Extramedullary plasmacytoma: a localized or systemic disease?
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Aged↗
Biomedical subjects
F J Laso
Publications and source records attributed to F J Laso.
Increased interleukin-12 serum levels in chronic alcoholism.
BACKGROUND/AIMS: In the present study the serum levels of interleukin-12 were analyzed in alcoholic patients in order to explore the possible relationship between them and both the ethanol intake status and the existence of alcoholic liver disease. METHODS: For that purpose interleukin-12 levels were analyzed in a total of 26 alcoholic patients. Additionally, both interferon-gamma and interleukin-4 serum levels were measured in the same patients as a means of exploring the balance between the T-helper-1 and T-helper-2 immune responses. All patients had consumed at least 90 g of ethanol per day for more than 5 years. Fourteen were alcoholics without liver disease (AWLD group) and the other 12 patients were diagnosed as having alcoholic liver cirrhosis. In parallel to the patients, 10 age- and sex-matched healthy volunteers were included in the study. RESULTS: Our results show that interleukin-12 serum levels are significantly increased in AWLD patients as compared to normal controls (p<0.05). In patients with cirrhosis, interleukin-12 serum levels varied, depending on the ethanol intake status at the time of evaluation. Accordingly, as compared to normal controls, significantly increased concentrations of serum interleukin-12 were found in the alcoholic liver cirrhosis patients with active ethanol intake (ALCET group) (p<0.01), while in the cirrhotic individuals with at least 1 year of alcohol withdrawal interleukin-12 serum levels remained within the normal range. Only the cirrhotic patients had increased interferon-gamma serum levels. Among them, the highest levels were found for individuals from the ALCET group, the differences with respect to the healthy subjects being close to statistical significance (p=0.05). No significant differences were detected regarding interleukin-4 serum levels for any of the groups of patients analyzed compared to the control individuals. CONCLUSIONS: Our results show the existence of a relationship between ethanol intake and increased interleukin-12 serum levels, suggesting that this cytokine may play an important role in the induction of the immunological abnormalities found in chronic alcoholism, independently of whether or not alcoholic liver disease is present.
Adult↗
Decreased natural killer cytotoxic activity in chronic alcoholism is associated with alcohol liver disease but not active ethanol consumption.
Chronic alcohol intake is associated with an increased incidence of certain neoplasms. Natural killer (NK) cells have been considered to be involved in control tumor development and growth. The goal of the present study was to contribute to a better understanding of the effects of ethanol (EtOH) per se on the NK-cell population. Both patients with chronic alcoholism without liver disease (AWLD) and subjects with alcohol-induced cirrhosis (ALC) were carefully selected for this study. Immunophenotypical and functional studies of peripheral blood (PB) NK-cells were performed during active EtOH intake and after 3 months of a withdrawal period. In the AWLD group a significant increase in number of NK-cells (CD3-/CD56+) (P < .05) associated with a parallel increase in NK-cell lytic activity (P < .01) was observed. In addition, the number of cytotoxic T cells displaying the CD3+/CD56+ phenotype as well as CD8-/CD57+ NK-cell subset was also increased (P < .01 and P < .001, respectively). By contrast, in ALC patients with active EtOH intake (ALCET group), although a significant increase in the number of NK PB lymphocytes was observed (P < .05), NK lytic activity was depressed (P < .05), suggesting the existence of a decreased lytic activity/NK-cell. After 3 months of EtOH withdrawal, PB mononuclear cells (PBMC) from the AWLD group patients still displayed an increased NK cytolytic activity; in addition, the number of PB NK-cells (CD3-/CD56+ and CD8-/CD57+) and CD3+/CD56+ PB T cells continued to be increased. Independently of the duration of withdrawal period, in ALC patients EtOH withdrawal was followed by a slight decrease in the NK lytic activity of PBMC with respect to the values in active alcoholism phase; slight differences observed in the NK lytic activity in ALC patients who quit drinking could be related to the tendency to decrease of the number of NK-cells toward normal values. Furthermore, although an increase in NK cytotoxic activity after stimulation of PBMC with interleukin-2 (IL-2) was observed in ALC, it did not reach the levels observed in healthy subjects. Overall, our results show that the behavior of PB NK-cell population in chronic alcoholism is different according to both the moment of EtOH consumption and the existence or not of ALC. Alcohol by itself induced an increase in the number and lytic activity of NK-cells. By contrast, the NK cytolytic activity is constantly depressed in the stage of alcoholic cirrhosis, supporting the notion that immunosurveillance mechanisms may be affected in these patients.
