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Viral load measurement is also vulnerable to contamination purchase 500 mg aleve amex pain treatment center memphis. If other examinations such as CD4 T cell count is done in the same lab generic 250 mg aleve with amex phoenix pain treatment center, it is recommended to send a sep- arated EDTA tube generic 500 mg aleve brunswick pain treatment center brunswick ga. One study showed a 5- to 160-fold elevated viral load during active tuberculosis (Goletti 1996) order aleve 500 mg visa pacific pain treatment center san francisco. Viral load can also increase significantly during syphilis and declines after successful treatment (Buchacz 2004, Kofoed 2006, Palacios 2007). In a large retrospective study, 26% of transient viremia in patients on ART were caused by intercurrent infections (Easterbrook 2002). In these situations, deter- mining the viral load does not make much sense. As the peak occurs one to three weeks after immunization, routine measurements of viral load should be avoided within four weeks of immunization. It should be noted that not every increase is indicative of virologic treatment failure and resistance. Slight transient increases in viral load, or blips, are usually of no consequence, as numerous studies in the last few years have shown (see chapter on Goals and Principles of Therapy). The possibility of mixing up samples always has to be considered. Unusually implausi- ble results should be double-checked with the laboratory, and if no cause is found there, they need to be monitored – people make mistakes. Should there be any doubt on an individual result; the lab should be asked to repeat the measurement from the same blood sample. Viral kinetics on ART The introduction of viral load measurement in 1996-1997 fundamentally changed HIV therapy. The breakthrough studies by David Ho and his group showed that HIV infection has significant in vivo dynamics (Ho 1995, Perelson 1996). The changes in viral load on antiretroviral therapy clearly reflect the dynamics of the process of viral production and elimination. The concentration of HIV-1 in plasma is usually reduced by 99% as early as two weeks after the initiation of ART (Perelson 1997). In one large cohort, the viral load in 84% of patients was already below 1000 copies/ml after four weeks. The decrease in viral load follows biphasic kinetics. The higher the viral load at initiation of therapy, the longer it takes to drop below the level of detection. In one study, the range was between 15 days with a baseline viral load of 1000 and 113 days with a baseline of 1 million viral copies/ml (Rizzardi 2000). The following figure shows a typical biphasic decrease in viral load after initial high levels. Monitoring 249 Figure 1: Viral load kinetics during the first months on first-line ART. The grey values derive from 10 patients who achieved a sustained virological suppression, the black values from 3 patients in which resistance mutations occurred during primary therapy (all 3 had NNRTI-based regimens) Numerous studies have focused on whether durable treatment success can be predicted early (Thiebaut 2000, Demeter 2001, Kitchen 2001, Lepri 2001). In a study on 124 patients, a decrease of less than 0. According to another prospective study, it is possible to predict virologic response at 48 weeks even after 7 days (Haubrich 2011). However, this has little clinical relevance, and in our opinion it is pointless to start measurement of viral load only one or two weeks after initiation of therapy. Many studies have evaluated the question whether long-term virological success can be predicted at early phases (Thibaut 2000, Demeter, Kitchen 2011, Lepri 2001). Many of them suggest that changes during the first days after treatment initiation are major correlates of longer-term virological responses. In a study on 124 HIV+ patients initiating a PI-based ART, a decline of less than 0. In another prospec- tive trial, week 1 HIV-RNA change was associated with virologic failure above 50 copies/ml at weeks 24 and 48 (Haubrich 2011). However, such an early measurement is not clinical routine. We recommend meas- uring viral load every four weeks until it has dropped to below detection of 20– 50 copies/ml. Once that is achieved, measurement every three to four months is enough. Eventually, longer intervals are possible (Chaiwarith 2010). In case of rebound, closer monitoring becomes necessary. Within the first 4 weeks of therapy initiation the viral load should be reduced by a factor of 100, after 3-4 months (6 months if viral load was high) it should be below the level of detection. Viral load can also be measured fairly reliably in body fluids other than blood or plasma (for example cerebrospinal, vaginal or seminal fluid). However, such tests are usually