Detection of HTLV-1 DNA by polymerase chain reaction in alveolar lymphocytes of patients with tropical spastic paraparesis.
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Biomedical subjects
Publications and source records attributed to L J Couderc.
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Three patients with lymphoid interstitial pneumonia (two HIV 1+ patients with chronic lymphadenopathic syndromes and one with a not-characterized autoimmune disease) have been studied with high-resolution computed tomography (HR-CT). This technique reveals septal lines, small reticulonodular opacities, polyhedral micronodular opacities, "ground-glass" opacities and a dense, subpleural, curved broken line in one patient. The lesions dominate in the bases of the lungs. They are not characteristic for lymphoid interstitial pneumonia. If a patient present with a chronic lymphadenopathic syndrome, the diagnosis of an opportunistic infection should not be automatically made, since the syndrome can be caused by lymphoid interstitial pneumonia.
STUDY OBJECTIVE: To determine the features of pulmonary involvement in patients with tropical spastic paraparesis associated with human T-cell lymphotropic virus type 1. DESIGN: Nonrandomized prospective case series. SETTING: Tertiary care units in two university medical centers. PATIENTS: Consecutive sample of 21 patients with tropical spastic paraparesis associated with human T-cell lymphotropic virus type 1 infection. INTERVENTIONS: Chest roentgenogram and bronchoalveolar lavage were done in all patients. Fifteen patients had pulmonary function tests. Alveolar T-lymphocyte subsets were analysed in 10 patients and thoracic computed tomographic scans were done in 10 patients. MEASUREMENTS AND MAIN RESULTS: All patients were free of clinical pulmonary symptoms and had normal chest roentgenograms. Thoracic computed tomographic scans were normal in 9 of 10 patients and showed mild interstitial pneumonitis in 1. Pulmonary function tests were within the normal range in 13 patients and showed a mild restrictive syndrome in 2. Eighteen patients had increased absolute numbers of alveolar lymphocytes (mean, 77 +/- 39 X 10(3) lymphocytes/mL; range, 13.5 X 10(3) to 259 X 10(3) lymphocytes/mL). Sixteen patients had percentages of alveolar lymphocytes higher than 20% of all alveolar cells (mean, 33.5 +/- 12.7; range, 9 to 69). In all 10 patients tested, 64.2% +/- 13.2% of alveolar lymphocytes were CD8+ cells. CONCLUSIONS: Excessive absolute numbers and percentages of alveolar lymphocytes were observed in 18 and 16 patients, respectively. Most alveolar lymphocytes were CD8+ cells.
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T-cell mediated and humoral responses directed to microbial antigens were investigated, at the time of the initial visit, in a group of 139 patients with HIV-1-related persistent generalized lymphadenopathy (PGL) enrolled in a longitudinal study. In vivo and in vitro cell-mediated responses to tuberculin were lower in patients than in controls. Differences were not significant for candidin and streptococcal antigen in vitro, whereas higher responses were observed in the patient group for cytomegalovirus antigen. Following immunization, a subgroup of patients did not have a significantly raised serum antitetanus antibody level, whereas in vitro lymphocyte proliferative responses to tetanus toxoid were lower than in controls. No association was found between these abnormalities and other immunological parameters, including the blood level of CD4+ lymphocytes. Lower responses to most microbial antigens were observed in patients with HIV-1-related symptoms in addition to lymphadenopathy, or the patients who progressed to AIDS in the 2 years following the study. Moreover, intravenous drug users showed higher responses than homosexual patients, possibly because of the influence of previous infections on immunological responses to microbial antigens.
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We report 31 cases of AIDS-Kaposi's sarcoma (KS) studied at the Hôpital Saint-Louis, Paris, France, from January 1983 to January 1986. Twenty-nine cases were cutaneous KS and 2 were lymph-node KS. Twenty-eight patients were homosexual or bisexual males, 1 was a woman with transfusion-AIDS and 1 was an intravenous drug-addict; one male had no known risk factor. Thirty were male and 1 female, mean age 35.5 years (+/- 8.4). All were Caucasian and positive for LAV antibodies (Elavia). 17/30 (56.6 p. 100) had a history of syphilis, 16/30 (53.3 p. 100) had a positive TPHA test, 12/30 (40 p. 100) had a history of urethral discharge, 26/31 (87 p. 100) had a history of sexually transmitted disease. 27/30 had antibodies against HBs or HBc. 14/31 (45 p. 100) presented with mild symptoms (fever, loss of weight). 