Lipid transfer protein syndrome: clinical pattern, cofactor effect and profile of molecular sensitization to plant-foods and pollens.

BACKGROUND: Multiple plant-food sensitizations with a complex pattern of clinical manifestations are a common feature of lipid transfer protein (LTP)-allergic patients. Component-resolved diagnosis permits the diagnosis of the allergen sensitization profile. OBJECTIVE: We sought to clinically characterize and describe the plant-food and pollen molecular sensitization profile in patients with LTP syndrome. METHODS: Forty-five subjects were recruited, after being diagnosed with multiple plant-food allergies sensitized to LTP, but not to any other plant-food allergen, according to the molecular allergen panel tested (Pru p 3 (LTP), Pru p 1 (Bet v 1-like), Pru p 4 (profilin) and those included in a commercial microarray of 103 allergenic components). IgE-mediated food-allergy symptoms and pollinosis were collected. Patients were skin prick tested with a plant-food and pollens panel, and specific IgE to Tri a 14 was evaluated. RESULTS: A heterogeneous group of plant-foods was involved in local and systemic symptoms: oral allergy syndrome (75.6%), urticaria (66.7%), gastrointestinal disorders (55.6%) and anaphylaxis (75.6%), 32.4% of which were cofactor dependent (Non-Steroidal Anti-inflammatory Drugs, exercise). All tested subjects were positive to peach and Pru p 3, Tri a 14 and to some of the LTPs included in the microarray. Pollinosis was diagnosed in 75.6% of subjects, with a broad spectrum of pollen and pollen-allergen sensitization. Plane tree and mugwort were the statistically significant pollens associated with Pru p 3. CONCLUSIONS AND CLINICAL RELEVANCE: Several plant-foods, taxonomically unrelated, independent of peach involvement, are implicated in LTP syndrome. Local symptoms should be evaluated as a risk marker for anaphylaxis because they are frequently associated with cofactor-dependent anaphylaxis. The association of these symptoms with pollinosis, especially plane tree pollinosis, could be part of this syndrome in our area.

Current Situation and Prognostic Evolution of Combined Heart-lung Transplantation in a European Union Country.

Background: This study aims to evaluate the entire experience in heart-lung transplantation (HLTx) in a country of the European Union with 47 million inhabitants according to the etiologies that motivated the procedure. Methods: A retrospective study on 1,751 consecutive transplants (HLTx: 78) was performed from 1990 to 2020 in two centers. Overall survival, adjusted for clinical profile and etiological subgroups, was compared. 7 subgroups were considered: 1) Cardiomyopathy with pulmonary hypertension (CM + PH). 2) Eisenmenger syndrome. 3) Congenital heart disease (CHD). 4) Idiopathic pulmonary arterial hypertension (IPAH). 5) Cystic fibrosis. 6) Chronic obstructive pulmonary disease (COPD)/Emphysema. 7) Diffuse interstitial lung disease (ILD). Results: Early mortality was 44% and that of the rest of the follow-up was 31%. There were differences between HTLx and HTx in survival, also comparing groups with a similar clinical profile with propensity score (p= 0.04). Median survival was low in CM + PH (18 days), ILD (29 days) and CHD (114 days), intermediate in Eisenmenger syndrome (600 days), and longer in IPAH, COPD/Emphysema and cystic fibrosis. Conclusion: HLTx has a high mortality. The etiological analysis is of the utmost interest to make the most of the organs and improve survival.

CD50 (intercellular adhesion molecule 3) stimulation induces calcium mobilization and tyrosine phosphorylation through p59fyn and p56lck in Jurkat T cell line.

The leukocyte differentiation antigen, CD50, has been recently identified as the intercellular adhesion molecule 3 (ICAM-3), the third counter-receptor of leukocyte function-associated antigen 1 (LFA-1). This molecule seems to be specially involved in the adhesion events of the initial phases of the immune response. To characterize the role of CD50 in leukocyte interactions, the different molecular events induced after cross-linking of CD50 on T cell-derived Jurkat cell line have been analyzed. When cells were incubated with anti-CD50 mAbs and cross-linked with polyclonal goat anti-mouse immunoglobulins, a rise in intracellular calcium concentration ([Ca2+]i) was observed. This increase in [Ca2+]i was mainly due to the uptake of extracellular Ca2+. This Ca2+ flux involved tyrosine phosphorylations and was further increased by CD3 costimulation. These data, together with those obtained by phosphotyrosine (P-Tyr) immunoprecipitation and in vitro kinase assays, suggested the involvement of protein-tyrosine kinases (PTK) in CD50 transduction pathways. By using specific antisera, the presence of p56lck and p59fyn protein tyrosine kinases (PTK) was clearly demonstrated in the CD50 immunoprecipitates. These findings suggest that the interaction of CD50 with its natural ligand (LFA-1) may result in T lymphocyte activation events, in which CD50 could play a very active role after antigen triggering.

