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Journal articles on the topic 'Zidovudin'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Kis, Heitzmann, Keusch, and Möddel. "Schwere Anämie im Rahmen der Zidovudin-Behandlung bei HIV-Erkrankung." Praxis 95, no. 4 (January 1, 2006): 119–22. http://dx.doi.org/10.1024/0369-8394.95.4.119.

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Eine 34-jährige Patientin mit einer HIV-Erkrankung im Stadium C3 nach CDC-Klassifikation wurde uns wegen einer symptomatischen Anämie zugewiesen. Die Patientin wurde seit 18 Monaten mit einer antiretroviralen Therapie mit Nukleosidanaloga (Combivir®: Zidovudin , Lamivudin) und HIV-Protease-Inhibitoren (Kaletra®: Lopinavir, Ritonavir) behandelt. Es wurde eine schwere hypoproliferative, makrozytäre Anämie (Hämoglobin 3.0 g/dl) festgestellt. Eine Blutungsanämie und ein Eisen-, Vitamin-B12- oder Folsäuremangel wurden ausgeschlossen. Die Knochenmarksuntersuchung zeigte bei fehlenden peripheren Retikulozyten eine isoliert verminderte Erythropoese bei ansonsten unauffälligen, normalreifenden Zellreihen. Es wurde die Diagnose einer Zidovudin-induzierten Pure red cell aplasia gestellt. Nach Absetzen von Zidovudin und Umstellung der antiretroviralen Therapie erholte sich die Erythropoese mit Normalisierung des Hämoglobin.

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2

Hirschel, B. "Indikationen und Kontraindikationen von Zidovudin." DMW - Deutsche Medizinische Wochenschrift 114, no. 34 (March 25, 2008): 1289–93. http://dx.doi.org/10.1055/s-2008-1066756.

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3

Kara, Ahu, Nuri Bayram, and İlker Devrim. "Postpartum Antiretroviral Prophylaxis with Zidovudine, Lamivudine, and Nevirapine during Intrapartum HIV Infection." Journal of Pediatric Infection 9, no. 4 (December 30, 2015): 178–80. http://dx.doi.org/10.5152/ced.2015.1714.

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4

Anggriani, Ani, Ida Lisni, and Olga Susana Liku. "POLA PENGGUNAAN OBAT ANTIRETROVIRAL (ARV) PADA RESEP PASIEN RAWAT JALAN DARI KLINIK HIV/AIDS SALAH SATU RUMAH SAKIT SWASTA DI KOTA BANDUNG." Jurnal Riset Kefarmasian Indonesia 1, no. 1 (January 19, 2019): 64–81. http://dx.doi.org/10.33759/jrki.v1i1.10.

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ABSTRACT The Human Immunodeficiency Virus (HIV) continues to be a major global public health issue, which targets the human immune system. The using of ARVs in the treatment of HIV / AIDS increased life expectancy for PLHIV (People With HIV / AIDS). This study aims to determine the description of the using of ARV drugs in outpatients of the HIV / AIDS Clinic and assessed their suitability with established treatment standards. This research was carried out in a descriptive non-experimental manner, with data collection carried out retrospectively, used patient prescription data from April to December 2017. The results of quantitative studies showed 87% were male patients, and the largest age group was 20-29 years (39%) . Class of antiretroviral drugs used were Nucleoside / Nucleotide Reverse Transcriptase Inhibitors (NRTIs), Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs), and Protease Inhibitors (PI), with a combination of antiretroviral drugs most was the combination of first-line tenofovir + lamivudine + efavirenz (69%) while the second-line drug zidovudine + lamivudine + lopinavir / ritonavir was 1%. The most commonly used comorbid drug was cotrimoxazole. For qualitative data, the accuracy of combination and dose of ARV drugs was 100% in accordance with Permenkes No. 87/ 2014, with 79% of patients adhered to antiretroviral treatment every month. The potential for most ARV drug interactions with other drugs for the moderate category was zidovudin + cotrimoxazole (11%) which occured pharmacokinetically by decreasing renal clearance of zidovudine and glucuronide metabolites. In conclusion, the pattern of used of ARV drugs had met the standard of Permenkes No.87/2014, with the most used were the first line combination of tenofovir + lamivudine + efavirenz.

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5

Rosaria, Iraisa. "Perbandingan Kadar CD4 dan Total Lymphocyte Count dengan Kombinasi Highly Active Antiretroviral Therapy pada pasien HIV/AIDS di RSUP Dr.Kariadi Semarang." Jurnal Kesehatan Andalas 9, no. 1 (April 30, 2020): 59. http://dx.doi.org/10.25077/jka.v9i1.1223.

