RESUMEN
In this study, the microbial community structure and carbon source utilisation profile of activated sludge samples collected from full-scale municipal wastewater treatment plants (WWTPs) operated under different conditions were characterised and compared, respectively, using terminal-restriction fragment length polymorphism (T-RFLP) analysis and Biolog assay. Samples were collected from each biological treatment tank of six conventional activated sludge, two anaerobic-oxic, two anaerobic-anoxic-oxic, and one step-aeration processes in eight full-scale WWTPs in Osaka, Japan. Results of the T-RFLP analysis of eubacterial 16S rDNA showed that microbial communities of activated sludge differed greatly among samples, and that they were affected by process-based operational conditions. In contrast, the carbon source utilisation profiles of activated sludge samples were mutually similar, but appeared to be influenced slightly by aerated conditions at each reaction tank. Similar carbon source utilisation profiles among all samples suggest that the activated sludge community possesses functions that are necessary for wastewater treatment even if the phylogenetic composition is different. Different results from the T-RFLP analysis and Biolog assay suggest that the phylogenetic composition of microbial community might not necessarily reflect the wastewater treatment functions of the activated sludge.
Asunto(s)
Aguas del Alcantarillado/microbiología , Eliminación de Residuos Líquidos/métodos , Aerobiosis , Anaerobiosis , Bacterias/clasificación , Bacterias/genética , Bacterias/aislamiento & purificación , Filogenia , Polimorfismo de Longitud del Fragmento de Restricción/genética , ARN Ribosómico 16S/genética , Microbiología del AguaRESUMEN
We report a case of mediastinal esophago-bronchogenic cyst in a patient with a high serum level of CA 19-9. A 49-year-old man presented with a complaint of dysphagia. Chest X-ray, CT, and MRI showed posterior mediastinal cystic shadow which was diagnosed preoperatively. The serum level of CA 19-9 was 158 U/ml. We underwent extirpation of the cyst through video-assisted thoracoscopic surgery (VATS) and confirmed to be a bronchogenic cyst histologically. The serum level of CA 19-9 returned to normal after the operation.
Asunto(s)
Quiste Broncogénico/inmunología , Antígeno CA-19-9/sangre , Quiste Mediastínico/inmunología , Cirugía Torácica Asistida por Video , Quiste Broncogénico/cirugía , Humanos , Masculino , Quiste Mediastínico/cirugía , Persona de Mediana EdadRESUMEN
The case was a 76-year-old male. After thoracoscopic left upper lobectomy against primary lung cancer with poor risks such as complication of systemic lupus erythematosus (SLE) and pulmonary emphysema, oral steroid treatment, heavy smoker, decreased renal function, the patient was complicated with intractable pulmonary fistula and MRSA pyothorax. Intracavitary administration of albumin preparation and fibrin glue (Beriplast P) was effective against pulmonary fistula though it was not helpful in the pleurodesis which was conducted 7 times. Teicoplanin (Targosid) was effective against MRSA pyothorax and maintained the renal function.
Asunto(s)
Carcinoma de Células Escamosas/cirugía , Fístula/cirugía , Enfermedades Pulmonares/cirugía , Neoplasias Pulmonares/cirugía , Complicaciones Posoperatorias/terapia , Anciano , Albúminas , Carcinoma de Células Escamosas/complicaciones , Empiema Pleural/tratamiento farmacológico , Adhesivo de Tejido de Fibrina , Humanos , Neoplasias Pulmonares/complicaciones , Lupus Eritematoso Sistémico/complicaciones , Masculino , Resistencia a la Meticilina , Neumonectomía , Enfisema Pulmonar/complicaciones , Infecciones Estafilocócicas/tratamiento farmacológico , Teicoplanina/uso terapéutico , Toracoscopía , Resultado del TratamientoRESUMEN
Inflammatory process plays an important role in the development and progression of atherosclerotic lesions. Recently, group-II phospholipase A(2) (PLA(2)), an inflammatory mediator, was reported to exist in human atherosclerotic lesions and to enhance the development of murine atherosclerotic lesions. Oxidized low density lipoprotein (Ox-LDL) stimulates the growth of several types of macrophages in vitro. Since proliferation of macrophages occurs in atherosclerotic lesions, it is possible to assume that the Ox-LDL-induced macrophage proliferation might be involved in the progression of atherosclerosis. In this study, the role of group-II PLA(2) in the Ox-LDL-induced macrophage growth was investigated using thioglycollate-elicited mouse peritoneal macrophages. Thioglycollate-elicited macrophages significantly expressed group-II PLA(2) and released it into the culture medium. The Ox-LDL-induced thymidine incorporation into thioglycollate-elicited macrophages was three times higher than that into resident macrophages, whereas under the same conditions, granulocyte/macrophage colony-stimulating factor (GM-CSF) equally induced thymidine incorporation into both types of macrophages. Moreover, the Ox-LDL-induced GM-CSF release from thioglycollate-elicited macrophages was significantly higher than that from resident macrophages. In addition, the Ox-LDL-induced thymidine incorporation into macrophages obtained from human group-II PLA(2) transgenic mice and the GM-CSF release from these cells were significantly higher than those from their negative littermates, and the Ox-LDL-induced thymidine incorporation into human group-II PLA(2) transgenic macrophages was significantly inhibited by a polyclonal anti-human group-II PLA(2) antibody. These results suggest that the expression of group-II PLA(2) in thioglycollate-elicited macrophages may play an enhancing role in the Ox-LDL-induced macrophage growth through the enhancement of the GM-CSF release.