Prognostic value of tyrosinase reverse transcriptase PCR analysis in melanoma sentinel lymph nodes: long-term follow-up analysis.

OBJECTIVE: To determine the prognostic value of detecting tyrosinase transcripts in melanoma sentinel lymph nodes (SLNs). METHODS: Reverse transcription (RT) PCR for tyrosinase mRNA was performed on negative SLNs of 76 patients with melanoma. RESULTS: Tyrosinase mRNA was found in 39 patients (51.3%). After a median follow-up period of 51 months, significant differences were found in overall survival (OS) but not in disease-free survival (DFS). The 5-year OS and DFS rates were 97.2% and 80%, respectively, for RT-PCR tyrosinase-negative (TN) patients vs. 78.67% and 66.24% for RT-PCR tyrosinase-positive (TP) patients (P = 0.019 and P = 0.38, respectively). Of four progressing patients in the TN group, three relapsed with subcutaneous, soft-tissue or lymph-node metastases, while seven out of nine progressing patients in the TP group relapsed at visceral sites. CONCLUSIONS: No significant differences in DFS were found by RT-PCR tyrosinase expression analysis at melanoma SLNs. Significant differences in OS could be related to a different pattern of relapse and must be confirmed after a longer follow-up time.

Expression of somatostatin receptors in human melanoma cell lines: effect of two different somatostatin analogues, octreotide and SOM230, on cell proliferation.

Somatostatin analogues (SAs) are potential anticancer agents. This study was designed to investigate the expression of somatostatin receptors (SSTRs) in melanoma cells and the effect of two SAs on cell proliferation and viability. Eighteen primary and metastatic human cutaneous melanoma cell lines were treated with octreotide and SOM230. Expression of SSTR1, SSTR2, SSTR3 and SSTR5 was assessed by real-time polymerase chain reaction. Proliferation, viability and cell death were assessed using standard assays. Inhibition was modelled by mixed-effect regression. Melanoma cells expressed one or more SSTR. Both SAs inhibited proliferation of most melanoma cell lines, but inhibition was < 50%. Neither SA affected cell viability or induced cell death. The results suggest that melanoma cell lines express SSTRs. The SAs investigated, under the conditions used in this study, did not, however, significantly inhibit melanoma growth or induce cell death. Novel SAs, combination therapy with SAs and their anti-angiogenic properties should be further investigated.

Molecular Alterations of Nucleocytoplasmic Transport in Patients on the Heart Transplantation Waiting List and Its Correlation With the Severity and Etiology of Heart Failure.

OBJECTIVES: To evaluate whether the levels of some molecules implicated in nucleocytoplasmic transport in human cardiomyocytes are related to the severity of heart failure (HF) in patients on the heart transplantation (HT) waiting list, and to determine whether there is a differential pattern of molecular alteration between ischemic cardiomyopathy (ICM) and non-ischemic dilated cardiomyopathy (DCM). METHODS: Sixty-three blood samples collected before HT were analyzed to identify the levels of IMPORTIN5 (IMP5); IMPORTINalpha2; ATPaseCaTransp (ATPCa); NUCLEOPORIN153kDa (Nup153); NUCLEOPORIN160kDa (Nup160); RANGTPaseAP1 (RanGAP1) and EXPORTIN4 (EXP4). These data were then compared between patients with advanced HF with or without the need for ventricular support with extracorporeal membrane oxygenation (ECMO) as a bridge for HT, as well as between patients with non-ischemic DCM and patients with ICM. RESULTS: Thirty-three patients had ICM, 26 had non-ischemic DCM, and 4 had heart disease. Seventeen patients required ventricular assistance as a bridge to HT. The levels of ATPCa, RanGAP1, and IMP5 were significantly higher in patients with ECMO, while EXP4 was significantly higher in patients without ECMO. Patients with DCM showed higher levels of IMP5, RanGAP1, and Nup153 than those with ICM. CONCLUSION: Patients with advanced HF in critical condition (with ECMO as a bridge for HT) presented with significantly higher levels of ATPCa, RanGAP1, and IMP5, while patients with DCM had significantly higher levels of RanGAP1, IMP5, and Nup153. It remains to be clarified whether the determination of these molecules would facilitate the early identification of this group or if their alteration occurs as consequence of circulatory support with ECMO.

