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Off- appear to provide satisfactory hemostasis and are not accompanied label drug use: None disclosed generic pamelor 25 mg with mastercard. The use of VWF concentrates with very low FVIII content should be accompanied by the coinfusion of recombinant FVIII to enhance the treatment of acute bleeding Correspondence episodes and to optimize surgical hemostasis order pamelor 25 mg otc. Any variances in Dr David Lillicrap, Department of Pathology and Molecular multimer content of the products have not resulted in obvious Medicine, Richardson Laboratory, Queen’s University, Kingston, differences in the clinical outcomes and the optimal dosing rationale ON, K7L 3N6, Canada; Phone: 613-548-1304; Fax: 613-548-1356; and schedule for these concentrates is still not reconciled defini- e-mail: dpl@queensu. Although dosing in FVIII:C units for surgical hemostasis is recommended by some, there may be more justification for using References VWF:RCo–based dosing to treat or prevent mucocutaneous bleeding. Human von Willebrand factor (vWF): isolation of complementary DNA The use of VWF-FVIII products for bleeding prophylaxis has been (cDNA) clones and chromosomal localization. Molecular musculoskeletal and mucosal bleeding, there is no consensus on the cloning of cDNA for human von Willebrand factor: authentica- concentrate dose and administration schedule. Bowman M, Hopman WM, Rapson D, Lillicrap D, James P. The prevalence of symptomatic von Willebrand disease in primary care practice. The clinical trial of this new concentrate has demonstrated excellent 6. Epidemiological investiga- hemostatic efficacy and safety, with effective bleeding control and tion of the prevalence of von Willebrand’s disease. Update on the 258 American Society of Hematology pathophysiology and classification of von Willebrand disease: a spectrum of type 1 von Willebrand disease: results from a report of the Subcommittee on von Willebrand Factor. Sequence and structure genotype of a cohort of families historically diagnosed with relationships within von Willebrand factor. Intersection of mecha- Type 1 von Willebrand Disease (MCMDM-1VWD). Use of a mouse model to have type 1 von Willebrand disease. Willebrand factor mutations and new sequence variations 12. Clinical and identified in healthy controls are more frequent in the African- molecular predictors of thrombocytopenia and risk of bleeding American population. Mutation and promoter of the von Willebrand factor gene in type 1 von ADAMTS13-dependent modulation of disease severity in a Willebrand disease. Willebrand factor mutations identified in patients with type 1 14. Mutation-specific von Willebrand disease from the MCMDM-1VWD study. J hemostatic variability in mice expressing common type 2B von Thromb Haemost. Platelet-type von Willebrand disease and type 2B Willebrand factor survival by assay of the VWF propeptide in von Willebrand disease: a story of nonidentical twins when two the European study: molecular and clinical markers for the different genetic abnormalities evolve into similar phenotypes. Haberichter SL, Balistreri M, Christopherson P, et al. Assay of within the A3 domain of von Willebrand factor (VWF) in two the von Willebrand factor (VWF) propeptide to identify related patients leads to a defective binding of VWF to patients with type 1 von Willebrand disease with decreased collagen. Cellular and W1745C and S1783A, two novel collagen binding defects in molecular basis of von Willebrand disease: studies on blood the A3 domain of von Willebrand factor. Critical von storage and secretion of von Willebrand factor in blood Willebrand factor A1 domain residues influence type VI outgrowth endothelial cells derived from patients with von collagen binding. Gill JC, Endres-Brooks J, Bauer PJ, Marks WJ Jr, Montgomery Willebrand disease: clinical manifestations, pathophysiology, RR. The effect of ABO blood group on the diagnosis of von laboratory diagnosis and molecular biology. Congenital von Willebrand disease type 3: multiple genetic loci with plasma levels of factor VII, factor clinical manifestations, pathophysiology and molecular biol- VIII, and von Willebrand factor: The CHARGE (Cohorts for ogy. Heart and Aging Research in Genome Epidemiology) Consor- 21. The C-type lectin co-dominant inheritance of mutant alleles. The evolution and value of bleeding patients and carriers of severe von Willebrand disease. Shelton-Inloes BB, Chehab FF, Mannucci PM, Federici AB, 7836.