per- formed for scientific purposes and are not officially licensed for other reasons. CD4 T cells CD4 T cells are T lymphocytes that express the CD4 receptor on their surface. This lymphocyte subpopulation is also referred to as T helper cells. Alongside viral load, measurement of the CD4 T cell level is the most important parameter or surrogate marker in HIV medicine. It allows for a reliable estimate of the individual risk of developing AIDS. Two reference values are generally accepted: above 400–500 CD4 T cells/µl, severe AIDS-related diseases are very rare; below 200 CD4 T cells/µl, the risk of AIDS-related morbidity increases significantly with increased duration of immunosuppression. Most AIDS-related illnesses occur below 100 CD4 T cells/µl. Several points should be considered when measuring CD4 T cells (usually by flow cytometry). The lower normal values are between 400 and 500 cells/µl, depending on the laboratory. Samples should always be sent to the same (experienced) laboratory. The same applies for viral load as for CD4 T cells: the higher the level, the greater the variability. In one study, the 95% confidence intervals with a real value of 500 cells/µl were between 297 and 841 cells/µl. At 200 CD4 T cells/µl, the 95% confidence interval was between 118 and 337 cells/µl (Hoover 1993). Measurement of CD4 T cells should only be repeated in the case of highly implau- sible values. As long as the viral load remains below the level of detection, there is no need to be concerned even with decreases in CD4 T cells.
SHORT a long-lasting beta 2-adrenoceptor agonist order 250mg aleve with amex pacific pain treatment center victoria, against methacholine- induced bronchoconstriction generic 500 mg aleve pain home treatment. Bronchodilating effect of formoterol but not of 5 salmeterol in two asthmatic patients buy 500 mg aleve joint and pain treatment center santa maria ca. Salbutamol dry powder 6-POWDER inhaler: efficacy purchase 250 mg aleve otc treatment for nerve pain from shingles, tolerability, and acceptability study. Long-term effects of inhaled beta 2-agonists on 1 bronchial hyperresponsiveness in asthmatics. Outcomes and humanistic issues related to treatment of 5 acute bronchospasm. Double-blind trial of a new bronchodilator in 3 asthmatic children. Assessing the effects of 4 racemic and single-enantiomer albuterol on airway secretions in long- term intubated patients. The effects of inhaled albuterol and salmeterol in 6-LONG VS. SHORT 2- to 5-year-old asthmatic children as measured by impulse oscillometry. Bricanyl Turbuhaler in the treatment of 6-POWDER asthma: a six week multi-centre study carried out in Sweden, the United Kingdom, Denmark, Norway and Finland. Tolerability of short-term, high-dose formoterol in healthy 5 volunteers and patients with asthma. Comparison between fenoterol and 6-DESIGN salbutamol in asthmatic patients. Palmqvist M, Balder B, Lowhagen O, Melander B, Svedmyr N, 6-LONG VS. Late asthmatic reaction decreased after pretreatment with salbutamol and formoterol, a new long-acting beta 2-agonist. Salmeterol is a partial beta-2- 5 agonist in relation to formoterol in asthmatic patients. Comparison of the relative 6 efficacy of formoterol and salmeterol in asthmatic patients. Quick-relief medications for asthma Page 103 of 113 Final Report Update 1 Drug Effectiveness Review Project Citation Exclusion Code Pansegrouw DF, Weich DJ, Le Roux FP. Airway reactivity is a determinant of bronchodilator 6 responsiveness after methacholine-induced bronchoconstriction. Effects of prolonged administration of 3 pirbuterol by mouth in chronic asthma. Patessio A, Podda A, Carone M, Trombetta N, Donner CF. SHORT effect and duration of action of formoterol aerosol on exercise-induced asthma. Variability of onset and 5 duration of effect of salmeterol and formoterol in patients with moderate and severe stable asthma. Formoterol--where does it fit in the current guidelines? Pauwels RA, Hargreave FE, Camus P, Bukoski M, Stahl E. A 1-year 6-POWDER comparison of turbuhaler vs pressurized metered-dose inhaler in asthmatic patients. SHORT medication in asthma: a worldwide safety and effectiveness trial. Pearlman D, Milgrom H, Andriano K, Feldman J, Ziehmer B. Long-acting beta 2-agonist salmeterol compared with 6-LONG VS. SHORT salmeterol with albuterol in the treatment of mild-to-moderate asthma. SHORT compared with salbutamol in large-scale multicentre studies. Cardiopulmonary 3 effects of terbutaline and a bronchodilator combination in chronic obstructive pulmonary disease. Comparison of 6-DELIVERY innovator and generic salbutamol inhalers: a double-blind randomized study of efficacy and tolerance. Pleskow W, LaForce CF, Yegen U, Matos D, Della Cioppa G. SHORT Formoterol delivered via the dry powder Aerolizer inhaler versus albuterol MDI and