Asunto(s)
Factor Estimulante de Colonias de Granulocitos y Macrófagos/metabolismo , Lipoproteínas LDL/farmacología , Macrófagos/citología , Macrófagos/metabolismo , Fosfolipasas A/fisiología , Animales , División Celular/fisiología , Fosfolipasas A2 Grupo II , Humanos , Macrófagos/efectos de los fármacos , Masculino , Ratones , Ratones Endogámicos C3H , Tioglicolatos/farmacologíaRESUMEN
Macrophage-derived foam cells are known to play an essential role in the development and progression of atherosclerotic lesions. Probucol prevents oxidative modification of low-density lipoprotein (LDL) and lowers plasma contents of LDL and high-density lipoprotein (HDL). A recent report using apoE -/- mice demonstrated that probucol treatment enhanced atherosclerosis in apoE -/- mice more rapidly than that in untreated apoE -/- mice, and a reduction in plasma cholesterol by probucol was not the cause of enhancement of atherosclerotic lesions in probucol-treated apoE -/- mice. Moreover, probucol was reported to inhibit apoA-I mediated cholesterol efflux from mouse macrophages. These reports suggested that probucol might directly affect cholesterol metabolism in mouse macrophages. Thus, we investigated the effects of probucol on cholesterol metabolism in mouse resident peritoneal macrophages. Probucol did not affect degradation of acetylated LDL (Ac-LDL), degradation of LDL and endogenous cholesterol synthesis in mouse macrophages. However, it significantly inhibited HDL-mediated cholesterol efflux. Moreover, probucol partially (30%) inhibited the binding of HDL to mouse macrophages, and significantly activated acyl-coenzyme A:cholesterol acyltransferase (ACAT). Our results suggested that probucol inhibited HDL-mediated cholesterol efflux by inhibiting the binding of HDL to mouse macrophages and reducing HDL-accessible free cholesterol content by ACAT activation, thereby worsening atherosclerotic lesions in apoE -/- mice. However, it remains unclear whether probucol inhibits HDL-mediated cholesterol efflux from human macrophages.
Asunto(s)
Anticolesterolemiantes/farmacología , Colesterol/metabolismo , Macrófagos Peritoneales/metabolismo , Probucol/farmacología , Animales , Células Cultivadas , HDL-Colesterol/metabolismo , Activación Enzimática/efectos de los fármacos , Masculino , Ratones , Esterol O-Aciltransferasa/metabolismoRESUMEN
The arbitrarily primed polymerase chain reaction (AP-PCR) was used to detect somatic genetic alterations in lung carcinomas. DNA fingerprints generated by a single arbitrary primer were compared between normal and tumor tissues of the same individuals. We adapted the technique to the use of tissue fixed with methanol, which allowed the analysis of small areas of tissue by microdissection. This improvement of the fingerprinting technique permitted the study of tumors at early stages of progression. Loss of sequences from chromosome 7 was detected in 41.7% of adenocarcinomas and from chromosome 22 in 84.6% of small-cell carcinomas. Gains of sequences from chromosomes 1, 8 and 13 were detected in more than 40% of adenocarcinomas and in chromosome 2 in 63.3% of squamous-cell carcinomas. Our results indicate that allelic imbalances at these chromosomal regions are common genetic abnormalities in lung carcinomas. Loss of sequences from chromosome 22q13.3, found in 11 of 13 small-cell carcinomas, were confirmed by microsatellite PCR analysis. We show that the use of our improved AP-PCR fingerprinting permits the detection of both losses and gains of novel chromosomal regions early during lung cancer development. Our results indicate that early-stage tumors tend to have more allelic imbalances than relatively advanced tumors, suggesting a high tumor genetic heterogeneity in the early stages of lung tumor progression.