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Nausea and vomiting in pregnancy: a mized 25 mg pamelor, double-blind discount pamelor 25mg with visa, placebo-controlled trial. Am J review of the problem with particular regard to psycho- Obstet Gynecol 1995;173:881–4 logical and social aspects. A placebo-controlled trial of oral 102:6–8 pyridoxine in hyperemesis gravidarum. Psychological factors in the Invest 2009;67:151–7 etiology and treatment of severe nausea and vomiting in 54. Use and safety of antipsychotic health in early pregnancy: relationship with nausea and drugs during pregnancy. The Hyper- methylprednisolone in the treatment of hyperemesis emesis Impact of Symptoms Questionnaire: develop- gravidarum: a randomized, double-blind, controlled ment and validation of a clinical tool. Am J Obstet Gynecol 1998;179:921–4 2010;47:67–77 57. Day-case management dose of prednisolone in the treatment of hyperemesis of hyperemesis gravidarum: feasibility and clinical effi- gravidarum. Treatment for double-blind, placebo-controlled trial of corticosteroids hyperemesis gravidarum in the home: an alternative to for the treatment of hyperemesis gravidarum. Pulsed steroid esis gravidarum: home care implications. Home Healthc therapy is an effective treatment for intractable hyper- Nurse 2009;27:347–51 emesis gravidarum. Teratogenic potential of cortico- cutaneous metoclopramide therapy for hyperemesis steroids in humans. Bendectin and safety of ginger in the treatment of pregnancy-induced birth defects: I. A meta–analysis of the epidemiologic nausea and vomiting. Eur J Obstet Am Fam Physician 2003;8:121–8 Gynecol Reprod Biol 1991;38:19–24 51 GYNECOLOGY FOR LESS-RESOURCED LOCATIONS 63. Wernicke’s encephalopathy and nausea and vomiting in pregnancy: randomized, central pontine myelinolysis associated with hypereme- double-masked, placebo-controlled trial. Effect of a ginger ex- ciation with severe hyperemesis gravidarum. Obstet tract on pregnancy-induced nausea: a randomised con- Gynecol 2002;100:1119–21 trolled trial. Saving Mothers’ Lives: review- controlled trial of ginger to treat nausea and vomiting in ing maternal deaths to make motherhood safer – 2003–2005. Obstet Gynecol 2004;103:639–45 The Eighth Report on Confidential Enquiries into 66. London: tive comparative study of the safety and effectiveness of CEMACH, 2011 ginger for the treatment of nausea and vomiting in preg- 79. Am J Obstet Gynecol 2003;189:1374–7 Thrombosis and Embolism during Pregnancy and the Puer- 67. J Perinat Neonat Nurs 2004;18: ciated with elective termination of pregnancy among 312–28 Canadian and American women with nausea and vomit- 69. J Psychosom Obstet Gynaecol 2001;22: tions associated with peripherally inserted central cath- 7–12 eter use during pregnancy. Obstet Gynecol 2004;104:467–76 cemia in a pregnant woman with hyperemesis receiving 82. Hyperemesis gravidarum: epidemiologic find- parenteral nutrition. Obstet Gynecol 2006;107:535–7 ings from a large cohort. Haemostasis in normal 811–14 pregnancy: a balancing act? Outcomes of pregnan- 428–32 cies complicated by hyperemesis gravidarum. Venous thrombo- Gynecol 2006;107:285–92 sis associated with the placement of peripherally inserted 84. 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.

