ABSTRACT Human herpesvirus 8 (HHV-8), or Kaposi's sarcoma-associated herpesvirus, is highly prevalent in certain risk groups (human immunodeficiency virus-infected patients, transplant recipients, and patients on hemodialysis). Heath care workers caring for these patients were found to be more frequently infected with HHV-8 than staff caring for other patients ( P < 0.01).

A 68-year female patient with increasing cognitive impairment in combination with affective disturbance is presented. The patient had previous history of Hashimoto's thyroiditis. Cerebral spinal fluid revealed an elevated protein level without pleocytosis. Cerebral MRI demonstrated only unspecific changes. EEG showed diffuse slow-wave abnormality. Suspecting Hashimoto's encephalopathy we initiated high-dose steroid treatment. Subsequently we could find improvement of the previously progressive cognitive decline. We conclude that the possibility of an endocrine or autoimmune etiology should always be taken into consideration examining the cause of progressive dementia.

Epstein-Barr virus (EBV) has been identified as a cofactor in the pathogenesis of a significant proportion of human immunodeficiency virus (HIV)-related or transplantation-related lymphoproliferative disorders (2, 3). Furthermore, EBV reactivation occurs more frequently in patients on hemodialysis due to the uremic immunodeficiency (5). Currently, EBV reactivations are almost exclusively diagnosed by antibody assays. We investigated whether the indirect detection of EBV by serological assays is correlated with the direct detection of the EBV viral DNA load in patients with immunosuppression (30 HIV-positive individuals, 30 transplant recipients, 23 patients on hemodialysis) and in 30 blood donors as controls. EBV primary infections and seronegatives were excluded. First, immunofluorescence analysis of immunoglobulin G (IgG), IgM, and IgA antibodies to virus-capsid antigen (VCA), early antigen (EA-IgG), and EBV nuclear antigens 1 and 2 (EBNA1-IgG and EBNA2-IgG, respectively) were carried out. Serological reactivations were detected when at least one of the following parameters was found: VCA-IgM titer, >32; VCA-IgA titer, >32, EA-IgG titer, >64; EBNA1-IgG ≤ EBNA2-IgG (5). EBV DNA present in peripheral leukocytes was quantified by a competitive nested PCR assay of EBV-p23 (1). The detection limit was determined as 20 EBV copies in 105 EBV-negative leukocytes. In the latent stage, not more than 5 cells in 106 leukocytes are EBV infected; thus, latent infections were not detectable with this PCR (4). Serological reactivation and EBV DNA content were not correlated, since serological reactivations were found with almost the same frequency in PCR-positive as in PCR-negative individuals (Table ​(Table1).1). No PCR-positive subjects were present in controls; however, 13% exhibited serological markers for reactivation. Furthermore, no differences were found when single serological reactivation parameters such as EA-IgG or EBNA1-IgG ≤ EBNA2-IgG were correlated with PCR. Finally, PCR results failed to correlate with the number of different reactivation markers in individual subjects. Four patients with a high viral load (>106 copies/μg of DNA) were found in the group of PCR-positive subjects. Even among these patients, no serological reactivations were detected. In contrast, 4 of 11 patients (36%) with moderate (104 to 106 copies/μg of DNA) and 6 of 7 patients (85%) with low viral load (<104 copies/μg of DNA) showed such serological reactivations, suggesting that antibody production and the loss of antibodies are individually different, particularly in immunosuppressed patients. TABLE 1 Comparison of serological reactivations detected by antibody assays and EBV DNA by PCR in leukocytes In summary, we suggest that the serological parameters that are currently employed as an indicator for EBV reactivation may be of limited use as they fail to correlate with viral load.