Adult↗
Abnormalities of peripheral blood T lymphocytes and natural killer cells in alcoholic hepatitis persist after a 3-month withdrawal period.
Present information about the behavior of the different lymphoid subsets in alcoholic hepatitis (AH), including cells displaying cytotoxic activity, is scanty and contradictory. The aim of this study was to gain further insight into knowledge of the immunological abnormalities involved in AH and the possible role of ethanol (EtOH) consumption in these changes. We analyzed the distribution of a wide range of peripheral blood (PB) lymphoid subsets, both during active EtOH intake and after a 3-month withdrawal period, using multiple stainings with monoclonal antibodies and flow cytometry, as well as natural killer (NK) cytotoxic activity. AH patients entering the study were selected strictly; only those undergoing their first episode of AH with no other lesions at liver biopsy were enrolled. Regarding the alcohol intake period, the most striking finding was a significant increase of the absolute number of PB T cells affecting both CD4+ and CD8+ lymphocytes. These changes were associated with a higher expression of T-cell activation antigens, such as HLA DR and CD11c. Simultaneously, a significant increase in both NK cells (CD3-/CD56+) and the cytotoxic T cells coexpressing the CD3 and the CD56 molecules together with an increased NK cytotoxic activity were observed. By contrast, the CD19+/CD5+ B-cell subset was significantly decreased. No significant changes were observed with EtOH withdrawal except in CD5+ B lymphocytes, which returned to normal values. Our results show that, in AH patients, a significant expansion of both activated T cells and NK lymphocytes occurs in the PB, which is associated with an increased NK cytotoxic activity. Interestingly these abnormalities persist during the withdrawal period.
Adult↗
Alterations in tumor necrosis factor-alpha, interferon-gamma, and interleukin-6 production by natural killer cell-enriched peripheral blood mononuclear cells in chronic alcoholism: relationship with liver disease and ethanol intake.
No previous studies have been reported on human alcoholism in which the pattern of cytokine secretion by natural killer (NK) cells is explored. The goal of the present study was to evaluate the role of NK cells in the production of cytokines in patients with chronic alcoholism, analyzing at the same time the possible relationship between cytokine production and both alcoholic liver disease and ethanol (EtOH) intake. A total of 30 chronic alcoholic patients-11 without liver disease [alcoholics without liver disease (AWLD) group] and 19 diagnosed of alcoholic liver cirrhosis-were included in this study. Twenty-five age- and sex-matched healthy volunteers were analyzed as controls. Production of interferon (IFN)-gamma, tumor necrosis factor-alpha (TNF-alpha), and interleukin (IL)-6 was performed on NK-enriched peripheral blood mononuclear cells (PBMC) after stimulation with IL-2 and IFN-alpha. In AWLD patients, the production of TNF-alpha was significantly reduced, compared with normal controls, under both IFN-alpha (p < 0.01) and IL-2 (p < 0.05) stimulation. In patients with cirrhosis, TNF-alpha production by PBMC enriched in NK cells varied depending on the EtOH intake status at the moment of evaluation. Accordingly, an increased concentration of this cytokine was detected in the supernatants of cirrhotic patients and active EtOH intake, particularly after IFN-alpha stimulation (p < 0.05); whereas, in patients with at least 1 year of alcohol withdrawal, TNF-alpha levels remained within normal range. The results on the production of IL-6 and IFN-gamma in AWLD and cirrhotic patients showed that only cirrhotic patients with a prolonged EtOH withdrawal period display abnormal production. Accordingly, in this group of patients, a significantly increased release of IL-6 was observed after both IFN-alpha and IL-2 stimulation (p < 0.01 and p < 0.05, respectively). By contrast, a lower IFN-gamma production (p < 0.005) was detected with respect to the control group. Our results point to the existence of an abnormal cytokine secretion by NK cells from chronic alcoholism patients, which depend on both the existence of liver disease and the status of EtOH intake.