Idarucizumab in High-risk Thoracic Surgery.

Direct oral anticoagulants have suggested a favorable profile compared with vitamin K antagonists. However, the lack of treatment to reverse the effect of direct oral anticoagulants has limited its use in some patients who require rapid reversal of anticoagulation, as those included in the transplant waiting list. Idarucizumab is a recently approved drug to reverse the anticoagulant effect of dabigatran. However, the clinical experience when using this drug is scarce. Herein, we present a clinical case on anticoagulation reversal with idarucizumab to perform heart and lung transplantation in a patient with Eisenmenger syndrome.

Melanoma inhibiting activity protein (MIA), beta-2 microglobulin and lactate dehydrogenase (LDH) in metastatic melanoma.

BACKGROUND: Serum levels of melanoma markers may have a role in monitoring disease evolution in metastatic melanoma. PATIENTS AND METHODS: Serial measurements of melanoma inhibiting activity protein (MIA), lactate dehydrogenase (LDH), S-100 and beta2-microglubulin were obtained from 42 metastatic melanoma patients during their biochemotherapy treatment. RESULTS: High pre-treatment serum levels of S-100, LDH, MIA and P2-microglobulin were detected in 50%, 57%, 50% and 24% of the patients, respectively. Only S-100 had prognostic significance for both disease-free (p=0.011) and overall survival (p=0.021). In patients who responded to treatment, S-100 levels decreased significantly from pre-treatment to the time of response (p = 0.050). When patients progressed, levels of MIA and P2-microglobulin increased significantly (p =0.028 and p =0.030, respectively). CONCLUSION: Correlation with disease evolution was found for S-100, MIA and P2-microglobulin levels. Despite the small sample size of the study, S-100 was a significant prognostic marker for overall survival and disease-free survival.

Incidence of radiation-induced leukoencephalopathy after whole brain radiotherapy in patients with brain metastases.

INTRODUCTION: Whole brain radiation therapy (WBRT) remains a recommended treatment for patients with brain metastases in terms of symptom palliation, especially when extracranial systemic disease is present. The aim of the study was to determine the clinical correlation between pre-existing leukoaraiosis and posterior leukoencephalopathy secondary to WBRT. METHODS AND MATERIALS: We retrospectively reviewed the results of WBRT treatment in 44 patients with melanoma brain metastases. The neuroimaging abnormalities of the white matter (T2-weighted MRI) were graded over time. RESULTS: From the 37 evaluable patients the mean age was 53 years old, 23 male and 14 female. Vascular risk factors were present in 22 patients (59.5%). The WBRT total dose was 20 Gy/5fr (n=21) and 30 Gy/10fr (n=16). Leukoaraiosis pre-WBRT was observed in 9/37 patients (24.3%) and leukoencephalopathy post-WBRT in 2/37 (5.4%). Univariate analysis of prognostic factors (sex, age and vascular risk factors) for leukoaraiosis was conducted observing statistically significant differences for patients with age>or=65 years old (p=0.003). Nineteen patients survived more than 3 months. Twelve patients (63.2%) suffered from vascular risk factors. Univariate analysis demonstrated previous leukoaraiosis as a prognostic factor for developing further leukoencephalopathy after WBRT (p=0.015). CONCLUSIONS: Radiation-induced leukoencephalopathy is greater in patients with pre-existing leukoaraiosis. Because of the potential of long-term survival in a small subset of patients with brain metastases and the risk of radiation-induced dementia, neurotoxicity reduction in patients with leukoaraiosis is an important goal of treatment.

Incidence of development of obesity after heart transplantation according to the calcineurin inhibitor.