Objective: To study syphilis in HIV infection focusing on immunocompromised patients with an atypical or aggressive clinical course of syphilis, inappropriate serological reactions or an unreliable response to therapy.Study design: A multicentre retrospective chart review using a standardised questionnaire for all patients with active syphilis.Settings: Thirteen dermatological and medical centres throughout Germany, all members of the German AIDS Study Group (GASG).Patients: Clinical data of 11368 HIV infected patients have been analysed for cases of active syphilis requiring treatment. Asymptotic patients with reactive serological parameters indicating latent syphilis without a need for treatment were excluded.Results: Active syphilis was reported in 151 of 11 368 HIV infected patients (1.33%, range per centre 0.3%-5.1%). Most of the 151 syphilis patients were male (93%) and belonged to the homosexual or bisexual exposure category for HN infection (79%); another 6% were iv drug users. Among the 151 syphilis patients primary syphilis was diagnosed in 17.2%, maculopapular secondary syphilis in 29.1%, ulcerating secondary syphilis in 7.3%, neurosyphilis in 16.6% and latent seropositive syphilis without clinical symptoms but serological abnormalities indicating active syphilis in 25.2%.A history of prior treatments for syphilis was reported in 50%. At the time of syphilis diagnosis 26.5% of the patients were in CDC stage II, 33.8% in stage III and 24.5% in stage IV of HIV disease (CDC classification 1987). CD4 cell count was lowest in those with ulcerating secondary syphilis (mean 307, SD 140/mu l) and neurosyphilis (351, SD 235/mu l). The highest CD4 count was found in patients with early primary and early secondary syphilis (444, SD 163/mu l and 470, SD 355/mu l). Inappropriate serological response to syphilis infection was found in 81 of 151 patients (54%). Remarkable findings were false negative VDRL titres (11 patients with non primary syphilis), false negative TPHA (1) or 19S-IgM-FTA-ABS-tests (16), and strongly reactive VDRL (greater than or equal to 512, 8) or TPHA titres (greater than or equal to 10 240, 47). Treatment failures were reported in at least 6 of 151 cases (4%).Conclusions: Atypical clinical and serological courses of syphilis were observed in HIV infected patients. Ulcerating secondary syphilis with general symptoms (''malignant syphilis'') was 60 times more frequent than in historic syphilis series. Neurosyphilis was found in one sixth of those with active syphilis. Therefore lumbar puncture should be considered a routine in coinfections with HIV and syphilis. Treatment efficacy should be monitored carefully.

OBJECTIVE:To study syphilis in HIV infection focusing on immunocompromised patients with an atypical or aggressive clinical course of syphilis, inappropriate serological reactions or an unreliable response to therapy.STUDY DESIGN:A multicentre retrospective chart review using a standardised questionnaire for all patients with active syphilis.SETTINGS:Thirteen dermatological and medical centres throughout Germany, all members of the German AIDS Study Group (GASG).PATIENTS:Clinical data of 11,368 HIV infected patients have been analysed for cases of active syphilis requiring treatment. Asymptotic patients with reactive serological parameters indicating latent syphilis without a need for treatment were excluded.RESULTS:Active syphilis was reported in 151 of 11,368 HIV infected patients (1.33%, range per centre 0.3%-5.1%). Most of the 151 syphilis patients were male (93%) and belonged to the homosexual or bisexual exposure category for HIV infection (79%); another 6% were iv drug users. Among the 151 syphilis patients primary syphilis was diagnosed in 17.2%, maculopapular secondary syphilis in 29.1%, ulcerating secondary syphilis in 7.3%, neurosyphilis in 16.6% and latent seropositive syphilis without clinical symptoms but serological abnormalities indicating active syphilis in 25.2%. A history of prior treatments for syphilis was reported in 50%. At the time of syphilis diagnosis 26.5% of the patients were in CDC stage II, 33.8% in stage III and 24.5% in stage IV of HIV disease (CDC classification 1987). CD4 cell count was lowest in those with ulcerating secondary syphilis (mean 307, SD 140/microliters) and neurosyphilis (351, SD 235/ microliters). The highest CD4 count was found in patients with early primary and early secondary syphilis (444, SD 163/microliters and 470, SD 355/microliters). Inappropriate serological response to syphilis infection was found in 81 of 151 patients (54%). Remarkable findings were false negative VDRL titres (11 patients with non primary syphilis), false negative TPHA (1) or 19S-IgM-FTA-ABS-tests (16), and strongly reactive VDRL (> or = 512, 8) or TPHA titres (> or = 10 240, 47). Treatment failures were reported in at least 6 of 151 cases (4%).CONCLUSIONS:Atypical clinical and serological courses of syphilis were observed in HIV infected patients. Ulcerating secondary syphilis with general symptoms ("malignant syphilis") was 60 times more frequent than in historic syphilis series. Neurosyphilis was found in one sixth of those with active syphilis. Therefore lumbar puncture should be considered a routine in coinfections with HIV and syphilis. Treatment efficacy should be monitored carefully.