Adult↗
Long lasting immunological effects of ethanol after withdrawal.
The aim of the present study was to analyze on chronic alcoholic patients the effect of ethanol (EtOH) withdrawal on the immune system through the investigation of the distribution of PB lymphoid subsets, using multiple-stainings with monoclonal antibodies and flow cytometry. For this purpose a group of 20 patients with active alcoholism without liver disease, negative for hepatitis virus, and without malnutrition was analyzed and followed for 9 months after alcohol consumption had been discontinued. Twenty-five age- and sex-matched healthy volunteers were included in the study. The following panel of monoclonal antibodies combinations (FITC/PE/PerCP or PE-Cy5) was used: TCR alpha beta/CD3/HLA DR, CD25/CD56/CD3, TCR gamma delta/CD3/HLA DR, CD45RA/CD45R0/CD4, CD3/CD8, CD19/CD5, and CD3/CD11c. Analysis was performed on at least 1,500 events/tube at flow cytometry using the Lysys II software program. During the alcohol intake period, the most striking findings were a significant (P < 0.05) expansion of the CD8+ T-lymphocyte subset, which coexpresses the activation associated antigens HLA DR and CD11c, as well as a significant increase in both NK-cells (CD3-/CD56+) and the T-cell subset with NK activity coexpressing CD3 and CD56 (P < 0.05 and P < 0.01, respectively). In addition, a decrease in the CD5+ B-cells (P < 0.05), associated with reduced serum gamma-globulin levels, was also observed. During alcohol withdrawal, a rapid decrease towards normal values of activated CD8+/HLA DR+ and CD11c+ T-lymphocytes was observed as well as a normalization of CD19+/CD5+ B-cells and gamma-globulin serum levels; these changes might be directly related to EtOH suppression. Surprisingly, however, new immunological imbalances emerged in spite of the absence of alcohol intake. Thus, a progressive and significant expansion (P < 0.05) of CD4+ T-cells associated with an increased expression of the CD25 activation-related antigen and a preferential use of the CD45R0 isoform by CD4+ T-cells were observed. In parallel, there was an even more evident increase (P < 0.01) in the number of PB NK-cells. Our results show that EtOH consumption induces changes in the immune system, its effects persisting or even becoming more evident after suppression of EtOH intake for a 9 month period.
Alcoholism↗
Distribution of peripheral blood lymphoid subsets in alcoholic liver cirrhosis: influence of ethanol intake.
