interleukin-15 receptor (IL-15R) and IL-2R have the same beta and gamma chains, but IL-15R has a specific alpha chain distinct from that of IL-2Ralpha, which is indispensable for the high affinity binding of IL-15. In the present study, we examined four IL-2-dependent adult T-cell leukemia (ATL) cell lines for their IL-15R expression. All cell lines bound IL-15, which was not inhibited by a 100-fold excess amount of IL-2, proliferated in response to IL-15 to the same degree as to the stimulation with IL-2, and were maintained without IL-2. The responses to 1L-15 were inhibited by the antibodies against IL-2R beta or gamma chains but was not by the IL-2R alpha chain antibody. [125I]-IL-15 exhibited a single high-affinity binding with an apparent kd of 0.17 nmol/L. Reverse transcription-coupled polymerase chain reaction (RT-PCR) showed that the cell lines had the mRNA of IL-15R alpha. The cell lines also had IL-15 mRNA. Despite the presence of IL-15 mRNA, the cell lines did not secrete IL-15, and the culture supernatants of fresh ATL cells and plasma from the patients did not contain a detectable amount of IL-15 with a few exceptional cases, although fresh ATL cells also responded to IL-15. These results suggest that ATL cells have the complete form of IL-15R and respond to IL-15. Such an IL-15-dependent cell proliferation mechanism might be used in the development of ATL and for the invasion and proliferation of ATL cells in the visceral organs.

Adult↗
PubMed1998

Possible association between adult T-cell leukemia/lymphoma and acute myeloid leukemia.

BACKGROUND: To the authors' knowledge, an association between adult T-cell leukemia/lymphoma (ATL) and acute myeloid leukemia (AML) has been reported only in four patients. The authors identified five additional patients with both neoplasms. METHODS: A review of the clinical records of patients with AML, ATL, or lymphoid neoplasms other than ATL diagnosed between 1986 and 1995 was performed. Cytokine levels were assayed in selected patients. The authors searched for reports from other institutions using MEDLINE and the proceedings of two Japanese hematology societies. RESULTS: ATL was diagnosed in 134 patients, whereas 180 had AML. Five patients with both neoplasms were identified (3.7% of ATL patients and 2.8% of AML patients). In seven of the nine patients (including four patients in the literature) with ATL and AML, the ATL was diagnosed prior to the AML, whereas in the remaining two patients both neoplasms were diagnosed simultaneously. Six of the nine cases were therapy-related (t)-AML, which developed after chemotherapy for ATL. Monoclonal integration of proviral human T-lymphotropic virus type 1 was detected in ATL cells but not in AML cells in the six patients examined. The plasma levels of macrophage colony-stimulating factor (M-CSF), granulocyte-colony stimulating factor, and granulocyte-macrophage-colony stimulating factor (GM-CSF) were elevated in 3, 1, and 1, respectively, of the 4 patients examined at AML onset who had active ATL. In one case, the levels of several cytokines, including GM-CSF and M-CSF, in the supernatant fluid of short term cultured ATL cells were elevated. Three patients with de novo ATL and AML received remission induction therapy, and two achieved a complete remission (CR) of both diseases. Among the four patients who received chemotherapy for t-AML, two achieved CR. CONCLUSIONS: ATL patients also can develop AML, irrespective of treatment with chemotherapy for ATL. This association does not indicate exclusive chemoresistance of both neoplasms. Cytokines produced by ATL cells may support the growth of AML cells.

Acute Disease↗
PubMed1998

The methylthioadenosine phosphorylase gene is frequently co-deleted with the p16INK4a gene in acute type adult T-cell leukemia.