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Tujuan: Membuktikan perbedaan jenis pemberian kombinasi Highly Active Antiretroviral Therapy dengan perubahan kadar CD4 dan Total Lymphocyte Count pada pasien HIV/AIDS di RSUP Dr. Kariadi Semarang. Metode: Penelitian ini bersifat analitik yang dilakukan dengan rancangan studi potong lintang. Sampel diambil secara total sampling, yaitu seluruh pasien HIV/ AIDS yang berobat di RSUP Dr. Kariadi Semarang selama 2018 sampai 2019 yang memenuhi kriteria inklusi dan mendapat pengobatan salah satu dari kombinasi Highly Active Antiretroviral Therapy (HAART). Keenam jenis kombinasi HAART tersebut adalah kombinasi I (Efavirens+ Lamivudin+ Tenofovir), II (Evafirenz+ Lamivudin+Zidovudin), III(Nevirapine+ Lamivudin+ Tenofovir), IV (Lamivudine+Zidovudine+Nevirapine), V (Lamivudine+Tenofovir+Rilvipirine), VI (Tenofovir+ Rilvipirine+ Emtricitabine). Data dikumpulkan dari rekam medis pasien dan dianalisis dengan uji Kruskal-Wallis. Hasil: Dari 89 pasien, didapatkan keenam kombinasi HAART tersebut memberikan efikasi yang baik berdasarkan kenaikan jumlah CD4 dan TLC rerata. Ada perbedaan kenaikan CD4 rerata yang bermakna pada pasien HIV/AIDS antara yang mendapat obat HAART kombinasi I (p = 0,038), II (p = 0,034), IV (p = 0,001), V (p = 0,040), VI (p = 0,006). Pada Total Lymphocyte Count (TLC) didapatkan perbedaan kenaikan rerata (p< 0,05) pada semua kombinasi HAART. Simpulan: Tidak ada perbedaan jenis pemberian kombinasi Highly Active Antiretroviral Therapy dengan perubahan kadar CD4 dan Total Lymphocyte Count (p> 0,05) pada pasien HIV / AIDS di RSUP Dr. Kariadi Semarang.Kata kunci: CD4, highly active antiretroviral therapy, ODHA, total lymphocyte count

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6

Kusumayanti, Ratu Ratih, Evy Yunihastuti, Dyah Purnamasari, F. Witjaksono, and Esthika Dewiasty. "Faktor-Faktor yang Berperan terhadap Terjadinya Lipodistrofi pada Pasien HIV yang Mendapatkan Terapi Antiretroviral Lini Pertama." Jurnal Penyakit Dalam Indonesia 2, no. 4 (February 1, 2017): 223. http://dx.doi.org/10.7454/jpdi.v2i4.90.

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Pendahuluan. Seiring dengan perkembangan antiretroviral, harapan hidup pasien HIV terus meningkat namun menjadi rentan terhadap efek samping pengobatan. Salah satu efek samping pengobatan adalah sindrom lipodistrofi, meliputi lipoatrofi, lipohipertrofi, atau gabungan keduanya. Faktor risiko yang dikaitkan dengan lipodistrofi pada HIV adalah usia, jenis kelamin, lama terapi antiretroviral, CD4 awal, Stadium HIV, dan pemakaian Stavudin. Belum ada publikasi di Indonesia yang meneliti kejadian lipodistrofi pada populasi pasien HIV yang mendapat terapi ARV lini pertama serta faktor-faktor yang memengaruhinya. Berdasarkan hal tersebut, penelitian ini dilakukan untuk mengetahui kejadian lipodistrofi pada pasien HIV dalam terapi ARV lini pertama berbasis Stavudin dan Zidovudin minimal 6 bulan serta faktor-faktor yang memengaruhinya yang berobat di Pokdisus RSCM.Metode. Penelitian dilakukan dengan desain potong lintang dan kasus kontrol untuk mengetahui prevalensi lipodistrofi pada pasien HIV dengan ARV lini pertama serta faktor-faktor yang memengaruhinya. Analisis statistik menggunakan uji chi square atau uji Kolmogrof Smirnoff untuk mendapatkan hubungan antara masing-masing faktor risiko dengan terjadinya lipodistrofi. Analisis multivariat dilakukan dengan regresi logistik.Hasil. Sebanyak 346 pasien terlibat dalam penelitian ini. Didapatkan prevalensi lipodistrofi sebesar 27,5%, dengan rincian 70,5% lipoatrofi, 8,4% lipohipertrofi, dan 21,1% gabungan keduanya. Lokasi lipoatrofi terbanyak di daerah wajah. Prevalensi lipodistrofi pada subjek yang menggunakan Stavudin sebesar 43.3%, dan Zidovudin sebesar 10,7%. Faktor yang berhubungan dengan kejadian lipodistrofi adalah penggunaan Stavudin [p= <0,001; adjusted OR 5,34 IK95% (2,59 – 10.98)].Simpulan. Didapatkan prevalensi Lipodistrofi pada pasien HIV yang mendapatkan terapi ARV lini pertama adalah 27.5%, dan didapatkan hubungan antara kejadian lipodistrofi pada pasien HIV dengan penggunaan Stavudin.

