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Biomedical subjects

F Agbalika

Publications and source records attributed to F Agbalika.

At least 19 recordsLinked to original sources

HHV8 status in Kaposi's sarcoma associated with multiple myeloma.

Kaposi's sarcoma in its sporadic or HIV-related form is due to a gamma herpesvirus, the human herpes virus 8 (HHV8). No data have been published on the potential role of the HHV8 in Kaposi's sarcoma occurring in multiple myeloma patients. A case is reported of a patient in whom four serum samples taken between the diagnosis of multiple myeloma and the occurrence of a Kaposi's sarcoma one year later tested positive for antibody to the HHV8. Similar findings have been reported in patients with other types of Kaposi's sarcoma. PCR studies for HHV8 DNA were positive on a Kaposi's sarcoma biopsy but negative on a bone biopsy, militating against a role for the HHV8 in the genesis of multiple myeloma.

Aged

Lymphomas in patients with Sjogren's syndrome are marginal zone B-cell neoplasms, arise in diverse extranodal and nodal sites, and are not associated with viruses.

The occurrence of non-Hodgkin's lymphoma (NHL) is the most serious complication of Sjogren's syndrome (SS). We performed a study of 16 NHLs occurring in patients with an underlying SS. These lymphomas arose not only in salivary glands (7 cases) but also in other mucosal extranodal sites (the stomach [4 cases], the lung [3 cases], the skin [3 cases], the buccal mucosa [1 case], the thymus [1 case]) and in nodal sites (8 cases). Low-grade marginal zone lymphomas (MZL) were diagnosed in 12 of the 16 patients, 9 of mucosa-associated lymphoid tissues (MALT) type in mucosal sites and 3 exclusively nodal. The 4 other patients presented with a high-grade B-cell lymphoma that was probably a histological transformation of an underlying low-grade MZL at least in 3 of the cases involving skin, stomach, and parotid, respectively. A t(14;18) translocation was detected in 1 of 8 lymphomas tested. We detected serum anti-p53 antibodies in 2 of the 14 studied patients. p53 protein was detected in 1 of 11 lymphomas tested. LMP protein and Eber RNAs of Epstein-Barr virus (EBV) were not detected in the 16 NHL biopsies. Using polymerase chain reaction, EBV was never detected except in 1 of 4 parotid lymphomas. No human T-lymphotropic virus 1 or human herpes virus 8 DNAs were detected in NHL biopsies. None of the patients had hepatitis C virus infection found using serological methods. Chemotherapy was usually efficient. In conclusion, lymphomas occurring in patients with an underlying SS are in most cases MZL. These lymphomas are not associated with viruses known to be present in other types of lymphomas. Some of the translocations or mutations of oncogenes or antioncogenes described in other lymphomas are detected in SS-associated lymphomas.

Adolescent

Fulminant Pneumocystis carinii pneumonia in 4 patients with dermatomyositis.

Between 1989 and 1996, 4 cases of Pneumocystis carinii pneumonia (PCP) were observed in patients seronegative for the human immunodeficiency virus who were receiving corticosteroid therapy for dermatomyositis in our institution. These cases were considered unusual in light of the short delay of their onset after initiation of immunosuppressive therapy and their fulminant course: 3 of these patients died of PCP occurring during the first month of treatment with prednisone. In all 4 patients lymphopenia was observed before the initiation of corticosteroid treatment and low CD4 and CD8 cell counts were evident at the time of PCP. These observations support the view of an increase in both the severity and incidence of PCP in patients without human immunodeficiency virus infection and question the need for a primary prophylaxis in patients with connective tissue diseases receiving high-dose corticosteroid therapy.

Adult

Detection of human herpesvirus 8 and human T-cell lymphotropic virus type 1 sequences in Kaposi sarcoma.