placebo in mild-to-moderate asthma: a randomized, double-blind, double-dummy trial. Comparison of formoterol, 6 salbutamol and salmeterol in methacholine-induced severe bronchoconstriction. Quick-relief medications for asthma Page 104 of 113 Final Report Update 1 Drug Effectiveness Review Project Citation Exclusion Code Price DB, Cargill K, Wolfe S, Darby H. Salmeterol xinafoate: an analysis 6-DESIGN of outcomes and cost-effectiveness using a primary care database. Quebe-Fehling E, Brambilla R, Bromly CL, Fishwick K, Walters EH, 6-LONG VS. The duration of action of inhaled formoterol dry powder. Effect of different inhaled 6-DESIGN bronchodilators on recovery from methacholine-induced BROCHOPROVOCATION bronchoconstriction in asthmatic children. The cost effectiveness of levalbuterol versus racemic albuterol. Comparison of the 6 effects of salmeterol and formoterol on airway tone and responsiveness over 24 hours in bronchial asthma. Prolonged protection against methacholine-induced bronchoconstriction by the inhaled beta 2-agonist formoterol. Randell J, Hamalainen KM, Leinonen M, Keski-Karhu J, Silvasti M, 6-DELIVERY Tukiainen H. Salbutamol via Easyhaler(TM) multidose dry powder inhaler produces equivalent relief of histamine-induced bronchoconstriction to salbutamol via pressurised metered-dose inhaler. A comparison of salmeterol with salbutamol inhalation in 1 treatment of mild to moderate asthma. Effects of on-demand beta -agonist2 6-DESIGN inhalation in moderate-to-severe asthma. SHORT single dose salmeterol affect exercise capacity in asthmatic men? Quick-relief medications for asthma Page 105 of 113 Final Report Update 1 Drug Effectiveness Review Project Citation Exclusion Code Rosenborg J, Bengtsson T, Larsson P, Blomgren A, Persson G, Lotvall 6-LONG VS. Relative systemic dose potency tolerability of inhaled formoterol salbutamol healthy subjects and asthmatics.
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Hyperemesis gravidarum: epidemiologic find- parenteral nutrition discount aleve 250 mg with amex dna advanced pain treatment center west mifflin. Obstet Gynecol 2006;107:535–7 ings from a large cohort order aleve 500mg chronic pain treatment vancouver. Haemostasis in normal 811–14 pregnancy: a balancing act? Outcomes of pregnan- 428–32 cies complicated by hyperemesis gravidarum buy aleve 250mg low price pain treatment journal. Venous thrombo- Gynecol 2006;107:285–92 sis associated with the placement of peripherally inserted 84 generic 250 mg aleve with amex pain treatment machine. J Vasc Interv Radiol 2000;11:1309–14 hyperemesis gravidarum and the effect of laboratory 73. J Obstet emesis in pregnancy: an evaluation of treatment strate- Gynaecol Res 2007;33:457–64 gies with maternal and neonatal outcomes. Long-term neuro- Gynecol 2008;198:56e1–4 development of children exposed to maternal nausea 74. J Pediatr 2009; social morbidity among women with nausea and vomit- 155:45–50; 50 e1–2 ing of pregnancy: prevalence and association with 86. J Psychosom Obstet Gynaecol 2000; nausea and vomiting of pregnancy and hyperemesis 21:129–36 gravidarum. Diffuse pain should alert to the possibility of peritonitis4. Acute pelvic pain is a common presenting com- Acute pain due to ischemia, or viscus injury plaint in women. The diagnosis of pelvic pain in such as in ovarian torsion or intestinal obstruction, women can be challenging because many symp- 1 is accompanied by autonomic reflex responses such toms and signs are insensitive and unspecific. The Prompt diagnosis and effective management pre- 2 suggested causes of pain in endometriosis include vent complications and may help preserve fertility. The definition of acute pelvic pain is arbitrary; often the duration is only a few hours, but it can be days. CLASSIFICATION It usually presents with a sudden onset, but may be insidious and the pain increasing with time. Gener- Classification of cases of pelvic pain is necessary as ally, any pain in the lower abdomen or pelvis lasting it highlights and provides rational consideration of less than 3 months is considered acute pelvic pain1,3. Different classifications of acute pelvic pain have Incidence been proposed1,4. A convenient and useful example classifies acute pelvic pain broadly as gynecological The incidence of the different etiologies varies and or non-gynecological pain (Figure 1; Table 1). More information on pel- vic pain in pregnancy is provided in Chapter 3. Pathophysiology ALGORITHM OF EVALUATION OF PELVIC The pathophysiologies are influenced by the differ- PAIN ent etiological factors and are mediated via the pain pathway along the pelvic innervations. Distinguish- The diagnosis of pelvic pain in women can be chal- ing pain arising from the genital organs from that of lenging because many symptoms and signs are in- gastrointestinal origin is