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Isolation is generally indicated to prevent the spread of the infec- tion purchase 25 mg pamelor with amex. Effective treatment according to the drug resistance profile of the TB case seems most relevant to control infectiousness also in HIV+ TB patients (Escombe 2008) buy pamelor 25mg mastercard. Recent evidence suggests that effectively treated, although smear and culture- positive, cases might not be infectious any more (Dharmadhikari 2014). Until further evidence is gathered, culture negativity seems the safest marker of non-infectious- ness for drug-susceptible and drug-resistant cases. In pulmonary TB sputum should be regularly collected (weekly in the initial phase, later monthly), evaluated for AFB by direct microscopy and for viable M. TB therapy Drug susceptible TB is treated with the first-line drugs rifampicin (RIF), isoniazid (INH), pyrazinamide (PZA) and ethambutol (EMB). INH and especially RIF are the most potent first-line drugs. To prevent the development of drug resistance, active TB should always be treated with a combination of four drugs in the initial phase. The standard therapy consists of a 2-month course of daily RIF, INH, EMB and PZA, followed by a continuation phase of 4 months with daily RIF and INH. The four drugs of the initial treatment phase Opportunistic Infections (OIs) 359 should be administered until a culture-based drug susceptibility result of M. Anti-tuberculosis drug doses, side effects and drug inter- actions are shown in Table 1. Table 1: Anti-tuberculosis drug doses, side effects and drug interactions Drug Recommended Common adverse Drug interactions daily dose events and comments Rifampicin (RIF) 10 mg/kg Toxic hepatitis; allergy, Many drug interactions: Also available as >50 kg: 600 mg fever; gastrointestinal (see Drug Chapter), liver IV injection <50 kg: 450 mg disorders; discoloration monitoring, safe up to (orange) of body fluids; 35 mg/kg (Boeree 2015) thrombopenia Isoniazid (INH) 5 mg/kg Peripheral neuropathy; Avoid d4T, ddI Also available as maximum elevated liver enzymes, Avoid INH if pre-existing IV or IM injection 300 mg/day toxic hepatitis; CNS side liver damage; avoid Administered effects: psychosis, with vitamin B6 seizures Ethambutol (EMB) 15 mg/kg Optic neuritis (contra- Baseline/monthly screen Also available as (15–20 mg/kg) indicated in case of for visual acuity and colour IV injection pre-existing lesions of perception optic nerve); peripheral Antacids decrease neuropathy (rare) absorption Pyrazinamide (PZA) 25 mg/kg Arthralgia, hyperuricemia, Hyperuricemia: uricosuric (20–30 mg/kg) toxic hepatitis, gastro- drug (allopurinol); intestinal discomfort monitor LFTs Streptomycin (S) 15 mg/kg Auditory and vestibular Audiometry; monitor IV/IM administration maximum cumula- nerve damage; renal function; do not use only tive dose 50 g! Diacon 2014) prolongation should be avoided ECG at 2,4,8, 12 and 24 weeks, LFT monthly Delamanid (DLM) 100 mg BID Nausea, vomiting, Avoid strong C3A4 for 24 weeks dizziness, QT prolongation inducers, drugs with QT-prolongation. ECG at 2, 4, 8, 12 and 24 weeks Clofazimine (CFZ) 100–200 mg/d Red skin discoloration, Avoid use with dry skin, pruritus, gastro- QT-prolonging drugs intestinal intolerance, Avoid direct sunlight photosensitivity, QT prolongation Meropenem/ 1000 mg TDS IV Nausea, vomiting Only active in Clavulanic acid plus 125 mg diarrhea combination. Data from a systematic review and meta- analysis suggest that a minimum of 8 months duration of rifamycin (rifampicin or rifabutin) therapy and concurrent ART might be associated with better outcomes (Khan 2010). When there is initially a high bacterial load, and sputum smear con- version is not achieved by two months of therapy or when PZA is not part of the induction regimen, continuation phase treatment with RIF and INH should be pro- longed for a total treatment of 9 months (BHIVA 2012). Opportunistic Infections (OIs) 361 Treatment of MDR-TB Bacillary resistance to RIF and INH is defined as multidrug-resistance (MDR) although mono-resistance to RIF is de facto comparable to MDR-TB. Patients with MDR-TB can be successfully treated with second-line drugs. Second-line injectable drugs (SLID) are amikacin, capreomycin and kanamycin. Second-line oral drugs include levofloxacin, moxifloxacin, prothionamide, cycloserine, para-aminosalicylic acid. When there is bacillary resistance to any fluoroquinolone or any SLID, the resist- ance level is termed extensively drug-resistant (XDR). In advanced MDR-TB or XDR- TB alternative drugs like clofazimine, linezolid and/or meropenem in combination with amoxicillin/clavulanic acid are frequently included in a drug regimen. Treatment of M/XDR-TB should always be guided by an experienced physician (Lange 2014). Drug resistant tuberculosis should be treated with at least four drugs to which the bacilli are susceptible by drug testing. WHO recommends including an SLID in the first 8 months of treatment. The total duration of MDR-TB treatment recommended by the WHO is 20 months (WHO 2011). Treatment recommendations are currently based on a retrospective cohort analysis (Ahuja 2011) and are likely inadequate for individual patients (Heyckendorf 2014). Clinical trials with new and shorter regi- mens including HIV+ patients are ongoing.

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