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7

Mossdorf and Hirsch. "Adhärenz, pharmakokinetischer «Toleranzbereich» und HIV-Resistenzbildung." Praxis 95, no. 33 (August 1, 2006): 1237–39. http://dx.doi.org/10.1024/0369-8394.95.33.1237.

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Anlässlich einer Kontrolle wird bei einem 43-jährigen, HIV-positiven Patienten mit ART neu eine HIV-Viruslast von 2032 Kopien/mL festgestellt. Zuvor war unter einer Therapie mit Lamivudin und Zidovudin (NRTI) sowie Nelfinavir (nicht-geboosteter PI) die Viruslast während 18 Monaten undetektierbar (< 50 Kopien/mL). Es konnte die Diagnose einer sekundären HIV-Resistenz des ungeboosteten PIs bei pharmakokinetischer Non-Adhärenz gestellt werden. Die HIV-Resistenzprüfung legte eine Salvage-Therapie mit einem geboosteten PI nahe. Neben der regelmässigen Medikamenteneinnahme erbringen diese antiretroviralen Medikamente mit ihren hohen Serumspiegeln und langen Halbwertszeiten eine dauerhafte Virussuppression und vermindern das Risiko von Resistenzentwicklungen.

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8

GONCHIKOVA, YU A., N. V. CHMELEVSKAYA, and E. A. ILLARIONOVA. "ANALYSIS OF MIXED COMBINATIONS OF MEDICINAL PRODUCTS BASED ON ABAKAVIR, LAMIVUDIN, ZIDOVUDIN USING THE METHOD OF MICROCOLONIES LIQUID CHROMATOGRAPHY." Kuban Scientific Medical Bulletin 25, no. 3 (July 26, 2018): 46–50. http://dx.doi.org/10.25207/1608-6228-2018-25-3-46-50.

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Aim.To develop a technique for the detection and separation of abacavir, lamivudine, zidovudine, both individually and combined with adaptol, azaleptin, analgin, amitriptyline, haloperidol, melipramine, neuleptil, phenobarbital, fluoxetine, and chlorprotixen using high performance liquid chromatography (HPLC).Materials and methods. A column filled with ProntoSIL-120-5-C18 AQ was used, eluting with A [0.2 M lithium perchlorate − 0.005 M perchloric acid] − water (5: 95); eluent B is acetonitrile. Chromatography conditions: a linear gradient of the solvent is 3700 μl from 5 to 70% at a flow rate of 100 μl / min. The temperature of the column was 40°C. The results were processed with the help of the computer program MultiChrome (ZAO Ampersend, Moscow).Results. The method of separation and detection of combinations of abacavir, lamivudine, zidovudine with adaptol, azaleptin, analgin, amitriptyline, haloperidol, melipramine, neuleptil, phenobarbital, fluoxetine and chlorprotixene by reversed-phase high-performance liquid chromatography was developed.Conclusion. The developed technique allows detecting abacavir, zidovudine, lamivudine with the help of the HPLC method after isolation from urine separately or at combined poisonings with adaptolom, azaleptinom, dipyrone, amitriptilinom, galoperidolom, melipraminom, neuleptilom, phenobarbital, fluoxetine and hlorprotiksenom

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9

AR, Indrati, Van Crevel R, Sumantri R, and Wisaksana R. "KADAR PENERIMA TRANSFERIN TERLARUT (sTFR) DI PENDERITA HIV/AIDS DENGAN ANEMIA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 15, no. 3 (March 16, 2018): 105. http://dx.doi.org/10.24293/ijcpml.v15i3.963.

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Anemia is the most common hematologic abnormality associated with HIV which affecting 60 to 80 percent of patients in the latestage of the disease. The presence of anemia is associated with increased of morbidity and mortality in patients with HIV infection. Irondeficiency, chronic inflammation and antiretroviral treatment (ACT) may cause HIV associated anemia. The differentiation of irondeficiency anemia from chronic disease anemia is a diagnostic challenge. Maybe it is helpful in soluble transferrin receptor (sTfR), thecleaving of the extra cellular domain related to transferrin receptor. Because the elevated sTfR concentration is a marker of tissue irondeficiency and increased marrow erythropoietin activity. The aim of this study was to examine the diagnostic value of soluble transferrinreceptor level in anemia patients with HIV/AIDS. The Study was the part of the IMPACT (Integrated Management for Prevention, Controland Treatment of HIV/AIDS) baseline and cohort study. The study started since September 2007 in RSUP Hasan Sadikin Bandung.There were 179 HIV/AIDS patients with anemia included in this study. Complete blood count, reticulocytes, feritin, soluble transferringreceptor and hsCRP were tested in these patients. It was found that the mean of sTfR in HIV patients with anemia were 1238.42U/mL(304.5-30435). sTfR had a low correlation with MCV (r -0.174), feritin (r -0.65) and absolute reticulocyte counting (r 0.172). Feritinhad moderate and significant correlation with hsCRP (r:0.429; p 0.00). There was no significant difference of sTfR level between thepatients without ART, with Zidovudin and d4T (p 0.81). There was no significance difference of sTfR concentration between the low andnormal MCV level (p 0.341). sTfR can not differentiate the source of anemia in patients with HIV/AIDS. It can be concluded so far thatchronic disease and inflammation as reflected by the elevated hsCRP level and use of zidovudine are the main cause of anemia.