often difficult due to the sensitive and non-specific (Table 2). The goal of shared visceral innervations of the uterus, cervix management is to identify the correct diagnosis and and adnexa and gastrointestinal structures, i. A rapid initial evaluation to exclude life- travel through the same sympathetic nerves to the threatening conditions such as ectopic ovarian 53 GYNECOLOGY FOR LESS-RESOURCED LOCATIONS complications, and initial resuscitation with intra- Age venous fluid or blood may be required before a The age of the patient may indicate common con- comprehensive evaluation is undertaken. In young women the possibility of complication of abortion, ectopic ges- History taking tation and tubo-ovarian abscess or other sexually Careful history is an important first step towards transmitted infections (STIs) and pelvic inflamma- establishing a diagnosis. This should focus on pain tion disease (PID) should be excluded due to risky characteristics, review of systems and gynecologi- sexual behavior5. Appendicitis is also common in cal, sexual and social history1. Non-pregnant patient Pain characteristics Gynecological ĺ Cyclic Pain perception varies across cultures and it also in- fluences health-seeking behavior. The duration of pain may be important as sudden onset may suggest բ Non-cyclic acute appendicitis, while a long history before the acute episode may indicate typhoid perforation or intestinal obstruction4,7,8. Colicky intermittent pain may be sug- gestive of intestinal obstruction or ureteric colic7,8. Pain of sudden onset can hint at visceral perfora- tion, and is insidious in inflammation, e. The frequency of pain or its cyclic Non-gynecological nature could also be suggestive of dysmenorrhea which typically presents with pain around the men- Figure 1 Classification of acute pelvic pain in the strual period. Ovulation pain (Mittelschmerz) is non-pregnant patient typically felt around the mid cycle6,7. Table 1 Gynecological and non-gynecological causes of acute pelvic pain Gynecological causes Reproductive period/age Adenomyosis; degenerating fibroid; endometriosis; Mittelschmerz, ovarian torsion; pelvic inflammatory disease; ruptured cyst; tubo-ovarian abscess; dysmenorrhea Adolescents Similar to women of reproductive age, with addition of imperforate hymen and transverse vaginal septum Postmenopausal Causes similar to that of the reproductive age group except for ectopic pregnancy and menstruation-related causes like dysmenorrhea, endometriosis etc. Non-gynecological causes Gastrointestinal Appendicitis; bowel obstruction and constipation; diverticulitis; gastroenteritis; inguinal hernia; irritable bowel syndrome; mesenteric venous thrombosis Urinary Cystitis; pyelonephritis; ureterolithiasis Musculoskeletal Strain tendons/muscles; joint infection/inflammation; hernia Others Among the patients of African origin sickle cell crisis could present with acute abdominal– pelvic pain; dissecting aortic aneurysm; lead poisoning; drug abuse; porphyria; somatization disorder 54 Acute Pelvic Pain in Limited-resource Setting Table 2 Common causes of acute pelvic pain Diagnosis Common features Sexually transmitted infec- Lower abdominal pain, cervical excitation tenderness and adnexal tenderness tions and pelvic inflammatory disease (Chapter 17) Tubo-ovarian abscess Minor features include dyspareunia, fever, abnormal discharge (Chapter 11) Tubo-ovarian torsion Acute pain, initially unilateral, often started by rapid turning or twisting movements (e. Pain, often unilateral, may be associated with gastrointestinal symptoms and may resolve spontaneously after the next period or within several cycles Dysmenorrhea (Chapter 7) Cyclic lower abdominal, usually starts before and predominantly during the first 2 days of menses; may be associated with gastrointestinal symptoms such as lower back pain, diarrhea, nausea and vomiting Mittelschmerz Mid-cycle pain usually mild; may be associated with bleeding per vagina, severe symptoms mimic ruptured ectopic or acute appendicitis. Resolves spontaneously Appendicitis Pain starting at epigastric area later settling at right iliac fossa; pain, anorexia, nausea and vomiting. Fever at later stages Endometriosis (Chapter 6) Pelvic pain, dysmenorrhea, dyspareunia, pelvic tenderness, tender sacrouterine ligament. Most of the time it is a chronic disease, but can present with an acute exacerbation Urinary tract infection Dysuria, frequency, lower abdominal pain, urgency, suprapubic tenderness, systemic symptom is slight Pyelonephritis Sudden pain radiating to suprapubic area; systemic symptom is common fever, chills, nausea and vomiting Typhoid perforation General abdominal pain, fever, acute abdomen Although pain quality and severity are non- in acute appendicitis4,7,8. Frequency, dysuria, scald- specific, they may provide