BACKGROUND: Development of obesity after heart transplantation (HT) is a common complication, largely attributed to immunosuppressive therapy. The objective of this study is to compare the incidence of development of obesity after HT, according to the calcineurin inhibitor (CNI) used (cyclosporine [CsA] vs tacrolimus [Tac]). METHODS: We studied 101 consecutive HT patients from November 2006 to December 2010. A diagnosis of overweight-obesity was made by a body mass index of ≥25 kg/m(2), which was assessed before HT and at 1 year after HT. Patients were randomly assigned to the administration of CsA or Tac by a simple randomization method using a computer program (56% received CsA and 44% Tac). RESULTS: Of the 101 patients, 77% were men, and ischemic heart disease was the most common indication for HT. At baseline, there were no differences in weight between groups treated with CsA or Tac. The mean weight for each group was 71.5 ± 12 and 75 ± 14 kg, respectively (P = .2). The weight increase was greater among CsA patients: after HT, the weight gain was 6.9 ± 11 kg in the CsA group, whereas a minimal weight loss of 0.03 ± 14 kg (P = .008) was experienced in the group treated with Tac. The multivariate analysis showed that only CsA treatment was an independent predictor of development of obesity 1 year after HT (odds ratio, 3.84; 95% CI, 1.04-14.21; P = .01). CONCLUSION: Weight gain after HT may be related to the CNI used and CsA seems to be the CNI that produces the greatest increase.

Osteoblasts in HIV-infected patients: HIV-1 infection and cell function.

BACKGROUND: HIV-infected patients have been shown to have a severe alteration in osteoblast function that appears to be related to the infection. OBJECTIVE: To determine whether normal human osteoblasts express CD4, whether osteoblasts from patients with HIV infection are infected by HIV-1 and whether osteoblast dysfunction observed in vivo also occurs in vitro. METHODS: Osteoblast cultures from bone marrow biopsies of HIV-infected patients (n = 14) and control patients (n = 10) were used in a cross-sectional study and a case-control prospective study. Expression of CD4 was analysed using flow cytometry and reverse transcriptase polymerase chain reaction; the presence of HIV-1 particles was determined by measuring p24 antigen in the supernatants of osteoblast cultures and viral DNA or RNA in the osteoblasts using the polymerase chain reaction. Osteoblast function was assessed by measuring cell proliferation, type I collagen and osteocalcin synthesis. RESULTS: In human osteoblasts, CD4 expression could not be determined using flow cytometry, although low levels of mRNA coding for CD4 were detected. HIV infection was not observed in osteoblast cultures from HIV-infected patients nor was there any alteration in replication and synthesis of type I collagen, although osteocalcin synthesis was increased. CONCLUSIONS: It is unlikely that HIV-1 infects human osteoblasts in vivo; therefore, the hypothesis that these cells could act as local HIV-1 reservoirs should be reconsidered.

Monoclonal antibodies against the human lymphocyte differentiation antigen CD 76 bind to gangliosides.

Two monoclonal antibodies, HD 66 and CRIS-4, by which the new CD 76 B-cell-associated cluster was defined, bound to several gangliosides (sialic acid containing glycolipids) of different polarity. One of the gangliosides recognized by HD 66 could be identified as NeuAc alpha 2-6Gal beta 1-4GlcNAc beta 1-3Gal beta 1-4Glc-beta 1-1'Cer. This antigen was enzymatically synthesized. Sialidase treatment of the ganglioside antigens abolished binding of HD 66 and CRIS-4.

An antiplatelet monoclonal antibody that inhibits ADP and epinephrine-induced aggregation.

A monoclonal antibody (Mab) named EDU-3, was produced by fusing splenocytes from one Balb/c mouse, immunized with a mixture of platelets and non-T cells from heparinized human peripheral blood, with the HAT-sensitive myeloma line P3-NS1/1.Ag4.1. By indirect immunofluorescence (IF) it was seen that this Mab reacted with all normal human platelets and bone marrow megakaryocytes, but did not react with lymphoid cells from normal donors, or platelets from Glanzmann's thrombasthenia (GT) patients. Immunoprecipitation and SDS-PAGE experiments demonstrated that this Mab recognized an epitope on the IIb-IIIa glycoprotein complex (GPC). EDU-3 inhibited platelet aggregation and release of ATP induced by ADP and epinephrine. Aggregation induced by arachidonic acid, ristocetin and bovine factor VIII were not inhibited by EDU-3. The difference between EDU-3 and other Mab directed against the IIb-IIIa GPC is discussed.

Monoclonal antibody against HLA-Aw32 + A25. Is HLA-Aw32 an allele with no unique antigenic determinant?