The aim of the present study was to investigate the effect of chronic ethanol (EtOH) consumption on the immune system in patients with alcoholic liver cirrhosis (ALC), as analyzed by the distribution of peripheral blood (PB-) T, B, and NK lymphoid subsets using multiple stainings with monoclonal antibodies and flow cytometry. For that purpose, we have analyzed a group of patients with ALC and active EtOH intake (ALCET group) which were re-evaluated 3 months after alcohol withdrawal. As controls, both ALC patients with at least 1 year of alcohol withdrawal (ALCAW group) and healthy subjects were used. Regarding the alcohol intake period, the most relevant findings were a significant activation of the PB T-cell compartment, and specifically of the TCR alpha beta + subset, as reflected by an increased expression of both the HLA DR and CD11c antigens as well as a significant increase of both the PB NK cells (CD3-/CD56+) and the cytotoxic T cells coexpressing the CD3 and CD56 molecules. In addition, a decrease of both the numbers of total B cells and their CD5+/CD19+ subset were observed. After a relatively short withdrawal period (3 months), the abnormalities of T, P, and NK cells disappeared. These findings suggest the existence of a close relationship between EtOH consumption and the abnormalities of the immune system observed during active alcoholism. Nevertheless, ALCAW individuals displayed marked alterations on the immunophenotypic profile, as reflected by a significantly decreased number of total T cells, due to reduced levels of the CD3+/TCR alpha beta+, CD4+, CD8+, and CD4+/CD45RA+ T-cell subsets. In addition, a significantly decreased number of total PB B cells was observed in this group of patients. Our results show that in patients suffering from ALC, the abnormalities of the immune system due to a direct effect of EtOH intake (or its metabolites) should be distinguished from the immunological alterations related to the liver disease itself.
Alcohol Drinking↗
Hypokalemia in opiate overdose.
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Drug Overdose↗
Esophageal brucellosis: a new location of Brucella infection.
The case of a patient with acute brucellosis presenting as lower dysphagia from a paracardial esophageal mass is described. Brucella melitensis biotype 3 was isolated from cultured esophageal biopsy material. This is the first case of esophageal brucellosis described in the literature.
Adolescent↗
[Sudden death, exercise, and blood potassium].
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Death, Sudden↗
"Open eyes" during examination of the motor system.
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Adaptation, Physiological↗
[Adrenergic regulation of potassium homeostasis].
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Adrenergic beta-Agonists↗
Hormonal regulation of potassium shifts during graded exhausting exercise.
Serum potassium, aldosterone and insulin, and plasma adrenaline, noradrenaline and cyclic adenosine 3':5'-monophosphate (cAMP) concentrations were measured during graded exhausting exercise and during the following 30 min recovery period in six untrained young men. During exercise there was an increase in concentration of serum potassium (4.74 mmol.l-1, SEM 0.12 at the end of exercise vs 3.80 mmol.l-1, SEM 0.05 basal, P less than 0.001), plasma adrenaline (2.14 nmol.l-1, SEM 0.05 at the end of exercise vs 0.30 nmol.l-1, SEM 0.02 basal, P less than 0.001), plasma noradrenaline (1.10 nmol.l-1, SEM 0.64 at the end of exercise vs 1.50 nmol.l-1, SEM 0.05 basal, P less than 0.001), serum aldosterone (0.92 nmol.l-1, SEM 0.14 at the end of exercise vs 0.36 nmol.l-1, SEM 0.05 basal, P less than 0.01), and plasma cAMP (35.4 nmol.l-1, SEM 2.3 at the end of exercise vs 21.4 nmol.l-1, SEM 4.5 basal, P less than 0.05). While concentrations of serum potassium, plasma adrenaline and cAMP returned to their basal levels immediately after exercise, those of plasma noradrenaline and serum aldosterone remained elevated 30 min later (1.90 nmol.l-1, SEM 0.01, P less than 0.01; and 0.85 nmol.l-1, SEM 0.12, P less than 0.01, respectively). Serum insulin concentration did not change during exercise (6.47 mlU.l-1, SEM 0.58 at the end of exercise vs 5.47 mlU.l-1, SEM 0.41 basal, NS) but increased significantly (P less than 0.02) at the end of the recovery period (7.12 mlU.l-1, SEM 0.65).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Amplitude of the distribution of erythrocyte size in the differential diagnosis of microcytic anemia].