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10

Wunder and Evison. "Antiretrovirale Medikamente und Schwangerschaft." Therapeutische Umschau 62, no. 1 (January 1, 2005): 37–42. http://dx.doi.org/10.1024/0040-5930.62.1.37.

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Während die vertikale Transmissionsrate bei unbehandelten HIV-positiven Müttern rund 30% beträgt, konnte 1994 durch Zidovudin (Retrovir®) eine um knapp 70% reduzierte vertikale Transmission auf 10.4% gezeigt werden. Damit kam es zum Durchbruch der antiretroviralen Therapie in der Schwangerschaft. Von großer Bedeutung ist die für jede Patientin individualisierte, optimale antiretrovirale Kombinations-Therapie, die idealerweise im zweiten Trimenon oder bei mütterlicher Indikation oder sehr hohem Viral load bereits im ersten Trimenon begonnen wird. Außerdem sollte als zusätzliche Prävention der vertikalen Transmission eine intravenöse Zidovudintherapie unter der Geburt und für das Neugeborene per os während vier Wochen postnatal gegeben werden. Wenn zusätzlich ein Kaiserschnitt am wehenlosen Uterus ohne vorzeitigen Blasensprung erfolgt, kann die Übertragungsrate der HIV-Infektion von der Mutter auf das Kind auf unter 2% gesenkt werden. Langzeitdaten zur Sicherheit der antiretroviralen Therapie nach intrauteriner Gabe zeigen mit wenigen Ausnahmen weder ein teratogenes Potential beim Menschen noch Langzeitschäden. Kritisch ist die Situation in den Entwicklungsländern, wo aus logistischen und Kostengründen die optimale antiretrovirale Therapie der HIV-positiven Schwangeren sowie das primäre Abstillen nicht realisiert werden können und es nach wie vor zu hohen vertikalen Transmissionsraten kommt. Deshalb werden immer häufiger antiretrovirale Kurzprotokolle entwickelt mit immerhin rund 50-prozentiger Reduktion der vertikalen Transmission. Die Betreuung von HIV positiven Schwangeren sollte interdisziplinär erfolgen.

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11

Kinpara, Shuichi, Mami Kijiyama, Ayako Takamori, Atsuhiko Hasegawa, Amane Sasada, Takao Masuda, Yuetsu Tanaka, Atae Utsunomiya, and Mari Kannagi. "Interferon-α (IFN-α) suppresses HTLV-1 gene expression and cell cycling, while IFN-α combined with zidovudin induces p53 signaling and apoptosis in HTLV-1-infected cells." Retrovirology 10, no. 1 (2013): 52. http://dx.doi.org/10.1186/1742-4690-10-52.

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12

Giovannini, M., G. V. Zuccotti, V. Locatelli, and E. Riva. "Combined Zidovudine and Interferon-α2a Therapy in Children with Acquired Immune Deficiency Syndrome." Journal of International Medical Research 20, no. 3 (June 1992): 295–301. http://dx.doi.org/10.1177/030006059202000312.

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A study was carried out in five children with acquired immune deficiency syndrome to assess the effect of combined zidovudine/interferon-α2a therapy with that of zidovudine given alone on immunological profiles and plasma zidovudine concentrations. Immunoglobulins A, G and M, total and absolute CD4 lymphocyte counts, and p24 antigen concentrations did not differ significantly when children were treated with 300 mg/m2 zidovudine given orally once every 12 h, or with 150 mg/m2 zidovudine plus 1.5 or 3 MIU interferon-α2a given intramuscularly three times weekly. Peak plasma zidovudine concentrations were significantly ( P < 0.05) lower when combined treatment with 150 mg/m2 zidovudine/1.5 MIU interferon-α2a was administered compared with 300 mg/m2 zidovudine alone, or combined 150 mg/m2 zidovudine/3 MIU interferon-α2a The results suggest that combination zidovudine/interferon-α2a therapy may be more efficacious than zidovudine alone and that the normal zidovudine dose may be reduced if interferon-α2a is given in addition, thus reducing the side-effects associated with zidovudine.

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13

&NA;. "Zidovudine see Probenecid/zidovudine." Reactions Weekly &NA;, no. 302 (May 1990): 12. http://dx.doi.org/10.2165/00128415-199003020-00052.