In the present paper we describe the production and characterization of a monoclonal antibody (Mab) recognizing HLA-Aw32 + A25 antigens. NS1 murine myeloma cells were fused with splenocytes from a BALB/c mouse immunized with normal human peripheral blood (PB) lymphocytes of phenotype A1, Aw32; B7,B37,Cw-,Cw-;DR2,DRw10. Supernatants were first screened against Cr51-labeled immunizing cells by complement dependent cytotoxicity 51Cr-CDC). Cultures identified as producing cytotoxic antibodies were subcultured and the supernatants tested against a selected panel of HLA typed cells by the NIH microcytotoxicity method. One culture producing antibody reacting with an HLA polymorphism was detected. This hybrid, designated CATA 1, was cloned twice by limiting dilution and obtained in ascitic form. Specificity of CATA 1 Mab was evaluated against a panel of 120 PB T cells from normal donors. CATA 1 reacted with cells bearing HLA-A25 or HLA-Aw32 antigens. In addition, a reaction was observed with a cell of phenotype A2,Aw31; B17,Bw49. Isoelectric focusing revealed the monoclonal nature of CATA 1, with immunofixation identifying it as an IgG molecule. Absorption studies have demonstrated that CATA 1 recognizes a common determinant on HLA-A25 and HLA-Aw32. The finding that this Mab recognizes the same CREG as alloantisera against HLA-Aw32 suggests that this antigen has no unique epitopes.

Immunophenotype of blast cells in acute myelofibrosis.

The immunophenotype of peripheral blood blast cells from six patients with acute myelofibrosis was studied using a panel of monoclonal antibodies directed against granulocytic, erythroid, megakaryocytic and lymphoid antigenic determinants. In all patients most of the blast cells were labeled with anti-HLA-DR and with the early myelomonocytic antibodies My7 (CD13), My9 (CD33) and B1-3C5 (CD34) (3/3). In three cases, platelet antibodies Edu3 (CD41) and GPIIIa (CD61) reacted with about 30% of blast cells. TdT was positive in two out of six samples studied. Lymphoid markers T3 (CD3), Leu9 (CD7), J5 (CD10), B4 (CD19) and B1 (CD20) were negative in all cases. These results suggest that blast cells are mainly of immature myelocytic origin. However, the coexistence of megakaryoblasts cannot be ruled out in the cases with a proportion of cells that are positive with Edu3 and GPIIIa antibodies.

Specific immune response to Parietaria judaica plant profilin: a low T cell proliferative response supports high IgE and skin prick test.

BACKGROUND: allergic disease caused by Parietaria judaica (Pj) has been widely documented in Mediterranean area. Profilins have been identified as widely distributed allergenic proteins. The role of Pj profilin in specific immune response in Pj-sensitized patients is unknown. METHODS: skin prick test and determination of specific and total IgE levels in serum were performed in all patients (n = 28) and non-allergic controls (n = 18). Peripheral blood mononuclear cells (PBMC) were isolated from both groups and stimulated with crude extract or highly purified Pj profilin. The production of type I and type II cytokines was determined by specific and polyclonal stimuli in patients and controls. T-cell lines specific to Pj profilin were established and cross-reactivity with another highly purified profilin from Phleum pratense (Phl p) was evaluated. RESULTS: Pj profilin-sensitized patients showed a small but significantly increased in T-cell proliferative response to this profilin compared with non-atopic controls. The production of interleukin (IL)-4 and interferon (IFN)-γ in response to the specific stimulus was undetectable. However, the production of IL-4 in response to a polyclonal stimulus [phytohemagglutinin (PHA)] was significantly higher in atopic patients than in controls. The T-cell response did not correlate with the magnitude of response to skin prick tests with Pj profilin or with Pj-specific serum IgE levels. In addition, the production of IL-4 in response to a polyclonal stimulus (PHA) did not correlate with the individual skin prick tests to Pj profilin or with Pj-specific IgE levels in serum. The T-cell lines tested showed no cross-reactivity with Phl p profilin. CONCLUSIONS: our results suggest that Pj profilin is partly responsible for the T-cell-mediated response in patients allergic to Pj. The high skin reactivity to Pj profilin is these patients was accompanied by a small increase in the T-cell response to this profilin. The response was highly specific since Pj profilin specific T-cell lines showed no cross-reactivity with a highly homologous profilin from Phl p. The lack of correlation between the proliferative T-cell response and polyclonal IL-4 production with allergen-specific serum IgE and skin reactivity probably indicates that some of the responding T-cells may be involved in immune reactions other than those supporting IgE production.