Asunto(s)
Aberraciones Cromosómicas , Dermatoglifia del ADN/métodos , Neoplasias Pulmonares/genética , Reacción en Cadena de la Polimerasa/métodos , Adenocarcinoma/genética , Adenocarcinoma/patología , Carcinoma de Células Pequeñas/genética , Carcinoma de Células Pequeñas/patología , ADN de Neoplasias/análisis , Humanos , Neoplasias Pulmonares/patología , Metanol , Fijación del TejidoRESUMEN
Glucocorticoid, an anti-inflammatory agent, inhibits the development of atherosclerosis in various experimental animal models. This is partially explained by its ability to inhibit smooth muscle cell migration and proliferation in the intima and to reduce chemotaxis of circulating monocytes and leukocytes into the subendothelial spaces. We have recently demonstrated that oxidized LDL (Ox-LDL) has a mitogenic activity for macrophages in vitro in which Ox-LDL-induced granulocyte/macrophage colony-stimulating factor (GM-CSF) production plays an important role. Proliferation of cellular components is one of the characteristic events in the development and progression of atherosclerotic lesions. In the present study, we investigated the effects of glucocorticoids on Ox-LDL-induced macrophage growth. Dexamethasone, prednisolone, and cortisol inhibited Ox-LDL-induced thymidine incorporation into macrophages by 85%, 70%, and 50%, respectively. Ox-LDL induced a significant production of GM-CSF by macrophages, which was effectively inhibited by dexamethasone, prednisolone, and cortisol by 80%, 65%, and 50%, respectively. Dexamethasone-mediated inhibition of Ox-LDL-induced GM-CSF mRNA expression and macrophage growth was significantly abrogated by RU-486, a glucocorticoid receptor antagonist. Our results suggest that the inhibitory effects of glucocorticoids on macrophage growth may be due to the inhibition of Ox-LDL-induced GM-CSF production through transactivation of the glucocorticoid receptor.
Asunto(s)
Dexametasona/farmacología , Factor Estimulante de Colonias de Granulocitos y Macrófagos/antagonistas & inhibidores , Lipoproteínas LDL/antagonistas & inhibidores , Macrófagos/efectos de los fármacos , Animales , División Celular/efectos de los fármacos , Factor Estimulante de Colonias de Granulocitos y Macrófagos/biosíntesis , Factor Estimulante de Colonias de Granulocitos y Macrófagos/genética , Lipoproteínas LDL/metabolismo , Lisofosfatidilcolinas/metabolismo , Macrófagos/fisiología , Masculino , Ratones , Ratones Endogámicos C3H , Mifepristona/farmacología , ARN Mensajero/análisisRESUMEN
BACKGROUND: The plasma concentration of 5-hydroxytryptamine (5-HT) in diabetic patients is higher than that in normal subjects. Since recent reports have demonstrated the presence of 5-HT2A receptor in glomerular mesangial cells, it is possible that 5-HT may be involved in the development of diabetic nephropathy through the 5-HT2A receptor in mesangial cells. Because expansion of the glomerular mesangial lesion is a characteristic feature of diabetic nephropathy, we examined the effect of 5-HT on the production of type IV collagen by human mesangial cells. METHODS: Human mesangial cells were incubated with 5-HT with or without 5-HT receptor antagonists, protein kinase C (PKC) inhibitor or transforming growth factor-beta (TGF-beta) antibody. Type IV collagen mRNA and protein concentration in medium were measured by Northern blot analysis and enzyme-linked immunosorbent assay (ELISA), respectively. TGF-beta mRNA and bioactivity in the medium were measured by Northern blot analysis and bioassay using mink lung epithelial cells, respectively. RESULTS: 5-HT stimulated the production of type IV collagen by human mesangial cells, which was inhibited by ketanserin and sarpogrelate hydrochloride, 5-HT2A receptor antagonists, but not by ondansetron, a 5-HT3 receptor antagonist. 5-HT increased the bioactivities of both active and total TGF-beta. However, the 5-HT-enhanced production of type IV collagen was completely inhibited by an anti-TGF-beta antibody. Furthermore, a PKC inhibitor, calphostin C, inhibited the 5-HT-induced increase in type IV collagen secretion, and the activity of membrane PKC was increased by 5-HT. Phorbol ester activated type IV collagen production as well as active and total TGF-beta. Calphostin C completely inhibited the 5-HT-enhanced activity of active TGF-beta, but did not inhibit exogenous TGF-beta-induced increase in type IV collagen secretion. CONCLUSIONS: Our results suggest that 5-HT-enhanced production of type IV collagen by human mesangial cells is mediated by activation of PKC and subsequent increase in active TGF-beta activity.
