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H Rasokat

Publications and source records attributed to H Rasokat.

At least 37 records · Page 2Linked to original sources
PubMed1989

[The atypical course of syphilis in HIV infection].

We report on 3 HIV patients showing atypical courses of syphilis. Both the history and serology of the first patient proved a recent re-infection with T. pallidum, whereas the histopathological findings corresponded to an advanced stage of the disease (S II-III). The second patient showed the clinical picture of syphilis maligna with slowly converting and slightly positive serological reactions. The third patient had a refractory syphilis and an early relapse. Our observations suggest that syphilis might take an unusual course in HIV patients. Considering our total HIV clientèle (800 patients greater than or equal to WR 2) the frequency of these atypical cases must be rated very low (0.38%).

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Aseptic skin necrosis after subcutaneous injection of alpha interferon].

Aseptic necrosis of the skin developed in two patients with HIV-associated disseminated Kaposi's sarcoma after subcutaneous injection of recombinant interferon-alpha. Both patients were given it at a daily dosage of 20 x 10(6) IU/m2 body surface area. One of the patients, after full remission had been achieved, received a reduced dosage of 3 x 10(6) IU/m2, twice weekly. The clinical picture and course of the changes were similar to those of embolia cutis medicamentosa (Nicolau's syndrome), which can occur after injection of various drugs, intended to be intramuscular but by mistake given intra-arterially.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Striated nail discoloration caused by zidovudine].

We report on 2 male patients treated with zidovudine (azidothymidine), who developed longitudinally striated coloration of their nails and lentigines. Both patients are suffering from advanced HIV disease with opportunistic infections. Following treatment with zidovudine 1200 mg daily for 3 and 6 months resp., we observed longitudinal streaks of brownish color in both patients; they did not receive any other drugs known to induce discoloration of the nail plate. Our cases possibly reflect antiproliferative effects of zidovudine at the particularly susceptible nail matrix.

Acquired Immunodeficiency Syndrome↗
PubMed1989

[Endothelial precipitates and cytomegalovirus infection].

In patients with the typical features of intraocular cytomegalovirus infection endothelial precipitates were identified that had a characteristic morphology, which included subtle, non-pigmented linear deposits with reticular arrangement that can spread diffusely over the corneal endothelium without preference for the inferior quadrants. The appearance of these precipitates was comparable to heterocromic cyclitis. Specular microscopy identified lymphocytes and macrophages on the endothelial layer. The present observations are based on five case reports of necrotizing retinitis, typical for intraocular cytomegalovirus infection, in connection with the atypical endothelial precipitates. In four of the five patients reported, HIV-infection was confirmed. In one patient with serologically confirmed cytomegalovirus infection (however without HIV-infection), a diagnostic work-up of the aqueous humor was carried out. Local production of specific antibodies against cytomegalovirus was identified in the aqueous humor. Topical treatment with antiviral and/or steroidal drugs was unsuccessful. The antiviral drug gancyclovir was applied systemically in two patients, but there was no impact on the corneal precipitates described. No intravitreal therapy was given. If these endothelial changes can be regarded as pathognomonic for cytomegalovirus infection, thorough slit lamp examination may be important for diagnosis of the presence of or the reactivation of cytomegalovirus infection in the eye. So far, no correlation has been found between the time course of corneal/endothelial precipitation and necrotizing retinitis.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Treatment of advanced, progressive epidemic Kaposi's sarcoma (EKS): a phase-II study.

The design of a prospective phase-II study on the treatment of Kaposi's sarcoma (KS) in patients with HIV infection is described. In this study the toxicity and antineoplastic activity of high-dose alpha-interferon (20 x 10(6) U/m2 s.c. daily) will be investigated in patients with advanced and progressive KS. Patients with progressing KS during IFN treatment or with relapsing KS after IFN will be treated with vinblastine (4 mg/m2 i.v., days 1, 8, and 15) and bleomycin (15 mg i.v., days 1 + 8). The study was only recently activated; results are so far not available.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Plasma amino acid pattern of patients with HIV infection.

We measured the free amino acids in plasma of 58 patients with HIV infection and in six persons in the risk group. The HIV+ patients had significantly increased concentrations of arginine, phenylalanine, and glutamate in comparison with both age- and sex-matched controls and the members of the risk group. Glutamate concentrations increased only in an advanced stage of the disease (WR 5 and 6 of the Walter Reed staging classification), whereas arginine and phenylalanine increased independently of the stage. There was no correlation between the amino acid concentrations and the number of T4 and T8 lymphocytes, the sedimentation rate, and the existence or absence of Kaposi's sarcoma. The amino acid pattern of HIV-infected persons is similar to that of cancer patients or those with other immune deficiencies.

Acquired Immunodeficiency Syndrome↗
PubMed1986

[Psoriasis in HTLV-III-induced immunologic defect--status of cellular immunity and immunohistologic findings].

Four patients suffering from immune deficiency related to HTLV III developed psoriasis vulgaris. All patients showed lymphadenopathy and cutaneous hypergy or anergy. In three of them, the count of peripheral helper cells was critically decreased (less than 400/microliter), and they showed oral candidosis. One patient suffered from disseminated Kaposi's sarcoma and developed pneumocystis carinii pneumonia. The psoriasis was extensive, exsudative, and almost refractory to therapeutical approaches. The bulk of dermal infiltrating mononuclear cells were T lymphocytes, mostly the T 8 positive phenotype. The majority of these cells were HLA-DR positive, so were many epidermal cells. OKT6 positive epidermal Langerhans' cells were not diminished. Thus we observed the development of psoriasis in spite of severe disturbances of cellular immunity. We suppose that immune mechanisms mediated by T cells--after having got out of control--might play some role in the pathogenesis of the disease.

Acquired Immunodeficiency Syndrome↗
PubMed1985

Prevalence of antibodies to human T-lymphotropic virus-III (HTLV-III) in hemophiliacs and other patients chronically substituted with blood products.

The prevalence of antibodies to human T-lymphotropic virus III (HTLV-III) was determined in a total of 140 hemophiliacs and 36 polytransfused patients from three medical centers by an enzyme linked immunosorbent assay (ELISA) and confirmatory tests. 58 hemophiliacs (41.4%) were seropositive. In all instances where the origin of the coagulation factors given to these patients could be determined, blood products came from the United States. In addition, 2 of 36 polytransfused patients, mostly with acute leukemias, who were transfused with blood products from local donors were positive for HTLV-III antibodies. No HTLV-III antibodies were detected in 237 blood donors selected in part from the donor pool of the polytransfused patients.

Antibodies, Viral↗
PubMed1985

Immunopathology of AIDS (acquired immune deficiency syndrome) observations in 75 patients with pre-AIDS and AIDS.

Sequential changes in the morphology of immunocompetent and other organs, in the accompanying immunocytological and immunovirological measurements are described in 75 patients with lymphadenopathy syndrome and with AIDS. The data presented demonstrate a stepwise development of the disease from a hyperimmunization syndrome to T-cell immune deficiency. Excessive antigenic stimulation by a large number of infectious organisms or by transfusion of blood and blood products account for antigenic overloading and hyperimmunization. Among such infectious organisms are certain viruses which per se interfere with cells of the immune system as for instance Epstein-Barr virus, cytomegalovirus, and HTLV3. Developing immunological incompetence will favor the persistence of these and other infectious organisms enhancing the damage of the immune reactivity and finally allow lethal infections or malignant tumors to occur.

Acquired Immunodeficiency Syndrome↗