Adult T-cell leukemia (ATL) is a retrovirus-associated leukemia with poor prognosis and often has deletions of the p16INK4a and p15INK4b genes on chromosome 9p21. The gene for methylthioadenosine phosphorylase (MTAP), a purine and methionine metabolic enzyme, resides approximately 100 Kb telomeric to the p16INK4a gene and is frequently co-deleted with the tumor suppressor gene in a variety of cancers. This enzyme deficiency can be exploited for selective chemotherapy with de novo purine synthesis inhibitors and/or methionine depletion. To determine whether ATL can be a candidate for selective chemotherapy based on genetic alterations on chromosome 9p21, we analyzed the MTAP gene in 41 samples from ATL patients (27 acute type and 14 chronic type ATL) and 3 cell lines established from ATL patients. Five samples from the acute type had deletions of the MTAP gene (4 total deletions and 1 partial deletion of exons 6-8). The MTAP gene was always co-deleted with p16INK4a. No deletion of the MTAP gene was detected in samples from the chronic type. Of 3 cell lines, 2 showed partial deletions of exons 5-8 of the MTAP gene, and 1 lost all exons. The p16INK4a gene was deleted in all cell lines. In conclusion, deletions of the MTAP gene were found in 5 of 27 acute type ATL samples. Acute type ATL with MTAP deficiency can be a good candidate for selective chemotherapy by depleting purines and/or methionine.

Adult↗
PubMed1998

Expression and cellular localization of low-density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor in human glioblastoma in vivo.

Low-density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP) has been proposed to mediate the cellular uptake and clearance of inactivated protease-inhibitor complexes in regulating proteinase activity at the cell surface, which is necessary for cellular migration and invasive processes. In this study, we investigated the presence of both LRP and urokinase-type plasminogen activator receptor (uPAR) in glioblastoma by reverse transcriptase-polymerase chain reaction (RT-PCR), and the cellular localization of LRP in glioblastoma tissues by immunohistochemical analysis. LRP mRNA was frequently expressed in glioblastomas and anaplastic astrocytomas compared with low-grade astrocytomas by RT-PCR analysis, and was well correlated with uPAR expression. The immunohistochemistry of LRP on sequential frozen sections showed that neoplastic glial cells and endothelial cells of glioblastomas exhibited intense LRP immunoreactivity, whereas LRP was almost undetectable in low-grade astrocytomas or in normal glial cells and endothelial cells of normal brain tissue. Glioblastomas from 11 patients in which the expression of LRP mRNA was observed by PCR displayed strong to moderate LRP immunoreactivity, with predominantly diffuse cytoplasmic and cell-surface localization. In normal brain tissues, LRP immunoreactivity was identified in the pyramidal neurons of the cerebral cortex. These results indicate that LRP is present both in the cellular cytoplasm and on the cell surface of glioblastomas with an increased expression of uPAR. Altered LRP expression might contribute to the stimulation of cell-surface proteolytic activity that in turn facilitates the invasiveness of glioblastoma in vivo.

Brain↗
PubMed1998

Stromal angiogenesis in human glioma: a role of platelet-derived endothelial cell growth factor.

BACKGROUND: Although several tumor angiogenic factors have been identified previously and characterized, it is not yet fully clear how tumor angiogenic factors induce endothelial cell transformation and proliferation. Platelet-derived endothelial cell growth factor (PD-ECGF) has been recently discovered to be an endothelial cell growth factor initially purified from human platelets. However, there has been no previous report describing the significance of PD-ECGF in the growth of brain tumors by angiogenic stimulation. We report the immunohistochemical localization of PD-ECGF in human gliomas and meningiomas, and discuss whether PD-ECGF could play a role in the modulation of stromal angiogenesis in human glioblastoma multiforme. METHODS: Twenty-eight cases of glioma (11 glioblastomas and 17 astrocytomas) derived from the neuroectoderm in embryogenesis and 12 meningiomas from the mesoderm were investigated by both immunohistochemical localization of the PD-ECGF and a semiquantitative assay to determine the degree of stromal angiogenesis. RESULTS: Numerous PD-ECGF positive cells were observed within and around the blood vessels of glioblastoma multiforme, especially on the borders of tumor tissue. The PD-ECGF positive cells were negative for anti-von Willebrand factor (vWF) and antiglial fibrillary acidic protein (GFAP) antibodies and were positive for antimacrophage (HAM-56). The expression of PD-ECGF by macrophages closely correlated with the degree of stromal vascularity in glioblastoma multiforme; no such correlation was found in either astrocytoma or meningioma. Proliferating cell nuclear antigen (PCNA) was found to be positive in some endothelial cells of stromal vessels in glioblastoma multiforme. These findings suggest that PD-ECGF expressed by macrophages plays an important role in the growth of glioblastoma multiforme with stromal angiogenesis.