Asunto(s)
Colágeno/biosíntesis , Mesangio Glomerular/efectos de los fármacos , Mesangio Glomerular/metabolismo , Serotonina/farmacología , Células Cultivadas , Nefropatías Diabéticas/etiología , Nefropatías Diabéticas/metabolismo , Humanos , Ketanserina/farmacología , Cinética , Proteína Quinasa C/metabolismo , ARN Mensajero/genética , ARN Mensajero/metabolismo , Receptor de Serotonina 5-HT2A , Receptores de Serotonina/efectos de los fármacos , Receptores de Serotonina/metabolismo , Antagonistas de la Serotonina/farmacología , Succinatos/farmacología , Factor de Crecimiento Transformador beta/genética , Factor de Crecimiento Transformador beta/metabolismoRESUMEN
A case of double primary adenocarcinoma of the lung with multiple atypical adenomatous hyperplasia (AAH) in a 77-year-old woman is reported. Histopathologically, in the resected left upper lobe of the lung, both cancers were diagnosed as well-differentiated papillary adenocarcinoma, and 161 lesions of AAH were also found. Both the cancer lesions and six AAH (greater than 3 mm in diameter) were examined with regard to immunoreactivity of carcinoembryonic antigen (CEA) and p53 gene product, microsatellite instability (MI) and loss of heterozygosity (LOH) on chromosome 9q and 17q by polymerase chain reaction (PCR). Although both cancers expressed CEA, they did not show clonal immunoreactivity for the p53 gene product. Atypical adenomatous hyperplasia expressed CEA weakly and showed no immunoreactivity for p53 gene protein. Both carcinomas showed LOH on chromosome 17q, and one of them showed LOH on chromosome 9q. In six AAH, LOH on chromosome 17q was detected in two tumors, and one of them also showed LOH on chromosome 9q. One AAH, which was negative for LOH on chromosome 17q and 9q, showed MI at D17S791. These results indicated that AAH is a clonal neoplastic lesion with genetic abnormalities and should be called intraepithelial pneumocyte neoplasia, and that each of the numerous papillary lesions in this case was considered to be an independent lesion.
Asunto(s)
Adenocarcinoma Papilar/patología , Adenoma/patología , Neoplasias Pulmonares/patología , Neoplasias Primarias Múltiples/patología , Adenocarcinoma Papilar/genética , Adenocarcinoma Papilar/metabolismo , Adenoma/genética , Adenoma/metabolismo , Anciano , Antígeno Carcinoembrionario/metabolismo , Cromosomas Humanos Par 17 , Cromosomas Humanos Par 9 , ADN de Neoplasias/análisis , Femenino , Humanos , Hiperplasia/genética , Hiperplasia/metabolismo , Hiperplasia/patología , Pérdida de Heterocigocidad , Neoplasias Pulmonares/genética , Neoplasias Pulmonares/metabolismo , Repeticiones de Microsatélite , Neoplasias Primarias Múltiples/genética , Neoplasias Primarias Múltiples/metabolismo , Reacción en Cadena de la Polimerasa , Proteína p53 Supresora de Tumor/metabolismoRESUMEN
To elucidate the mechanism of triglyceride (TG) accumulation in adipocytes induced by TG-rich lipoproteins, we examined the effect of beta-very low density lipoprotein (beta-VLDL) on TG accumulation in 3T3-L1 adipocytes. Beta-VLDL did not induce TG accumulation in 3T3-L1 preadipocytes but in 3T3-L1 adipocytes. TG accumulation was significantly inhibited by cytochalasin B, an inhibitor of receptor mediated endocytosis. In contrast, cytochalasin B did not inhibit free fatty acid induced TG accumulation in adipocytes. The binding of [125I]beta-VLDL to preadipocytes was inhibited completely by both beta-VLDL and LDL. In sharp contrast, the binding of [125I]beta-VLDL to adipocytes was inhibited completely by beta-VLDL, but partially by LDL. The VLDL receptor mRNA was only expressed in adipocytes. These results suggest that beta-VLDL induced TG accumulation in adipocytes may be mediated through the VLDL receptor pathway.