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14

&NA;. "Zidovudine see Ganciclovir/zidovudine." Reactions Weekly &NA;, no. 315 (August 1990): 8. http://dx.doi.org/10.2165/00128415-199003150-00041.

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15

Purvin, Shah, Parameswara Rao Vuddanda, Sanjay Kumar Singh, Achint Jain, and Sanjay Singh. "Pharmacokinetic and Tissue Distribution Study of Solid Lipid Nanoparticles of Zidovudine in Rats." Journal of Nanotechnology 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/854018.

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Zidovudine-loaded solid lipid nanoparticles (AZT-SLNs) and zidovudine in solution were prepared and administered in rats. The aim of this research was to study whether the bioavailability of zidovudine can be improved by AZT-SLNs perorally to rats as compared to oral administration of zidovudine. Zidovudine was determined in plasma and tissues by reverse phase high performance liquid chromatography. The pharmacokinetic parameters of zidovudine were determined after peroral administration: area under curve of concentration versus time (AUC) for AZT-SLNs was 31.25% greater than AZT solution; meanwhile mean resident time (MRT) was found to be 1.83 times higher for AZT-SLNs than AZT solution. Elimination half life of zidovudine was also increased for SLN formulation. Tissue distribution pattern of zidovudine was changed in case of AZT-SLNs. AUC of zidovudine in brain and liver was found to be approximately 2.73 and 1.77 times higher in AZT-SLNs than AZT solution, respectively, indicating that AZT-SLNs could cross blood brain barrier. Distribution of zidovudine was approximately 0.95 and 0.86 times lesser in heart and kidney, respectively. It can be concluded from the study that oral administration of AZT-SLNs modifies the plasma pharmacokinetic parameters and biodistribution of zidovudine.

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Burger, David M., Pieter L. Meenhorst, Cornells H. W. Koks, and Jos H. Beijnen. "Pharmacokinetics of Zidovudine and Acetaminophen in a Patient on Chronic Acetaminophen Therapy." Annals of Pharmacotherapy 28, no. 3 (March 1994): 327–30. http://dx.doi.org/10.1177/106002809402800306.

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OBJECTIVE: To report a case of a potential interaction between acetaminophen and zidovudine in a patient who had used high daily doses of acetaminophen over many years. CASE SUMMARY: A 43-year-old man presented with HIV-1 infection, recurrent oral candidiasis, and chronic use of acetaminophen, codeine, and diazepam before he started zidovudine therapy. Although literature was available regarding short-term combined use of acetaminophen and zidovudine, information was lacking on zidovudine therapy and kinetics after long-term use of acetaminophen. Acetaminophen and zidovudine pharmacokinetics were determined on several occasions. The results showed extremely rapid absorption of both drugs (tmax, the time to reach maximum concentration. 10–15 minutes for acetaminophen and 15–20 minutes for zidovudine) and, consequently, relatively high maximum plasma concentration (Cmax). No influence on other pharmacokinetic parameters of either drug could be detected. Because the effect of high Cmax values of zidovudine is unknown, the patient was treated with a third of the dose of zidovudine used at that time (zidovudine 100 mg q6h). No toxicity or opportunistic infections developed within the next 8 months, after which the patient died of a cause unrelated to HIV infection. DISCUSSION: The observed pharmacokinetic profiles of both drugs are discussed and compared with two studies dealing with zidovudine therapy in combination with short-term use of acetaminophen and with a case report of acetaminophen-induced hepatotoxicity during concomitant use of zidovudine. CONCLUSIONS: Long-term use of acetaminophen may accelerate the absorption of zidovudine. Although other causes cannot be ruled out, there was no influence on other pharmacokinetic parameters of zidovudine. No influence of zidovudine on acetaminophen concentrations was found. Combined use of zidovudine 100 mg q6h and acetaminophen 500 mg q4h appeared to be safe and effective for at least eight months.

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Lee, B. L., S. Safrin, V. Makrides, and J. G. Gambertoglio. "Zidovudine, trimethoprim, and dapsone pharmacokinetic interactions in patients with human immunodeficiency virus infection." Antimicrobial Agents and Chemotherapy 40, no. 5 (May 1996): 1231–36. http://dx.doi.org/10.1128/aac.40.5.1231.