A prospective study was carried out in 83 patients with microcytic anemia. 43 had iron deficiency anemia, 28 had heterozygous beta thalassemia not associated with iron deficiency (beta-THNID) and 12 had both conditions. The behavior of red blood cell volume distribution width (RDW) was evaluated in all patients. RDW was higher in patients with iron deficiency (20.62 +/- 4.64) and beta-THNID (15.76 +/- 1.41) than in controls (13.29 +/- 0.92) (p less than 0.0001 for both comparisons). There also were statistically significant differences (p less than 0.0001) between both patient groups. In patients with both heterozygous beta thalassemia and iron deficiency (beta-THID), RDW reached similar values to those from patients with only iron deficiency anemia. A significant negative correlation was also found between the transferrin saturation index and RDW (r = -0.614, p less than 0.02). In 34 patients controlled during iron replacement therapy a significant increase of RDW was found after one month of treatment, while hemoglobin concentration and mean corpuscular volume became normal. When 18 was taken as cutoff value for RDW, its positive predictive value was very high in iron deficiency (95%), while it was only 59% in beta-THNID. England's index may help to differentiate between isolated iron deficiency anemia and beta-THID: in patients with RDW higher than 18, the positive predictive value of England's index was 89% for iron deficiency and 57% for beta-THID.(ABSTRACT TRUNCATED AT 250 WORDS)
Anemia, Hypochromic↗
Inter-relationship between serum potassium and plasma catecholamines and 3':5' cyclic monophosphate in alcohol withdrawal.
Serial analyses of serum potassium and plasma epinephrine, norepinephrine and adenosine 3':5'-cyclic monophosphate (cyclic AMP) concentrations were measured in 13 patients with alcohol withdrawal, six of whom presented delirium tremens. Patients with delirium showed at admission levels of potassium (3.45 +/- 0.45 mmol/l) lower (P less than 0.02) than patients without delirium (3.81 +/- 0.14 mmol/l). Three patients were hypokalemic, all of them with delirium. Serum potassium increased significantly in all the patients during evolution. A close negative correlation (r = -0.751) between the intensity of withdrawal and serum potassium was observed. Plasma epinephrine concentrations were increased at admission (623 +/- 192 pmol/l), patients with delirium showing greater values (705 +/- 137 pmol/l). As the alcohol withdrawal improved, plasma epinephrine concentration decreased. Plasma norepinephrine concentrations were also increased at admission (3422 +/- 1451 pmol/l), but did not change significantly during evolution, being similar in patients with and without delirium. Plasma cyclic AMP levels were high at admission (40.4 +/- 24.3 nmol/l) and increased significantly (P less than 0.05) during evolution. The data obtained suggest that in patients with alcohol withdrawal, as symptomatology improves, plasma epinephrine decreases, while plasma norepinephrine remains increased. The combined actions of the two facts--less beta-stimulus, maintaining of alpha-stimulus--would comprise a significant increase of kalemia, that in cases of initial hypokalemia would lead to normal values of serum potassium.
Alcohol Withdrawal Delirium↗
[Gallbladder torsion: report of a case].
A case of an 81 year old woman who had fever, abdominal pain and a palpable mass in epigastrium and right hypochondriac region is presented. She was diagnosed as having acute cholecystitis and hydrops of the gallbladder. The surgical operation was performed and the findings were: dilated gallbladder with necrotic aspect, free floating with torsion of the cystic duct (greater than 180 degrees) wrapped in the mentum. There was no hepatic bed of the gallbladder. After correcting the torsion, the gallbladder was extirpated, with good clinical evolution. The etiopathogenia is discussed and the literature is reviewed. Despite the rareness of the gallbladder's torsion and the disease being relatively unknown, it has to be considered in the differential diagnosis of acute abdomen in the elderly.
Aged↗
Werner's syndrome and astrocytoma.
Werner's syndrome, a relatively rare and autosomal recessive disorder, is well known to be characterized by a high frequency of malignant neoplasms. Werner's syndrome has not infrequently been associated with meningiomas. We report a case of Werner's syndrome and temporal astrocytoma in a 49-year-old male. As far as we are aware, this is the first report of the association of Werner's syndrome and astrocytoma.
Astrocytoma↗