BACKGROUND: Ultrastructural studies have shown retroviral particles in Kaposi sarcoma (KS) unrelated to infection with the human immunodeficiency virus (HIV). Recently, DNA sequences from a new herpesvirus, human herpesvirus 8 (HHV-8), were detected in KS tissues. OBJECTIVES: To screen for the presence of HHV-8 sequences in patients with KS not related to HIV infection and correlate HHV-8 sequence detection and clinical staging and to screen for the presence of human T-cell lymphotropic virus type 1 (HTLV-1) sequences in the peripheral blood mononuclear cells (PBMCs) of such patients. DESIGN: Tumor and normal skin samples and PBMCs were investigated by polymerase chain reaction using primers for HHV-8 and HTLV-1 pX gag, pol, and env sequences. SETTING: Ambulatory or hospitalized patients from a university hospital associated with a research laboratory. PATIENTS: Thirty-one patients with KS not related to HIV infection (21 classic cases, 3 endemic cases, 1 case associated with Castleman disease, 4 homosexual men, 1 post-transplantation patient, and 1 patient taking corticosteroids). Stages involved included I (13 patients), II (8 patients), III (7 patients), and IV (3 patients). RESULTS: Human herpesvirus 8 sequences were found in 100% of KS specimens, 70% of distant normal skin specimens, and 42% of PBMC samples. The percentage of HHV-8 detection in PBMCs was higher in patients with KS stage III or IV than in patients with stage I or II. Human T-cell lymphotropic virus type I pX sequences were detected in 2 of 19 patients while gag, pol, and env test results were negative using polymerase chain reaction analysis. CONCLUSIONS: Our data suggest no significant association between HTLV-1 infection and KS. Detection of HHV-8 infected cells in normal skin samples from the majority of KS tissues, regardless of clinical staging, can be paralleled to the multifocal pattern of the disease. Human herpesvirus 8 detection in PBMCs could be related to the tumor burden.

Adult

Long-term follow-up of non-HIV Kaposi's sarcoma treated with low-dose recombinant interferon alfa-2b.

BACKGROUND AND DESIGN: We reviewed the follow-up of 16 patients with Kaposi's sarcoma not related to human immunodeficiency virus (13 with classic Kaposi's sarcoma and three with endemic Kaposi's sarcoma; median age, 58 years) treated by low-dose recombinant interferon alfa-2b (5 million U three times weekly for at least 6 months). RESULTS: One patient had a complete response, nine had a major response, three had stable disease, and one had a minor response. Visceral disease stabilized and symptoms improved in three patients. Limited relapse was noted in four patients after withdrawal of interferon. CONCLUSION: Our results confirm the efficacy and safety of low-dose recombinant interferon alfa-2b in the long-term treatment of both cutaneous and visceral lesions of Kaposi's sarcoma not related to human immunodeficiency virus.

Adolescent

Absence of cytomegalovirus and Epstein-Barr virus expression in labial salivary glands of patients with chronic graft-versus-host disease.

We investigated in 15 consecutive patients a possible correlation between expression of CMV or EBV in labial salivary gland (LSG) biopsies performed 100 days after allogeneic BMT and subsequent development of chronic GVHD. Three techniques were performed for the detection of each virus: immunohistochemistry, in situ hybridization and PCR. Eleven patients developed chronic GVHD. Histologic examination detected a moderate lymphoid infiltrate (grade 1 according to Sale's score) in LSG biopsy in only one patient. CMV genes or proteins could not be detected in any patients. Likewise, EBV genome or proteins were not detected by in situ hybridization and immunohistochemistry. However, in three of the 15 patients, EBV DNA was detected by PCR in LSG biopsies. Only one of these three patients developed chronic GVHD. Therefore, at the present time, the presence of a lymphoid infiltrate on lip biopsies performed at day 100 post-BMT does not appear to be sensitive enough for the diagnosis or the prediction of the subsequent development of chronic GVHD. Moreover, the absence of EBV and CMV expression in a day-100 LSG biopsy does not preclude the development of chronic GVHD.

Adolescent

[Do neuromyosites exist?].

Neuromyositis defined as the association of dermatomyositis or polymyositis and a neuropathy without any found cause is a very controversial entity because of the possibility of, in one hand, muscular modifications caused by neurological involvement and, on the other hand, neurogenic type manifestations caused by polymyositis. The study of 4 cases seen in an Internal Medicine department and the review of the literature allowed us to show that the concept of neuromyositis corresponds to a clinico-pathological reality when the diagnosis is based on the association of definite criteria of both primary muscle and nerve involvement excluding muscular abnormalities that could be the consequence of nerve involvement and vice versa. The criteria, most relevant when associated are: a) for muscular involvement: high increase of muscular enzyme over 6 times the superior limit of the normal values, pseudomyotonic electrical discharges, perifascicular atrophy, intense inflammatory infiltrates and massive necrosis, b) for neurological involvement: early abolition of tendinous reflexes in a patient without notable muscular atrophy and with little or no myalgia, sensitive abnormalities in areas other than those of muscular involvement, especially when they are intense, early weakness of distal muscles, decrease of nerve conduction speed, target fibers and lesions of nerve trunks (and albuminocytological dissociation in the particular case of polyradiculoneuritis). Once the diagnosis of neuropathy settled, it is necessary to exclude an usual cause (alcoholism, diabetes...) before concluding to neuromyositis. When we apply these restrictive (but nevertheless necessary for the validity of diagnosis) criteria, only 6 cases of the literature respond to this entity. It is a peripheral neuropathy in 5 cases (like two of ours) and a polyradiculoneuritis in one case (like our two others). Among these 6 cases, there is a vasculitis in two, frequency much higher to what is observed in adult polymyositis, which suggest a possible causative role of vascular involvement in neuropathy arising. In the other cases we can just give pathogenic hypothesis making the neuropathy and the polymyositis the result of the same process (immunological disturbance, paraneoplastic origin, viral disease). In one of our four patients, who have shown an HTLV-I infection by polymerase chain reaction in situ hybridization was positive in muscle which suggest a direct pathogenic role of the virus. HTLV-I infection should be considered as a possible cause of neuromyositis especially in endemic areas.