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Zidovudine is widely prescribed for the treatment of human immunodeficiency virus (HIV) infection. Trimethoprim and dapsone are commonly used in the management of Pneumocystis carinii pneumonia in HIV-infected patients. To examine the pharmacokinetic interactions among these drugs, eight HIV-infected patients (26 to 43 years old) with a mean CD4 count of 524.4 +/- 405.7 cells per mm3 received zidovudine (200 mg), trimethoprim (200 mg), and dapsone (100 mg) as single agents and in two- and three-drug combinations. Blood and urine samples were collected at a specified time and analyzed for zidovudine, zidovudine-glucuronide, trimethoprim, dapsone, and monoacetyl-dapsone concentrations under single-dose and steady-state conditions. Zidovudine did not influence the pharmacokinetic disposition of dapsone or trimethoprim. Dapsone had no effect on the pharmacokinetic disposition of zidovudine. Trimethoprim significantly decreased the renal clearance of zidovudine by 58% (5.0 +/- 1.8 versus 2.1 +/- 0.5 ml/min/kg of body weight [P < 0.05]). There was a concurrent 54% decrease in the mean urinary recovery of zidovudine (11.7 +/- 3.5 versus 5.4 +/- 3.0 [P < 0.05]), and the metabolic ratio was decreased by 78% (0.32 +/- 0.4 versus 0.07 +/- 0.05 [P < 0.05]). The mean area under the concentration-time curve from 0 to 6 h of the zidovudine-glucuronide/ zidovudine ratio was unchanged. We conclude that zidovudine, trimethoprim, and dapsone can be coadministered to patients with AIDS without significant pharmacokinetic interaction. However, in AIDS patients with liver impairment and impaired glucuronidation, doses of zidovudine may need to be decreased.

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Gass, Rebekah JA, Dave Shugarts, Russell Young, Michael Allen, Mary Rosandich, and Daniel R. Kuritzkes. "Emergence of Dual Resistance to Zidovudine and Lamivudine in Clinical HIV-1 Isolates from Patients Receiving Zidovudine/Lamivudine Combination Therapy." Antiviral Therapy 3, no. 2 (February 1998): 97–102. http://dx.doi.org/10.1177/135965359800300204.

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Susceptibility to zidovudine and lamivudine was determined on human immunodeficiency virus type 1 (HIV-1) isolates obtained from patients who added lamivudine after 6 months of treatment with zidovudine. Lamivudine-resistant isolates that were also zidovudine-resistant were recovered from 13/16 (81%) patients after 6 months of dual therapy. In contrast to findings in anti-retroviral therapy-naive patients, these results suggest that dual resistance to zidovudine and lamivudine emerges relatively quickly when lamivudine is added to zidovudine as a single agent in the majority of patients with extensive prior zidovudine treatment.

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Peyclit, Lucie, Maryem Ben Khedher, Lotfi Zerrouki, Seydina M. Diene, Sophie Alexandra Baron, and Jean-Marc Rolain. "Inactivation of thymidine kinase as a cause of resistance to zidovudine in clinical isolates of Escherichia coli: a phenotypic and genomic study." Journal of Antimicrobial Chemotherapy 75, no. 6 (February 26, 2020): 1410–14. http://dx.doi.org/10.1093/jac/dkaa057.

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Abstract Objectives The antiviral zidovudine has been recently identified as an active drug against resistant Enterobacteriaceae, but prevalence of resistance to this compound remains unknown. The aim was to estimate the prevalence of clinical Escherichia coli isolates resistant to zidovudine and to decipher the mechanism of zidovudine resistance. Methods We screened 537 isolates on zidovudine-containing agar plates and studied their thymidine kinase (tdk) gene sequences, the putative target involved in zidovudine resistance. Moreover, sequence analysis of 633 complete genomes of E. coli was performed to investigate mutation in the tdk gene. A comparative genomic analysis was done on an in vitro zidovudine-resistant mutant. Results After screening on our medium containing 2.7 mg/L (10 μM) zidovudine, nine strains had a zidovudine MIC >26.7 mg/L. The gene was absent in three isolates, inactivated by an IS (IS1X2 and ISApl1) in two isolates and mutated in four isolates. A genomic analysis of 633 E. coli genomes showed heterogeneity of the tdk gene sequence, with 27 different sequences. Among them, three genomes showed an inactivation of the gene (IS, stop codon and no tdk gene sequence). The in vitro mutant E. coli had 27 SNPs in eight genes of the core genome compared with the initial strain. Conclusions Our study reports zidovudine-resistant clinical isolates of E. coli, presumably related to tdk inactivation. Diversity of Tdk in bacterial genomes can be large. Other mechanisms need to be considered in zidovudine resistance. The use of zidovudine in antibiotic-resistant infections needs to be in combination and should be tested before clinical administration.

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Polis, M. A., S. C. Piscitelli, S. Vogel, F. G. Witebsky, P. S. Conville, B. Petty, J. A. Kovacs, et al. "Clarithromycin lowers plasma zidovudine levels in persons with human immunodeficiency virus infection." Antimicrobial Agents and Chemotherapy 41, no. 8 (August 1997): 1709–14. http://dx.doi.org/10.1128/aac.41.8.1709.