Asunto(s)
Adipocitos/metabolismo , Adipocitos/fisiología , Endocitosis , Lipoproteínas VLDL/fisiología , Receptores de LDL/fisiología , Transducción de Señal , Triglicéridos/metabolismo , Células 3T3 , Adipocitos/citología , Animales , Northern Blotting , Diferenciación Celular/efectos de los fármacos , Endocitosis/efectos de los fármacos , Ratones , Unión Proteica/efectos de los fármacos , Conejos , Transducción de Señal/efectos de los fármacos , Células Madre/citologíaRESUMEN
To elucidate the mechanism of foam cell formation in the mesangial region of a kidney observed in a familial type III hyperlipoproteinemic patient presenting with diabetes mellitus and nephrotic syndrome, we have examined, in the present study, the effect of human beta-VLDL (apo E2/E2) on foam cell formation in human mesangial cells, since an increase in beta-VLDL is a characteristic feature of this patient. Human beta-VLDL (apo E2/E2) induced foam cell formation in human mesangial cells. The binding of [125I]LDL to human mesangial cells was inhibited completely by both LDL and beta-VLDL. On the other hand, the binding of [125I]beta-VLDL was completely inhibited by beta-VLDL, but partially by LDL. The LDL receptor, but not the VLDL receptor was down-regulated by accumulation of cholesteryl esters. These results suggest that human beta-VLDL (apo E2/E2)-induced foam cell formation in mesangial cells is mediated through both the LDL receptor pathway and the beta-VLDL specific pathway, in which the VLDL receptor is one of the candidates.
Asunto(s)
Células Espumosas/patología , Mesangio Glomerular/patología , Lipoproteínas VLDL/fisiología , Northern Blotting , Células Cultivadas , Ésteres del Colesterol/metabolismo , Células Espumosas/efectos de los fármacos , Células Espumosas/metabolismo , Mesangio Glomerular/metabolismo , Humanos , Ligandos , Lipoproteínas VLDL/metabolismo , Unión Proteica/efectos de los fármacosRESUMEN
We investigated whether low density lipoprotein (LDL) under oxidative stress might induce the release of fructose, glucose-6-phosphate and fructose-6-phosphate from perivascular cells, and also whether these substances might accelerate the formation of advanced glycation end products (AGE) from proteins in vitro. When vascular smooth muscle cells were incubated with LDL in Ham's F10 at 37 degrees C for 48 h. release of all these substances was increased dose-dependently by oxidized LDL. Fructose release was increased in a dose-dependent manner by glucose. Indomethacin (20 microM) significantly (P < 0.01) suppressed the release of fructose (25.4 +/- 15.7% of control) and hexose phosphates (29.4 +/- 4.0) with the inhibition of release of lactate dehydrogenase (35.5 +/- 4.9) as well as probucol, whereas an aldose reductase inhibitor, epalrestat, significantly (P < 0.001) inhibited only the fructose release (0.9 +/- 0.8). Release of fructose and hexose phosphates from vascular endothelial cells was also induced by oxidized LDL. AGE immunoreactivities and AGE-related fluorescence formed from proteins and glucose were significantly increased (P < 0.001) in the presence of small amounts of the cellular glucose metabolites (6.6%) with glucose (93.4%). These data suggest that release of potent AGE initiators, fructose and hexose phosphates, from perivascular cells induced by oxidized LDL may be an important phenomenon for vascular complications.