Adult

Detection of human T lymphotropic virus type I tax gene in salivary gland epithelium from two patients with Sjögren's syndrome.

OBJECTIVE: To investigate whether human T lymphotropic virus type I (HTLV-I) could be involved in the pathogenesis of Sjögren's syndrome (SS). METHODS: Labial salivary gland (LSG) biopsy specimens from 9 patients with SS (4 with primary SS and 5 with SS secondary to rheumatoid arthritis) and 9 controls were studied for the presence of the tax gene of HTLV-I using in situ hybridization, and for the presence of tax, gag, pol, and env genes of HTLV-I using the polymerase chain reaction (PCR). Testing for antibodies to HTLV-I and examination of lymphocytes on blood smears were performed to determine whether systemic viral infection was present. RESULTS: Using in situ hybridization and PCR, we detected the tax gene, but not the gag, pol, or env genes, of HTLV-I in LSG sections from 2 of 9 patients with SS and from none of the control subjects. Tax DNA was present mostly in nuclei of epithelial cells, but also in some lymphoid cells. Serum of the 2 affected patients did not contain antibodies to HTLV-I. In 1 patient, examination of blood smears revealed rare convoluted lymphocytes, sometimes with the appearance of "flower cells," as observed in the blood of HTLV-I-infected patients. CONCLUSION: None of the known endogenous retroviral sequences is homologous to the tax gene. Thus, we suggest that HTLV-I (or another related retrovirus) can infect salivary epithelium. Transactivation properties of the tax protein could be implicated in the pathogenesis of SS. Alternatively, viral infection could cause de novo expression of HLA-DR antigens and favor the presentation of antigens by epithelial cells, leading, in some genetically predetermined subjects, to lymphoid infiltration of the gland.

Antibodies, Viral

[4 new cases of neuromyositis, one of them associated with HTLV-I infection].

Neuromyositis is a very rare type of polymyositis where, beside the usual muscular manifestations, there are signs of peripheral neuropathy which can be found at clinical, electromyographic and/or pathological examination. We have seen between 1983 and 1990 four cases of neuromyositis. The neurological disorder was an axonopathy in two cases which is usual in neuromyositis; in the other two cases, there was a polyradiculoneuritis which seems to be very rare in this syndrome. In the four patients the disease was particularly severe and unresponsive to treatment. One of our patients had HTLV-I infection diagnosed by polymerase chain reaction amplification and in situ hybridization, while the serological test was negative. To our knowledge only three cases of HTLV-I associated neuromyositis have been reported in the literature.

Adult

False-positive HIV antigens related to emergence of a 25-30 kD protein detected in organ recipients.

OBJECTIVE: The routine screening of organ donors for HIV-1 since 1985 has markedly reduced the risk of acquiring infection in organ recipients. However, commercial HIV-1 p24-antigen assays reveal false-positive reactivity in certain recipients. This observation will be discussed here. METHODS: Post-transplantation sera collected sequentially from different organ recipients were tested for HIV antigen: 79 samples were from 14 kidney recipients, 57 from seven bone-marrow allografts and 18 from two heart recipients. Neutralization assays to determine specificity were performed on reactive samples. Immunoblots prepared from sera containing high levels of antigens were tested by Western blot using polyclonal anti-HIV sera. RESULTS: Abbott HIV-1-EIA kits detected non-neutralizable antigens in early post-transplantation sera from 12 kidney, five bone-marrow and two heart recipients. Using in-house immunoblots prepared from positive non-neutralizing antigen sera, a 25-30 kD protein was detected and shown to be the cause of the false HIV antigen cross-reactivity. CONCLUSION: False-positive HIV antigens related to the emergence of a 25-30 kD protein in early post-transplantation sera are detectable in transplant recipients.

Adolescent