Astrocytoma↗
PubMed1998

Giant cell tumor of the sphenoid bone: long-term follow-up of two cases after chemotherapy.

BACKGROUND: Giant cell tumors rarely occur in the sphenoid bone. When they do occur in the base of the skull, surgical treatment is frequently difficult and therefore, the use of adjuvant therapy is important. However, there remains no optimal management regimen for giant cell tumors of the sphenoid bone. CASE DESCRIPTION: Two cases of a giant cell tumor involving the sphenoid bone that responded well to chemotherapy using adriamycin after a partial removal of the tumor are presented. In the first patient, the tumor was partially removed via a transcranial subfrontal approach and a transnasal transsphenoidal approach. In the second patient, the tumor was partially removed through a transcranial subfrontal approach. Both tumors demonstrated histologic features typical of giant cell tumors. The patients subsequently received adjuvant chemotherapy using adriamycin alone in the first patient, and chemotherapy combined with radiotherapy in the second patient. Partial regression of the tumors was later confirmed on a computed tomography (CT) scan after chemotherapy. In both patients, tumors have been stable for more than 12 years despite an incomplete removal of the tumors. CONCLUSION: Based on the above findings, postoperative adjuvant chemotherapy using adriamycin may be effective for incompletely resected giant cell tumors of the sphenoid bone.

Adult↗
PubMed1998

Postoperative subarachnoid clots and the pattern of cerebral ischemia associated with symptomatic vasospasm.

OBJECTIVE: We retrospectively evaluated the presence of subarachnoid clots and the development of symptomatic vasospasm in 125 patients who had early surgical treatment of a ruptured cerebral aneurysm. SUBJECTS AND METHODS: We studied 16 patients (aged 35-86 years; mean, 58.7 years) who underwent surgery 0 to 6 days (mean, 2.1 days) and then manifested symptomatic vasospasm on day 5-12 (mean, day 7.4), and 57 patients (aged 13-79 years; mean, 52.0 years) who underwent surgery 0-8 (mean, day 2.9) and did not manifest symptomatic vasospasm. The volume and location of subarachnoid clots were evaluated with computed tomographic (CT) scanning. Cerebral ischemia was evaluated clinically and also in eight patients, by measurement of cerebral blood flow (CBF) using xenon-enhanced CT. Angiographic evaluation was performed only on one patient. RESULTS: Of the 16 patients with symptomatic vasospasm, the subarachnoid clots were localized, distributed thickly, or associated with intracerebral hematomas in 15 and thin in 1 at the time of admission. Fifteen patients had CT evidence of a subarachnoid clot during vasospasm. Most of the clots were near the ruptured aneurysms, but in three cases, clots were located in the remote cisterns, which were not accessible operatively. The clinical manifestations of vasospasm in these three patients correlated with the site of the clot. CBF was reduced in the territory of the involved artery in all eight patients in whom it was measured. In two of the eight cases, the reduction occurred in the territory of a contralateral artery. In contrast, in the 57 patients without symptomatic vasospasm, the subarachnoid clots were already gone or disappeared soon after surgery in most patients. CONCLUSIONS: The continued presence of subarachnoid clots is an important risk factor for symptomatic vasospasm after the rupture of a cerebral aneurysm. The clot is not always located near the ruptured aneurysm, and the clinical course may be unpredictable.