Objective: Zidovudine (ZDV) is the only antiretroviral drug which has been shown to reduce mortality in patients with symptomatic HIV disease, but its use is restricted by intolerance in a significant proportion of patients. Additionally, the efficacy of ZDV therapy appears to decrease after prolonged treatment particularly in the advanced stage of HIV disease. Therefore, alternative antiretroviral regimens for patients are needed. In this study, didanosine (ddl; 2',3'-dideoxyinosine), another HIV reverse transcriptase inhibitor, was evaluated.Design: A total of 426 patients with AIDS or AIDS-related complex (ARC) who were intolerant to or clinically progressing on ZDV therapy and who had CD4+ cell counts less than or equal to 150 x 10(6)/l were randomized to receive either a high (750 mg for bodyweight greater than or equal to 60 kg or 500 mg for bodyweight < 60 kg) or a low (200 mg and 134 mg, respectively) dose of ddl daily.Setting: The patients were recruited from 31 German and Austrian AIDS clinical primary-care centres.Results: The study was stopped after the second interim analysis due to a statistically significant difference in the incidence of pancreatitis (nine versus 26; relative risk, 2.92; P=0.003) and neuropathy (28 versus 43; relative risk, 1.55; P=0.05) in favour of the low dose. There was no difference between the low and high dosage groups in survival rate at 6 (80 versus 80%) and 12 months (61 versus 65%), number of deaths [82 (43.6 per 100 patient-years) versus 84 (44.4 per 100 patient-years)], progression from ARC to AIDS or to AIDS or death, or average number of new/recurrent opportunistic infections (2.8 versus 3.0 per patient).Conclusions: This study cannot conclude on ddl efficacy but it shows that in patients with advanced HIV disease for whom no alternative antiretroviral therapy is available and ddl therapy is considered, daily doses < 750 mg should be administered.

The success of Cyclosporin A in organ transplantation naturally raises the question of its usefulness in treating autoimmune diseases such as systemic lupus erythematosus. Therefore, we performed a pilot study in which 10 cases of severe systemic lupus erythematosus were treated with Cyclosporin A.

Thirty-one samples representing Hodgkin's and non-Hodgkin's lymphomas, angioimmunoblastic lymphadenopathy (AILD), and benign follicular hyperplasia in HIV infections were examined for rearrangements of the immunoglobulin (Ig) and T cell receptor (TcR) beta-chain gene loci. In 11 of 12 non-Hodgkin's lymphomas (classified as Burkitt lymphoma (2), centrocytic lymphoma (1), centrocytic-centroblastic lymphoma (5), centroblastic lymphoma (3], only rearranged Ig genes could be detected. The exceptional case was an unclassified high-grade lymphoma, which represented a rearrangement of the TcR beta-chain. We also examined DNA from lymphoid neoplasms in which the lineage of the malignant cell was still controversial. Rearrangement of the TcR could exclusively be demonstrated in all 3 cases of AILD. One Ig gene rearrangement and 4 TcR beta-chain rearrangements were found in 13 samples of Hodgkin's lymphomas (11 lymph nodes, 1 pleura effusion and 1 bone biopsy with proven infiltration). Examination of 3 cases of benign follicular hyperplasia in HIV infection represented one Ig rearrangement.

11 Patienten mit einer Haarzell-leukämie wurden zwei bis sechs Monate lang mit Beta-Inferferon (IFN-β; 3 × 4 Mio. I.E./Woche i.v.) behandelt. Von 8 auswertbaren Patienten erreichten 3 eine partielle Remission, 2 eine minor response, während 3 Patienten keine Verbesserung ihrer hämatologischen Werte zeigten. Als Nebenwirkungen traten die für die IFN-Therapie typischen grippeähnlichen Symptome bei 9 der 11 behandelten Patienten auf. Bei einem Patienten wurde ein Rückgang der Knochenmarksinfiltration unter IFN-β beobachtet. Diese Daten zeigen, daß IFN-β bei der Haarzelleukämie wirksam ist.

: Eleven patients with histologically proven hairy-cell leukemia were treated for 2 to 6 months with a natural beta-interferon (beta-IFN) preparation (3 X 4 million units week i.v.). Three of the eight evaluable patients experienced a partial response, two a minor response, and three no improvement. A reduction of the hairy-cell infiltration of the bone marrow was observed in one patient. Typical IFN side-effects with flu-like symptoms were noted. These results demonstrate that IFN-beta has some clinical efficacy in hairy-cell leukemia.