10/28 (36 p. 100) had lymph node enlargement before the first cutaneous lesions of KS developed. Initial involvement included the trunk (32 p. 100), the legs (25 p. 100), the face (21 p. 100) and the lower limbs (11 p. 100). Seventy-one p. 100 of the patients had more than 10 lesions at the initial assessment. The palate was involved in 50 p. 100 of patients, the lymph nodes in 74 p. 100, the stomach in 38 p. 100, the colon in 31 p. 100. In 8 cases pulmonary involvement was present. Altogether, 55 p. 100 of the patients had visceral involvement. Enlargement of the spleen (16 p. 100) and liver (13 p. 100) was also noted. Nineteen p. 100 of the patients had chronic dermatophytic cutaneous infection, 39 p. 100 had oral candidiasis, 32 p. 100 had seborrheic dermatitis, 6 p. 100 had oral hairy leukoplakia and 26 p. 100 had trimethoprim-sulfamethoxazole eruption. Fifty-five p. 100 developed opportunistic infection (OI) (Pneumocystis carinii 8 cases, intestinal cryptosporidiosis 6 cases, cerebral toxoplasmosis 4 cases, CMV pulmonary infection 3 cases). In 14 cases KS preceded OI and in 3 cases OI preceded KS. Biological results are shown in tables II and III. Main findings were: mild inflammatory syndrome (ESR 33 +/- 24 mm, first hour), polyclonal hypergammaglobulinemia (18.6 g/l +/- 5.8), elevation of plasma factor VIII related antigen (191 +/- 66 U/dl), elevation of serum activity of angiotensin-converting enzyme (23.8 +/- 5 nmol/ml/min), low plasmatic cholesterol (3.77 +/- 1.1 mmol/l).(ABSTRACT TRUNCATED AT 400 WORDS)
Five male patients with the persistent generalized lymphadenopathy syndrome also had a sicca complex. Salivary gland biopsy specimens showed diffuse lymphocytic infiltration of the glandular parenchyma. Serum autoantibodies and rheumatoid factor were not detected. All patients had IgG antibodies to human immunodeficiency virus and IgG to the viral capsid antigen of Epstein-Barr virus. These five patients had benign lymphocytic infiltrates in other organs (lung, liver, and kidneys). Sicca complex may be one of the various manifestations of the lymphoid hyperplasia noted in human immunodeficiency virus-infected patients. In these patients, the sicca complex showed specific features related to male predominance, lack of serum autoantibodies, and peripheral-blood T-lymphocyte subset distribution.
Pre- and post-immunization serum antibodies to pneumococcal polysaccharides (PPS) and tetanus toxoid (TT) were measured in 25 patients with persistent generalized lymphadenopathy and serum antibodies to the human immunodeficiency virus (HIV). The increase in post-immunization anti-PPS antibodies was lower than 40% in 16/25 patients. Isotype analysis indicated that the IgM, IgA, IgG2, but not the IgG1 antibody responses were lower in patients that in healthy controls, whereas pre-immunization values were similar. For TT, no difference was found between the patients and the healthy group in total and IgG1 antibody response whereas IgG4 response was lower in patients. No significant association was found between the defect in anti-PPS antibody response and associated thrush or constitutional symptoms or other immunological parameters. These findings suggest that defective response to a thymo-independent polysaccharide antigen is a distinctive consequence of HIV infection.
Seven patients of Haitian and Central African origin were investigated for interstitial pneumonitis and unexplained chronic lymphadenopathy. A study of broncho-alveolar lavage fluid showed no opportunistic micro-organisms and disclosed a high alveolar lymphocyte count with more than 80% T8+ cells. In 3 patients, open lung biopsy showed lymphoid interstitial pneumonitis. Follicular hyperplasia was a constant finding in lymph nodes. Benign lymphocytic infiltration was found in other organs of all patients, associated with polyclonal hyperimmunoglobulinaemia, low peripheral T4+ cell count and LAV-Ig G antibodies.
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HLA-A B and DR typing were performed in 77 patients with AIDS related complex (ARC)--69 lymphadenopathy associated syndrome and 8 thrombocytopenic purpura LAV/HTLV III related--and 21 symptom free homosexual males. A significant increase in the frequency of HLA DR5 antigen was observed in patients with ARC mainly in purpura thrombocytopenic patients. We suggest that increase of HLA DR5 antigen support the view that DR5 antigen could be one of the factors necessary at the spreading out clinical symptoms.
An abdominal computed tomographic examination was performed to 20 patients with Acquired Immunodeficiency Syndrome (AIDS) and to 5 patients with Lymphadenopathy Syndrome (LAS). Intraabdominal lymph nodes were seen in 18 out of 20 cases of AIDS and in 5 cases of LAS. Lymph nodes have a normal size or are slightly enlarged but they are too numerous. Splenomegaly was found in 17 patients. Rectal modifications secondary to a proctitis were seen in the homosexual patients.
Serum IgG subclass levels were measured by an indirect competitive immunoenzymatic assay with monoclonal antibodies in 61 adult patients of different geographic origins affected either with the lymphoadenopathy syndrome (LAS, 46 cases) or with the acquired immune deficiency syndrome (AIDS, 15 cases). In spite of considerable variations from patient to patient, IgG-1 and IgG-3 levels were higher than in normal Caucasians, with IgG-1 levels much more elevated in LAS than in AIDS patients. In Caucasians with AIDS or LAS, IgG-4 levels were low. IgG-2 levels tended to be low and correlated negatively with IgG-1 levels. IgG subclass imbalances were especially striking in patients with lymphoid interstitial pneumonitis. The results suggest that the IgG increase predominantly affects the less T-dependent subclasses. The low levels of the more T-dependent isotypes do not appear to play a clear role in the occurrence of pyogenic infections in certain patients.