some clue about the ing and hematuria are suggestive of urinary tract etiology. Abrupt and severe pain is typically associ- disorder7,9. Presence of fever in association with ated with perforation (ectopic pregnancy), strangu- pelvic pain is suggestive of infection or inflamma- lation (ovarian torsion) or hemorrhage (ovarian tory etiology, such as appendicitis, PID, ovarian cyst). Dysmenorrhea and abortion may be associ- torsion or tubo-ovarian abscess (TOA)4. Colicky pain typifies and syncopal attack could be an associated feature ovarian torsion or nephrolithiasis. Burning or of ruptured ectopic gestation or hemorrhagic aching pain often occurs with inflammatory pro- ovarian cyst. Inflammatory conditions and hemo- cesses such as appendicitis or tubo-ovarian abscess peritoneum can sometimes present with non- and PID4,7. Progressively worsening pain would specific symptoms of nausea, vomiting and suggest visceral inflammation or perforation4. Headache, malaise and fever before on- set of pain are suggestive of typhoid perforation7,8. Associated symptoms Aggravating and alleviating factors Diagnosis is often considered based on the associ- ated symptoms (Table 3). Nausea and vomiting are Changes in pain may occur in relation to menses, associated with acute appendicitis, pyelonephritis coitus, activity, diet, bowel movement or voiding.
The clinical manifestations of sexu- ally transmitted HPV infections are genito-anal warts or Bowenoid papulosis as well as giant condyloma (Buschke-Lowenstein tumor) proven aleve 500 mg texas pain treatment center frisco, cervical or anal intraepithelial neo- plasias (classified CIN or AIN I-III lesions including the erythroplasia of Queyrat) or at least carcinoma cheap aleve 500mg with amex northside pain treatment center atlanta. In HIV-infected patients generic aleve 500mg with mastercard allied pain treatment center raid, the risk of persistent HPV infections is seven times higher and correlates inversely with the CD4 T cell count (Piketty 2003) cheap aleve 500mg free shipping pain solutions treatment center ga. In HIV+ patients, HPV infections are more often symptomatic and chronic. In addi- tion, the risk of relapse is considerably higher, even after treatment. Malignant trans- formation is the most important complication involving the high-risk HPV subtypes. Condylomata acuminata are hyperkeratotic and verrucous papules of the anogeni- tal region. Condylomata acuminata are usually caused by HPV 6 or HPV 11, so-called low-risk HPV types, which by themselves do not tend to induce malignant trans- formation. Therefore, fig warts are not inevitably the beginning of genito-anal intraepithelial neoplasms and carcinoma but it is difficult to differentiate between them. Besides the preferred localization in genital as well as peri- and intra-anal regions, fig warts may also occur enorally and in the urethra. Condylomata are usually asymptomatic but can affect the sexual life of patients and may cause hygiene and psychogenic problems. Pruritus, burning or bleeding are rare and are generally caused by mechan- ical stress. Diagnosis Analogous to cervical intraepithelial neoplasia (CIN) and cervical cancer in women, regular screening (every 1 to 3 years) for condylomata acuminata, anal intraepithe- lial neoplasia (AIN) and anal carcinoma is advised for all HIV+ patients. Screening should include clinical inspection, palpation, colposcopy, proctoscopy, cytology (Pap smear) and, if necessary, a histopathological examination of biopsies. An exploratory biopsy is recommended before therapy starts to confirm it is not a malignancy. In case of therapy resistance, early relapse or a fast or infiltrating growth, an exploratory biopsy is imperative. Meanwhile, cytologic examination of microscopic preparations (smear tests) are done in order to differentiate from preliminary cervical or anal carcinoma. Cytological results of smears from the cervix are divided with the classification of Papanicolaou. However, the sensitivity and specificity of these tests are still not sufficient (Panther 2004, Jablonka 2011). A review of anal cytologic examinations has shown a prediction of biopsy results for anal dysplasia with a sensitivity of 69-93% and a specificity of 32–59% (Chiao 2006). Every suspicious cytologic finding should be monitored with a contemporary col- poscopy or proctoscopy (Duerr 2006). Specialized centers offer the “High Resolution Anoscopy” as gold standard, which improves the test results of peri- and intra-anal inspections with regard to necessary exploratory biopsies, especially after the application of acetic acid (3 per cent mucosa, 5 per cent skin) and an additional staining with Lugol’s solution. Histologically, examinations of intralesional biopsies differ in Condylomata acuminata, intraepithe- lial neoplasia divided in