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The use of antiretroviral agents and drugs for the treatment and prophylaxis of opportunistic infections has lengthened the survival of persons with AIDS. In the era of multidrug therapy, drug interactions are important considerations in designing effective and tolerable regimens. Clarithromycin has had a significant impact on the treatment of disseminated Mycobacterium avium complex infection, and zidovudine is the best-studied and one of the most widely used antiretroviral agents in this population. We conducted a study to determine the maximally tolerated dose of clarithromycin and the pharmacokinetics of clarithromycin and zidovudine individually and in combination. Mixing studies were conducted to simulate potential interaction in the gastric environment. The simultaneous administration of zidovudine and clarithromycin had little impact on the pharmacokinetics of clarithromycin or of its major metabolite. However, coadministration of zidovudine and clarithromycin at three doses (500 mg orally [p.o.] twice daily [b.i.d.], 1,000 mg p.o. b.i.d., and 2,000 mg p.o. b.i.d.) reduced the maximum concentration of zidovudine by 41% (P < 0.005) and the area under the concentration-time curve from 0 to 4 h for zidovudine by 25% (P < 0.05) and increased the time to maximum concentration of zidovudine by 84% (P < 0.05), compared with zidovudine administered alone. Mixing studies did not detect the formation of insoluble complexes due to chelation, suggesting that the decrease in zidovudine concentrations results from some other mechanism. Simultaneous administration of zidovudine and clarithromycin appears to decrease the levels of zidovudine in serum, and it may be advisable that these drugs not be given at the same time. Drug interactions should be carefully evaluated in persons with advanced human immunodeficiency virus infection who are receiving multiple pharmacologic agents.

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Callender, Diana P., Nalini Jayaprakash, Aaron Bell, Vidmantas Petraitis, Ruta Petratienes, Myrna Candelario, Robert Schaufele, et al. "Pharmacokinetics of Oral Zidovudine Entrapped in Biodegradable Nanospheres in Rabbits." Antimicrobial Agents and Chemotherapy 43, no. 4 (April 1, 1999): 972–74. http://dx.doi.org/10.1128/aac.43.4.972.

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ABSTRACT The pharmacokinetic profile of oral zidovudine entrapped in a 50:50 polyactide-coglycolide matrix (nanospheres) was compared to those of standard oral and parenteral zidovudine formulations in rabbits. The bioavailability of zidovudine nanospheres at 50 mg/kg of body weight was 76%, and this dose achieved prolonged exposure to zidovudine compared to standard formulations without an increase in the drug’s peak concentration.

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Messori, Andrea, Paola Becagli, Valeria Berto, Sabrina Trippoli, Maria Font, Francesca Tosolini, Francesca Venturini, and Nello Martini. "Advanced HIV Infection Treated with Zidovudine Monotherapy: Lifetime Values of Absolute Cost—Effectiveness as a Pharmacoeconomic Reference for Future Studies Evaluating Antiretroviral Combination Treatments." Annals of Pharmacotherapy 31, no. 12 (December 1997): 1447–54. http://dx.doi.org/10.1177/106002809703101201.

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OBJECTIVE: This study was undertaken to evaluate the cost and the effectiveness of zidovudine monotherapy in patients with advanced HIV infection and to derive preliminary data on the cost—effectiveness of the triple treatment with saquinavir plus zalcitabine plus zidovudine compared with zidovudine alone. DESIGN: We used a combined method of survival analysis utilizing both the quality-adjusted time without symptoms or toxicity (Q-TWIST) method and the Gompertz approach. This combined method was applied to assess the absolute cost-effectiveness and cost—utility ratios of zidovudine monotherapy and to perform a preliminary incremental cost—effectiveness comparison of saquinavir plus zalcitabine plus zidovudine versus zidovudine alone. The clinical material used in our study was derived from two reports on the treatment of advanced HIV infection. Data of lifetime costs of HIV infection were obtained from published information. RESULTS: In patients with advanced HIV infection treated with zidovudine monotherapy, lifetime survival was 252.1 discounted person-years per 100 patients. Using an average lifetime cost of $93 000 (discounted) per individual, the absolute ratio of cost—effectiveness for zidovudine monotherapy was $36 980 per life-year, while the absolute cost—utility ratio was $47 112 per quality-adjusted life-year. In the comparative analysis of saquinavir plus zalcitabine plus zidovudine versus zidovudine alone, our calculations showed that the administration of the triple treatment can have an “average” cost—effectiveness, provided that mean lifetime survival per patient (discounted) is improved to at least 3.68 years (with an average survival gain of at least 14 mo per patient). CONCLUSIONS: The values of absolute cost—effectiveness and cost—utility ratios for zidovudine monotherapy are a useful reference point for further pharmacoeconomic studies in the area of antiretroviral drugs.

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Van Harken, D. R., J. C. Pei, J. Wagner, and I. M. Pike. "Pharmacokinetic interaction of megestrol acetate with zidovudine in human immunodeficiency virus-infected patients." Antimicrobial Agents and Chemotherapy 41, no. 11 (November 1997): 2480–83. http://dx.doi.org/10.1128/aac.41.11.2480.