[Diagnosis of paroxysmal nocturnal hemoglobinuria with cytofluorometric of molecules bound to the membrane by glycosylphosphatidylinositol groups]. / Diagnóstico de la hemoglobinuria paroxística nocturna mediante el análisis citofluorimétrico de moléculas unidas a la membrana por grupos glucosilfosfatidilinositol.

BACKGROUND: Paroxysmal nocturnal hemoglobinuria (NPH) is a clonal disease in which a deficit in the expression of molecules bound to the cell membrane by glycosyl-phosphatidylinositol (MUGFI) groups has been demonstrated. The MUGFI are widely distributed and among them proteins regulating the action of complement may be found. The development of monoclonal antibodies (MoAb) against MUGFI may allow the introduction of a new diagnostic method in this disease and increase the sensitivity, particularly in transfused individuals. METHODS: The erythrocytic and leukocytic phenotype of 14 patients with NPH clonality demonstrated by the classic tests of sensitivity to the complement was analyzed by immunofluorescence techniques and flow cytometry with the use of MoAb which recognize MUGFI (CD55, CD59, CD14, CD16 and CD24). RESULTS: Cells with a decrease or absence of MUGFI were observed in all the patients. The defect was demonstrated in the red cells, monocytes and neutrophils of all the patients, while it was only observed in the lymphocytes of three patients. The percentage of cells with a decrease in MUGFI was variable (2-100%) as well the pattern of deficiency against the different MoAb used. The MoAb with greatest sensitivity for the detection of clonal population were the CD59 in erythrocytes, the CD14 in monocytes and the CD24 in neutrophils. The CD16 was normal in one patient and the CD55 in two. The transfusion of packed red cells did not influence the abnormal leukocyte pattern, with abnormalities even being observed in the erythrocytary CD59. The Ham test was negative in those cases in which the percentage of negative CD59 erythrocytes was lower than 5% of the total erythrocytic population. CONCLUSIONS: The study of glucosylphosphatidylinositol by flow cytometry and monoclonal antibodies is a useful technique for the detection and quantification of the nocturnal paroxistic hemoglobinuria clone even in transfused patients.

[CD4+ lymphocytes and opportunistic infections and neoplasms in patients with human immunodeficiency virus infection]. / Linfocitos CD4+ e infecciones oportunistas y neoplasias en pacientes con infección por el virus de la inmunodeficiencia humana.

BACKGROUND: The CD4+ lymphocytes are the principal target cell for the human immunodeficiency virus (HIV). Their depletion originates a very severe cell immunosuppression, which conditions the appearance of opportunistic infections and neoplasms characteristic of AIDS. The aim of this study was to evaluate whether there is a relation between the degree of cell immunosuppression and the type of opportunistic infections and neoplasms which these patients develop in Spain. METHODS: The CD4+ lymphocyte counts in 400 adults with HIV infection who developed opportunistic infections or neoplasms were retrospectively reviewed (1987-1991). This determination was carried out during between two months prior to diagnosis of AIDS (CDC, 1987) to one month after such diagnosis. RESULTS: The results allowed opportunistic infections to be classified into three groups according to the grade of immunosuppression: 1) opportunistic infections with more than 0.2 x 10(9) CD4+ lymphocytes/l (45-60% of cases of tuberculosis, esophageal candidiasis and enteritis by Isospora belli); 2) opportunistic infections with 0-0.2 x 10(9) CD4/l (87-100% of the cases of pneumonia by Pneumocystis carinii, encephalic toxoplasmosis, visceral leishmaniasis and enteritis by Cryptosporidium); 3) opportunistic infections with 0-0.1 x 10(9) CD4 lymphocytes/l (70-100% of the cases of systemic cryptococcosis, retinitis by cytomegalovirus, progressive multifocal leukoencephalopathy and infection by Mycobacterium avium-intracellulare). With respect to the neoplasms, Kaposi's sarcoma was observed in patients with different degrees of immunosuppression. Seventy-five and 80% of the patients with non Hodgkin's lymphoma and primary cerebral lymphoma had less than 0.2 x 10(9)/l and less than 0.1 x 10(9)/l CD4+ lymphocytes, respectively. CONCLUSIONS: The CD4 lymphocyte counts may predict the type of opportunistic infections which patients with the human immunodeficiency virus infection may develop.