Serum beta 2 microglobulin in psoriasis and psoriatic patients.
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Biomedical subjects
Publications and source records attributed to S Storti.
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Methotrexate and Aracytin commonly employed in prophylaxis and treatment of leukaemic neuromeningosis, can induce neuromeningeal injury. Cerebrospinal fluid (CSF) protein disturbance may reflect the damage. In this study we have examined 141 CSF samples collected by lumbar puncture from 51 subjects: 15 normal controls and 36 leukaemic patients during the prophylaxis or the Central Nervous System (CNS) involvement treatment. In all the CSF samples, total proteins, IgG and IgA were examined. CSF total protein and albumin levels increased in the presence of leukaemic neuromeningosis and also after a prolonged CNS prophylaxis or therapy. The same behaviour was found in IgG levels. The IgA levels did not show any modification. We conclude that these parameters are not reliable indices of leukaemic CNS involvement.
The authors describe 2 cases of acute myeloid leukemia (AML) with ovarian granulocytic sarcoma (GS) and central nervous system (CNS) involvement. The patients had an unfavorable clinical course in a short period of time. It has been reported that GS or CNS involvement does not have a bad prognostic significance. We suggest that the association of these two complications worsens the prognosis of AML.
Cerebrospinal fluid (CSF) beta-2-microglobulin (B2m) has been proposed as a marker of central nervous system (CNS) involvement in myelo-lymphoproliferative diseases. Recently its reliability has been put in question because of false positive and false negative results. In our study, B2m was measured in 574 CSF samples collected from 74 patients affected by ALL, ANLL or lymphomas; 20 of these patients had CNS-involvement while they were under observation. There was a significant difference in CSF B2m between the patients with and without CNS-involvement (p less than 0.001). No false positive or false negative results were obtained. In 4 cases the rising of CSF B2m was observed 8, 6, 4 and 4 wk before the clinical and laboratory diagnosis of CNS-involvement. In all patients the clinical and laboratory improvement of the neurological disease was associated with a progressive decrease of CSF B2m. Some hypotheses about the origin of CSF B2m are discussed. The authors conclude that CSF B2m is a useful and reliable marker of CNS-involvement in myelo-lymphoproliferative disease.
The modifications of cell-mediated immunity in idiopathic thrombocytopenic purpura (ITP) were investigated using the technique of Moretta et al. [J. exp. Med. 151: 969-974, 1980] to study T lymphocyte subsets in 35 ITP subjects at various clinical stages. In all these patients, platelet-associated IgG (PAIgG) were measured by a complement lysis inhibition technique. Untreated ITP patients did not show significant modifications of T lymphocyte subsets. Patients with thrombocytopenia not responsive to corticoids or splenectomy and increased PAIgG levels showed significant reduction of Fc-gamma-bearing T lymphocytes (T-gamma). Patients 'cured' by splenectomy (12 out of 17) showed a normal PAIgG level, a marked increase of T-gamma cells and a reduction of T-mu cells; patients 'not cured' by splenectomy showed an increased PAIgG level and a reduction of T-gamma cells. An increase of PAIgG levels and a reduction of T-gamma cells were found in 2 splenectomized patients after relapse. An association between chronic nonresponsive ITP and decrease of T-gamma cells was established.
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The cerebrospinal fluid (CSF) and serum beta-2-microglobulin (B-2-m) level was determined in 15 patients affected by lymphoma with and without central nervous system (CNS) involvement and in 15 normal controls. No statistical difference in CNS B-2-m was found between patients affected by lymphoma without CNS involvement and normal subjects. CSF B-2-m was significantly increased (p less than 0.001) in patients with CNS involvement as compared to normal subjects or patients without CNS involvement. These findings suggest that CSF B-2-m can be used as a useful marker of CNS involvement in patients affected by lymphoma.
Plasma concentration of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured by radioimmunoassay in 45 patients with benign and malignant ovarian diseases. All patients with ovarian carcinoma showed increased beta-TG and PF4 levels. Among benign ovarian diseases the patients with serous cystadenoma more frequently showed signs of platelet activation, whereas those with endometriotic cyst and mucinous cystadenoma generally had normal beta-TG and PF4 values. These results indicate that an increased platelet activation is consistently associated with malignant tumors of the ovary, whereas benign tumors show a different capacity to induce platelet activation.
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In order to investigate the role of an immune mechanism in the pathogenesis of thrombocytopenia in hepatic patients, we measured platelet associated IgG (PAIgG) in 84 patients with various hepatic diseases. Increased PAIgG levels were found in 84% of patients with chronic active hepatitis (mean 21.32 +/- 8.45 fg/platelet) and in 75% of those with cirrhosis with hepatitis (mean 17.3 +/- 11.2 fg/platelet). In these patients there was no significant correlation between PAIgG and platelet count. Increased PAIgG amounts were also observed in some patients with inactive cirrhosis (18%). Normal PAIgG values were found in all patients with acute viral hepatitis and chronic persistent hepatitis. An immunologic mechanism may play a role in the pathogenesis of thrombocytopenia in hepatic patients. Furthermore, measurement of PAIgG may have a great usefulness in the differential diagnosis of chronic hepatic diseases.