severity grades I-III (IN) and invasive cancer. The abbrevia- tion of the anatomic location of the lesion is specified in front of the IN grade. The description AIN III is in accordance with an anal carcinoma in situ. The determina- tion of the HPV subtype allows for differentiation between high- and low-risk types and is still not a routine diagnostic method, because of its subordinate role in therapy decisions (Ledger 2000). When high-risk HPV-types are detected, some experts recommend to shorten the period between control examinations of the affected region. Just like women, HIV+ men, mainly those suffering from condyloma anamnesis, should have a proctological follow-up at least once a year (Chiao 2006, Scott 2008, Wexler 2008, Jamieson 2006, Esser 2011). To avoid fatal tumor growth and mutilat- ing operations (rectum amputation, etc) it is recommended to do thorough genito- anal inspections and regular proctological exams by means of high resolution anoscopy with cytological smears and exploratory excision, which are timely and specific (Kreuter 2009, Pindea 2008). Rectal palpation and external inspection of the anogenital regions are not sufficient as a preventive medical checkup for HIV+ patients. Should an anal carcinoma be palpable, it has, in general, already progressed extensively. Until today, there are no good reports on how often intra-anal, HPV- associated lesions are isolated without involving the external genito-anal regions. Nowadays there are surveys trying to find out how often colposcopic and procto- scopic exams should be offered in addition to the routine genito-anal palpations and inspections, and exactly who should be examined. Therapy Until now there is no satisfying therapy for Condylomata acuminata. Relapses still occur frequently even after adequate treatment in immune competent HIV-negative patients (40-60%). However, therapy delays (watch & wait) should be avoided and all clinically striking findings should be removed at an early stage even at the risk of operating multiple times. Therapy includes the most complete operative removal possible with histological follow-up of the nature of the tumor and its invasive depth. Besides surgical excision, electrosurgery, the condyloma may be removed by means of laser surgery, infrared coagulation, caustica (trichloroacetic or podophyllotoxin) or cryotherapy with liquid nitrogen (high healing effect initially – high relapse risk). Since virus-harboring keratinocytes can remain in the clinically normal surrounding tissue, relapses are as frequent as 50% in immunocompetent patients and in up to 70% in immunodefi- cient patients within 4 months. In clinical practice, attending physicians often try HIV and Sexually Transmitted Diseases 489 to reduce the high relapse risk by an adjuvant local immunotherapy with imiquimod (Aldara) cream or interferon beta. Both agents are expensive and a local therapy takes time (at least 3 months). Imiquimod is licensed for the topical treatment of HPV-associated lesions. As demonstrated in several controlled studies imiquimod treatment is safe and effective and has the lowest relapse rate of all treatments (6-13% in immunocompetent patients). Imiquimod is not approved for the treat- ment of anogenital warts in immunodeficient patients and intraepithelial neoplasias but results of successful treatments of genital warts (Cusini 2004), Bowenoid papu- losis and Bowen’s disease in HIV+ patients have been published (Kreuter 2008). In our own experience imiquimod can be successfully used as the sole therapy for flat, less hyperkeratotic condyloma. There are formulas for imiquimod-containing sup- positories (off-label). However, the treatment period takes several weeks without sur- gical intervention, often complicated by compliance-reducing side effects such as inflammation, pruritus and burning. Condyloma may also be systemically treated with interferon (there are often problems with health insurance due to a low success rate of 31% in the intial stages, although there are reports of a significantly lower relapse rate in comparison with other invasive therapies). Herbal 10% Camellia sinensis ointment (Veregen) is also approved for local therapy of genitoanal warts (Abramovits 2010). The only antiviral agent active against HPV is cidofovir but there is little experience in HIV+ patients (Snoeck 2001). In a prospective comparative trial, destruction of HPV-associated anogenital lesions with electrocautery was superior to local immunotherapy with imiquimod or topical chemotherapy in HIV+ MSM and had less adverse events (Richel 2013). While various vaccines have been successfully used as prophylaxis for certain HPV- subtypes (HPV 6, 11, 16, 18), there is still no progress in the development of an effec- tive therapeutic vaccination against symptomatic HPV infections.