Adult↗
PubMed1998

Quantitative electroencephalographic correlates of cerebral blood flow in patients with chronic subdural hematomas.

BACKGROUND: We have observed that the reduction in cerebral blood flow (CBF) of patients with chronic subdural hematomas is always most pronounced in the thalamus and has a linear correlation with the degree of brain deformity caused by the compression from the hematoma. When the brain is markedly displaced by a hematoma, electroencephalography (EEG) shows delta waves in the frontal region. We theorized that the flow reduction begins in the thalamus, spreading throughout the hemisphere as displacement progresses. METHODS: We measured CBF using the xenon/computed tomography (CT) method in 10 patients with chronic subdural hematomas who had hemiparesis and/or a mental disturbance and radiographic evidence of a midline shift or herniation. We correlated their flow reductions with topographic encephalograms. RESULTS: Flow reductions were more pronounced in the thalamus than in the hemisphere and cortex. Slow waves dominated over fast waves, especially in the frontopolar and frontal regions bilaterally. Flow values correlated negatively with the presence of delta and theta waves and positively with that of alpha and beta waves. On the side of the hematoma, the brain wave activity correlated significantly with thalamic flow, and the correlation was greater than with the hemispheric or cortical flow. Thalamic flow correlated more consistently with delta and alpha waves in the central, temporal, and occipital regions, and with beta waves in the frontopolar, frontal, and central regions. On the nonhematoma side, the correlation between brain wave activity and hemispheric flow was significant and greater than with cortical or thalamic flow. CONCLUSIONS: The correlation of EEGs with thalamic flow, which was maximally reduced, seems to substantiate the concept that the thalamus is primarily injured by brain distortion due to the compression from hematoma and that the remote areas are secondarily deactivated by a transneural depression ("diaschisis") originating from the dysfunctioning thalamus. Thalamic involvement seems to be the cause of the neurologic dysfunction and the abnormal EEG activity in chronic subdural hematomas.

Aged↗
PubMed1998

No parental origin bias for the rearranged chromosomes in myeloid leukemias associated with t(9;22), t(8;21) and t(15;17).

We investigated parental origin of rearranged chromosomes 9 and 22 (9q + and 22q -) in five patients with Ph-positive chronic myeloid leukemia (CML) using the C-banding and silver-staining methods of nucleolus organizer regions, respectively; of rearranged chromosome 21 (21q +) in seven patients with t(8;21)-positive acute myeloid leukemia (AML); and of rearranged chromosome 15 (15q +) in six patients with t(15;17)-positive AML. It was found that these rearranged chromosomes can be of either paternal or maternal origin. Although the number of patients examined was small, these results indicate that the genes rearranged as a result of these chromosome translocations (ABL, BCR, AML-1 and PML) are not genomically imprinted.

Adolescent↗
PubMed1998

A long term follow-up of a randomized trial comparing interferon-alpha with busulfan for chronic myelogenous leukemia. The Kouseisho Leukemia Study Group.

To evaluate the long-term effectiveness of interferon-alpha (IFN-alpha) therapy in patients with chronic myelogenous leukemia (CML) in chronic phase, we examined the updated outcomes of 159 patients who had been enrolled between 1988 and 1991 into a randomized trial comparing IFN-alpha with busulfan. At a median follow-up of 73 months, the median survival was 71 months in the IFN-alpha group and 55 months in the busulfan group (P=0.0563), and the median time of remaining in chronic phase was 58 months in the IFN-alpha group and 39 months in the busulfan group (P=0.4676). Landmark analysis showed a significant advantage in survival (P=0.009) and duration of chronic phase (P=0.0001) in patients with any cytogenetic response among the IFN-alpha group. About half patients were discontinued IFN-alpha administration in spite of cytogenetic response in this study. It appears that continuation of IFN-alpha might possibly confer a survival advantage. Pretreatment factors associated with cytogenetic response included high hemoglobin level, low percentage of peripheral basophils and low leukocyte counts. Multivariate analysis identified lower percentage of bone marrow basophilia (P=0.007) for survival advantage. If a group with a very good prognosis is predicted by a new prognostic model, it might be an option to wait for bone marrow transplantation.