BACKGROUND: It is known that patients with renal failure have normochromic normocytic anemia due to impaired endogenous erythropoietin (EPO) synthesis. The aim of this work was to determine whether low serum erythropoietin (s-EPO) levels play a role in the pathogenesis of anemia in patients with Type 1 diabetes without overt nephropathy. METHODS: We included in the study 13 patients with Type 1 diabetes whose Hb levels were <11 g/dl. Blood cell count, s-EPO, urinary albumin excretion rate (AER), HbA(1c), glomerular filtration rate, serum iron, serum ferritin, the presence of neuropathy, retinopathy and nephropathy were determined. RESULTS: Ten out of 13 patients with anemia (77%) had a blunted EPO response to anemia. All ten patients with low EPO levels had autonomic neuropathy; five had clinical nephropathy but with serum creatinine<1.6 mg/dl. Three patients were treated with rHuEPO and showed an improvement in their anemia after treatment. CONCLUSION: The majority of patients with Type 1 diabetes who had anemia also had low EPO levels. The pathogenesis of this phenomenon is probably multifactorial. Autonomic neuropathy appears to play a role, but it is not sufficient, per se, to be the only cause. Dysautonomia might enhance the effect of renal damage.
Serum lactate dehydrogenase (S-LDH) and its isoenzyme pattern were assayed in 63 non-Hodgkin's lymphoma (NHL) patients, 37 at diagnosis, 15 at relapse and 11 in complete remission (CR). S-LDH in NHL patients with active disease was higher than in normal subjects and CR patients (p less than 0.001). Among the isoenzymes, LDH-2 and LDH-5 showed no remarked differences; LDH-1 was reduced and LDH-3 and LDH-4 raised in comparison to the normal group (p less than 0.001). S-LDH levels and isoenzymes 1 and 4 were influenced by the stage, the histological subgroup and by the presence of general symptoms. In fact, cases in stage IV, with "high-grade malignancy" and with general symptoms, had higher S-LDH levels and more evident LDH-1 and LDH-4 changes than the other stages, the other histopathological subgroups and the cases classified as "A". S-LDH was the same as in normal subjects in the "low-grade" and "intermediate-grade" malignancies as was LDH-1 in stage II and LDH-4 in stages II and III, in "low-grade" malignancy and in the A cases. In contrast, LDH-3 was always high, with no significant difference in relation to the variables considered. Thus, in NHL, LDH-3 seems to be a reliable marker of the presence of the disease in any case, whereas S-LDH is more related to the spread of the lymphoma.
Eighteen acute nonlymphoblastic leukemia patients greater than 60 yr., 12 at diagnosis and 6 in first relapse, were treated with the association of oral Idarubicin and subcutaneous Aracytin. One patient was not evaluable. Eight out of 17 patients achieved complete remission (47%), 4 patients died in induction and 5 proved resistant to treatments. Mucocutaneous and gastrointestinal toxicity was mild. The most frequent extra-hematological complications were infections. We observed an important hepatic toxicity in 1 case.
The case of a patient with cystic fibrosis who developed an Hodgkin's lymphoma is reported. ABVD chemotherapy induced complete remission but caused a worsening of pulmonary function.
From December, 1985 to October, 1987, 16 patients aged from 14 to 62 (median 34) with acute leukemia in relapse (10 affected by ANLL and 6 by ALL) were treated with the following regimen: Idarubicin 12 mg/m2/day on days 1-2-3, Ara-C 600 mg/m2 twice a day from day 1 to 6. Twelve patients (75%) achieved complete remission (C.R.). Two (12%) died during the induction phase from alveolar pneumonitis. One patient was resistant. The median duration of C.R. and survival was respectively 12 (range 6 to 100 +) and 23 weeks (4 to 108 +). The median duration of granulocytopenia was 16 days (range 10 to 24 days). The most frequent non-hematological complications consisted of nausea, vomiting, diarrhea and mucositis. Four patients had hepatic and splenic microabscesses of suspected mycotic etiology, and one showed a transient cardiac arrhythmia. The C.R. rate obtained in this series may be considered satisfaying since all but 3 patients were on treatment at the time of relapse. Yet the short duration of C.R. suggests the opportunity of performing consolidation cycles or suprelethal therapy followed by bone marrow transplantation.
Thirty-five patients affected by Progressive System Sclerosis (PSS) (20 acrosclerosis and 15 diffuse sclerosis) were subjected to the following laboratory tests: Beta 2 microglobulin (B2m), Fibronectin, C3c, C4, Fibrinogen, Factor VIII Coagulant (F. VIII:C), Factor VIII related Antigen (F. VIII:Ag), IgG, ESR, Antithrombin III (AT III), alpha 1 Antitrypsin (alpha 1AT) and alpha 2 Macroglobulin (alpha 2M). The results showed that no difference was observed between the normal group and the groups of PSS patients with respect to alpha 1AT, alpha 2M, and AT III. In contrast the B2m, ESR, IgG, F. VIII:Ag results were significantly higher in the PSS patients, while Fibrinogen and C3c results were slightly higher, but no high enough to be of statistical significance. The two PSS patient subgroups did not produce significant results, only the C4 values were lower in the Diffuse Sclerosis subgroup. From these results it seem that the tests used are not very useful indifferentiating the two subgroups of the PSS patients.
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