Asunto(s)
Endotelio Vascular/metabolismo , Fructosa/metabolismo , Glicoproteínas/metabolismo , Hexosafosfatos/metabolismo , Lipoproteínas LDL/farmacología , Músculo Liso Vascular/metabolismo , Factor de Activación Plaquetaria/análisis , Aldehído Reductasa/antagonistas & inhibidores , Animales , Aorta Torácica , Células Cultivadas , Endotelio Vascular/citología , Endotelio Vascular/efectos de los fármacos , Inhibidores Enzimáticos/farmacología , Glicosilación , Humanos , Cinética , L-Lactato Deshidrogenasa , Músculo Liso Vascular/citología , Músculo Liso Vascular/efectos de los fármacos , Oxidación-Reducción , Estrés Oxidativo , Probucol/farmacología , Conejos , Rodanina/análogos & derivados , Rodanina/farmacología , Tiazolidinas , Sustancias Reactivas al Ácido Tiobarbitúrico , Venas UmbilicalesRESUMEN
To elucidate whether beta-migrating very low density lipoproteins (beta-VLDL) induce foam cell formation in mesangial cells or not, surface binding and foam cell formation with beta-VLDL were studied in mouse mesangial cells. Specific binding kinetics for beta-VLDL and low density lipoproteins (LDL) on the mesangial cells were observed with Kd = 3.8 and 13.7 micrograms/ml, and Bmax = 65.9 and 71.9 ng/ml cell protein at 4 degrees C, respectively. The binding of beta-VLDL was inhibited by excess amounts of LDL or beta-VLDL, but not by acetyl-low density lipoproteins. Ligand blotting using beta-VLDL or LDL and immunoblotting using anti-human LDL receptor monoclonal antibody detected the same apparent single protein (approx. 130 kDa). Incorporation of [14C]oleate into cholesteryl ester in mouse mesangial cells was enhanced by beta-VLDL to 3-fold higher than that by LDL, and it was inhibited by chloroquine or anti-human LDL receptor monoclonal antibody. The light microscopic findings also demonstrated that cholesteryl ester deposition increased in these cells incubated with beta-VLDL, but not with LDL. In conclusion, beta-VLDL was specifically taken up by receptor-mediated endocytosis in mouse mesangial cells through LDL receptors, resulting in foam cell formation.
Asunto(s)
Células Espumosas/citología , Mesangio Glomerular/efectos de los fármacos , Lipoproteínas VLDL/farmacología , Receptores de LDL/metabolismo , Animales , Unión Competitiva , Células Cultivadas , Ésteres del Colesterol/metabolismo , LDL-Colesterol/metabolismo , LDL-Colesterol/farmacología , Femenino , Células Espumosas/metabolismo , Mesangio Glomerular/citología , Immunoblotting , Lipoproteínas VLDL/metabolismo , Ratones , Ratones Endogámicos , Ensayo de Unión RadioliganteRESUMEN
A case of cholangiocellular carcinoma in the caudate lobe with intraluminal growth in the extrahepatic bile duct is reported. The main tumor in the caudate lobe was detected by computed tomography and angiography, and two intraluminal tumors at the hepatic hilus and at the root of the right posterior segmental duct were well demonstrated by cholangiography and percutaneous transhepatic cholangioscopy. Independent total caudate lobectomy with bile duct resection was performed. Cholangiocellular carcinoma of the liver with intraluminal growth in the extrahepatic bile duct is very rare and has not been reported in the literature. Independent caudate lobe resection requires a rather complicated technique. However, this method has the advantage of reducing to a minimum the hepatic volume to be resected, and is useful for poor-risk patients or for cases with localized carcinoma at the hepatic hilus.
Asunto(s)
Adenocarcinoma/diagnóstico por imagen , Neoplasias de los Conductos Biliares/diagnóstico por imagen , Neoplasias Hepáticas/diagnóstico por imagen , Neoplasias Primarias Múltiples/diagnóstico por imagen , Adenocarcinoma/patología , Adenocarcinoma/cirugía , Neoplasias de los Conductos Biliares/patología , Neoplasias de los Conductos Biliares/cirugía , Conductos Biliares/patología , Conductos Biliares/cirugía , Colangiografía , Humanos , Hígado/diagnóstico por imagen , Hígado/patología , Hígado/cirugía , Neoplasias Hepáticas/patología , Neoplasias Hepáticas/cirugía , Masculino , Persona de Mediana Edad , Neoplasias Primarias Múltiples/patología , Neoplasias Primarias Múltiples/cirugía , Tomografía Computarizada por Rayos XRESUMEN
The common staging systems for myeloma do not include IgD myeloma because its rarity makes analysis difficult. We studied a series of 165 Japanese patients with IgD myeloma retrospectively to assess which of the easily assessable parameters present at the time of diagnosis were of prognostic significance. The important individual variables detected in a previous univariate analysis were placed in a multiple regression model to identify the major prognostic factors for survival. This analysis showed that light-chain subtype and white blood cell (WBC) count had a strong predictive relationship for the length of survival. These two factors were used to construct a model containing four categories of patients at increased risk for shortened survival. These categories divided the patients into three groups with respective 5-year survival rates of 66% (low risk), 23% (moderate risk), and 0% (high risk). This new risk grouping showed prognostic validity for IgD myeloma.