Systemic lupus erythematosus (SLE) may give rise to an extremely variable symptomatology with different clinical pictures ranging from an acute attack with high fever, anaemia, leucocytopenia and thrombocytopenia, arthritis, exanthema and polyserositis to the isolated involvement of organs including the kidneys, bone marrow or joints. Over recent years, aggressive therapy has ensured a continual increase of survival rates. The 5- and 10-year survival rates have been given as 75% and 60% for SLE with nephrotic syndrome and as 88% and 79% for other forms of SLE [9]. In addition to immunosuppressive therapy with cyclophosphamide, azathioprine and steroids [4], more recently the prognosis has been improved by administering high doses of prednisone and by combining therapeutic plasma exchange (TPE) with immunosuppression.

Letters and Corrections1 May 1984Pseudothrombocytopenia and MexiletineGERD GIRMANN, M.D., HANS PEES, M.D., PAUL GERHARD SCHEURLEN, M.D.GERD GIRMANN, M.D.Search for more papers by this author, HANS PEES, M.D.Search for more papers by this author, PAUL GERHARD SCHEURLEN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-100-5-767_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Fasola and coworkers (1) recently have reported the second case (2) of a mexiletine-associated thrombocytopenia with platelets having been counted in edetic acid-anticoagulated blood. We have observed a hitherto unknown association between mexiletine and pseudothrombocytopenia, in which antibodies in patients' sera (3) react with platelets anticoagulated with edetic acid or other agents (4, 5) causing agglutination and spuriously low platelet counts.In July 1982, a 62-year-old man was hospitalized for thrombocytopenia. After a myocardial infarction in 1981, he received nifedipine, isosorbide dinitrate, and mexiletine (600 mg/d). He had no history of bleeding. After edetic acid treatment, an...References1. FASOLAD'OSUALDODE PANGHERBARDUCCI GFVE. Thrombocytopenia and mexiletine [Letter]. Ann Intern Med. 1984;100:162. LinkGoogle Scholar2. CAMPBELLKELLYSHANKSADGEY NJRA. Long term oral antiarrhythmic therapy with mexiletine. Postgrad Med J. 1977;53(suppl 1):143-5. MedlineGoogle Scholar3. PEGELSBRUYNESENGELFRIETVON DEM BORNE JECA. Pseudothrombocytopenia: an immunologic study on platelet antibodies dependent on ethylene diamine tetra-acetate. Blood. 1982;59:157-61. CrossrefMedlineGoogle Scholar4. CIMO P. Pseudothrombocytopenia. JAMA. 1974;229:766-7. CrossrefMedlineGoogle Scholar5. ONDERWEINSTEINHOYER OAL. Pseudothrombocytopenia caused by platelet agglutinins that are reactive in blood anticoagulated with chelating agents. Blood. 1980;56:177-82. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: First University Medical Center D-6650 Homburg/Saar, West Germany PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byEDTA’ya Bağlı Psödotrombositopeni: Olgu SunumuMexiletineSunitinib-associated pseudothrombocytopenia induced by IgM antibodyClinical Pharmacology of Antiarrhythmic DrugsANTIDYSRHYTHMIC DRUGSMolecular characterization of the variable domains of an ?IIb?3-specific immunoglobulin�M ? platelet cold agglutinin in a follicular lymphoma patient with treatment refractory autoimmune thrombocytopenia: idiotypic overlap between ?IIb?3 integrin antibodiesMexiletineOlanzapine-Induced EDTA-Dependent PseudothrombocytopeniaPlatelet cold agglutinins: a flow cytometric analysisPlatelet activation during myocardial ischaemia: A contributory arrhythmogenic mechanismA new type of pseudothrombocytopenia: EDTA-mediated agglutination of platelets bearing Fab fragments of a chimaeric antibodyEdta-dependent pseudothrombocytopenia: A clinical study of 18 patients and a review of the literatureCLASS IA AND CLASS IB ANTIARRHYTHMIC DRUGS - A Review of Their Pharmacokinetics, Electrophysiology, Efficacy, and ToxicityCLASS IA AND CLASS IB ANTIARRHYTHMIC DRUGS ? A Review of Their Pharmacokinetics, Electrophysiology, Efficacy, and ToxicityMexiletineMexiletine for the Management of Ventricular Arrhythmias in Ischemic Heart DiseasePseudothrombocytopenia: a cold autoantibody against platelet glycoprotein GP II bCardiac glycosides and drugs used in dysrhythmias 1 May 1984Volume 100, Issue 5Page: 767-767KeywordsAntibodiesBloodEthylenediaminetetraacetic acidHemorrhageMyocardial infarctionPlatelets Issue Published: 1 May 1984 PDF downloadLoading ...