Adult↗
PubMed1998

Chemotherapy vs HLA-identical sibling bone marrow transplants for adults with acute lymphoblastic leukemia in first remission.

There is controversy about whether chemotherapy or an HLA-identical sibling bone marrow transplant is better treatment for adults with acute lymphoblastic leukemia (ALL) in first remission. A previous study of patients treated in 1980-1987 showed similar leukemia-free survivals with these approaches. We re-examined this issue in more recently treated patients receiving different chemotherapy. Chemotherapy subjects (n = 76) participated in trial ALL-87 of the Japan Adult Leukemia Study Group (JALSG). Transplant subjects (n = 214) were reported to the International Bone Marrow Transplant Registry (IBMTR). Treatment-related mortality, relapse and leukemia-free survival were compared after adjusting for differences in subject- and disease-related variables and time-to-treatment. Outcomes differed in persons < or = and >30 years of age. Five-year treatment-related mortality in persons < or =30 years was 3% (95% confidence interval, 0-12%) with chemotherapy vs 32% (23-41%; P < 0.0001) with transplants. The difference was greater among persons >30 years, 13% (2-31%) with chemotherapy vs 57% (43-69%; P < 0.0001) with transplants. Five-year relapse probability in persons < or =30 years was 69% (50-84%) with chemotherapy vs 22% (14-32%; P < 0.0001) with transplants. Among persons >30 years, 5-year relapse was 70% (53-85%) with chemotherapy vs 32% (20-45%; P < 0.0001) with transplants. Leukemia-free survival at 5 years was significantly worse with chemotherapy than with transplants in persons < or =30 years (30% (15-48%) vs 53% (44-63%; P = 0.02)) but not in persons >30 years (26% (13-41%) vs 30% (20-41%; P = 0.70)). We concluded that transplants result in more treatment-related deaths but fewer relapses than chemotherapy. Leukemia-free survival is better with transplants than chemotherapy in persons < or =30 years of age but comparable in older persons.

Adolescent↗
PubMed1998

Circulating interleukin-6 levels are elevated in adult T-cell leukaemia/lymphoma patients and correlate with adverse clinical features and survival.

We measured the circulating levels of interleukin (IL)-6 in adult T-cell leukaemia/lymphoma (ATL) patients using an enzyme-linked immunosorbent assay. The IL-6 levels in 59 ATL patients (median 8.2 pg/ml; range < 1.0 to 185.7 pg/ml) were significantly higher than in 30 healthy controls (median < 1.0 pg/ml; range < 1.0 to 3.5 pg/ml) (P < 0.0001) or 32 human T-lymphotropic virus type-I (HTLV-I) carriers (median 4.2 pg/ml: range < 1.0 to 13.3 pg/ml) (P = 0.002). Among the ATL patients, the IL-6 levels in the acute- or lymphoma-type patients were significantly higher than those in the chronic-type patients (P < 0.0001). The IL-6 levels were also higher in the patients with B symptoms than in those without B symptoms (P = 0.039), and were significantly correlated with increased serum lactate dehydrogenase (LDH) (P = 0.0004) and C-reactive protein (CRP) (P < 0.0001) and decreased serum albumin (P = 0.0003) values. The patients with elevated IL-6 levels had inferior overall survival periods compared to those with normal IL-6 levels (P = 0.025). ATL is a single disease entity, although its clinical features are quite diverse; the increased production of cytokines may cause the diversity of clinical features. The results of our study indicate that IL-6 is one such cytokine.

Adult↗