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This nonrandomized, two-period crossover study was performed to assess whether concomitant administration of megestrol acetate influences the steady-state pharmacokinetics of zidovudine and its inactive 5'-O-glucuronide metabolite. Twelve HIV-positive, asymptomatic male volunteers received a 100-mg oral capsule dose of zidovudine at least 30 min before meals five times a day at 0700, 1100, 1500, 1900, and 2300 h on study days 1 to 3 and a single 100-mg dose at 0700 h on day 4. On days 5 to 17, 800 mg of megestrol acetate, as a 40-mg/ml aqueous suspension, was administered orally immediately before the 0700 h dose of zidovudine. On days 5 to 16, zidovudine was also administered at 1100, 1500, 1900, and 2300 h. Serial blood samples were collected for 12 h after the single 100-mg dose of zidovudine on days 4 and 17; trough samples were also obtained just before the 0700 h dose on days 2 to 4 and 15 to 17. Levels of zidovudine and its glucuronide in plasma were assayed by a validated radioimmunoassay. Statistical analysis of trough plasma level data indicated that steady-state levels of zidovudine and its glucuronide in plasma had been attained when pharmacokinetic assessments were made on days 4 and 17. When megestrol acetate and zidovudine were coadministered for 13 days, differences of -14, -6.5, and -4.6% in mean zidovudine peak concentration and areas under the curve at 0 to 4 and 0 to 12 h, respectively, +22.5% in mean trough concentration, +2.6% in mean plasma half-life, and no change in median time to peak were observed compared to conditions when zidovudine was administered alone; for zidovudine 5'-O-glucuronide the respective differences were -9, -7.3, -4.4, +2.3, and +10% and no change. None of the differences were statistically significant (P > 0.05). Concomitant therapy with megestrol acetate, at the dose employed to treat anorexia, cachexia, or an unexplained, significant weight loss in AIDS patients, did not alter the steady-state pharmacokinetics of zidovudine or its 5'-O-glucuronide metabolite.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 770 (September 1999): 12. http://dx.doi.org/10.2165/00128415-199907700-00038.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 437 (February 1993): 12. http://dx.doi.org/10.2165/00128415-199304370-00056.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 438 (February 1993): 12. http://dx.doi.org/10.2165/00128415-199304380-00051.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 444 (March 1993): 12. http://dx.doi.org/10.2165/00128415-199304440-00056.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 445 (April 1993): 12. http://dx.doi.org/10.2165/00128415-199304450-00064.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 448 (April 1993): 16. http://dx.doi.org/10.2165/00128415-199304480-00074.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 449 (May 1993): 12. http://dx.doi.org/10.2165/00128415-199304490-00052.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 450 (May 1993): 16. http://dx.doi.org/10.2165/00128415-199304500-00076.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 455 (June 1993): 12. http://dx.doi.org/10.2165/00128415-199304550-00057.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 464 (August 1993): 12. http://dx.doi.org/10.2165/00128415-199304640-00068.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 467 (September 1993): 12. http://dx.doi.org/10.2165/00128415-199304670-00058.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 474 (October 1993): 12. http://dx.doi.org/10.2165/00128415-199304740-00055.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 431 (December 1992): 12. http://dx.doi.org/10.2165/00128415-199204310-00057.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 286 (February 1990): 11. http://dx.doi.org/10.2165/00128415-199002860-00042.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 287 (February 1990): 8. http://dx.doi.org/10.2165/00128415-199002870-00033.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 292 (March 1990): 8. http://dx.doi.org/10.2165/00128415-199002920-00038.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 298 (April 1990): 8. http://dx.doi.org/10.2165/00128415-199002980-00042.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 299 (May 1990): 12. http://dx.doi.org/10.2165/00128415-199002990-00058.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 307 (June 1990): 8. http://dx.doi.org/10.2165/00128415-199003070-00043.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 1081 (December 2005): 25–26. http://dx.doi.org/10.2165/00128415-200510810-00081.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 1088 (February 2006): 22. http://dx.doi.org/10.2165/00128415-200610880-00069.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 317 (September 1990): 8. http://dx.doi.org/10.2165/00128415-199003170-00048.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 323 (October 1990): 8. http://dx.doi.org/10.2165/00128415-199003230-00051.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 329 (December 1990): 8. http://dx.doi.org/10.2165/00128415-199003290-00041.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 331 (December 1990): 12. http://dx.doi.org/10.2165/00128415-199003310-00065.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 339 (February 1991): 16. http://dx.doi.org/10.2165/00128415-199103390-00082.

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&NA;. "Zidovudine." Reactions Weekly &NA;, no. 340 (March 1991): 8. http://dx.doi.org/10.2165/00128415-199103400-00036.

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