News

News

January 17, 2017

January ID Update

Sign up here to receive monthly ID Updates by e-mail.
Links marked with an asterisk (*) provide details to Sanford Guide Web Edition subscribers, while all other links are universal.

 

Updated Treatment Guidelines

  • Updated guidelines for the prevention, detection, and management of surgical site infections* from the American College of Surgeons (ACS) and the Surgical Infection Society (SIS) have been published (J Am Coll Surg 224:59, 2017). The guidelines are available for download on the JACS website.
  • Current SIS recommendations regarding the management of patients with intra-abdominal infection are also available (Surg Infect 18:1, 2017). The guidelines were last updated in 2010.

Practice Pearls

  • The impressive final results of a trial designed to assess the efficacy of the rVSV-ZEBOV vaccine for prevention of Ebola virus disease* (EVD) are now available. The trial, conducted in Guinea, used the ring vaccination approach inspired by the surveillance-containment strategy that resulted in eradication of smallpox. After confirmation of a case of EVD, clusters of contacts and contacts of contacts were identified. Clusters were randomly assigned to immediate vaccination or vaccination delayed by 21 days. Vaccination was a single IM dose (2 x 107 plaque-forming units) administered in the deltoid muscle. Randomized assignment was eventually discontinued on the recommendation of an independent data and safety board because of interim analysis findings, and thereafter all clusters received immediate vaccination (including children). Immediate vaccination resulted in complete protection against subsequent onset of EVD ten days later or more. Headache, fatigue, and muscle pain were the most commonly reported adverse events across all age groups. The rVSV-ZEBOV vaccine is a recombinant, replication-competent, vesicular stomatitis virus-based vaccine expressing a surface glycoprotein of a Zaire Ebolavirus (Lancet 2016 Dec 23 [Epub ahead of print]).
    • A classic question: does concomitant treatment with an anti-infective agent enhance the pharmacologic effects of warfarin?First, some background. Warfarin is a racemic mixture of R-warfarin (half-life 37-89 hours) and S-warfarin (half-life 21-43 hours). R-warfarin is metabolized by CYP1A2, 2C19, and 3A4 whereas S-warfarin is metabolized by CYP2C9. The S enantiomer is five times as active as the R enantiomer. Therefore, anti-infectives that inhibit CYP2C9 would be expected to have the greatest impact on warfarin metabolism and INR. Here is a complete (hopefully) list of anti-infectives that inhibit CYP2C9:
      • Antibacterials: metronidazole, oritavancin (weakly), TMP/SMX (specifically SMX)
      • Antifungals: fluconazole, voriconazole
      • Antiretrovirals: delavirdine, efavirenz, etravirine

      There are at least five reasons why an anti-infective might enhance the effects of warfarin (listed in no particular order):

      1) Protein-binding displacement. The notion that a highly protein bound anti-infective might displace warfarin from its binding sites was one of the earliest explanations offered. However, we know that protein displacement results in an increased free fraction of unbound warfarin but also increased warfarin clearance since more is available to its metabolic enzymes. Thus, any increase in warfarin effect should be transient.

      2) Direct inhibition of clotting factor formation by the anti-infective. For years we all recited the specific cephalosporins containing an N-methylthiotetrazole (MTT) side chain at position 3 of the cephalosporin nucleus because of its known association with bleeding. MTT is a heterocyclic leaving group that inhibits the gamma-carboxylation of glutamic acid, a vitamin K-dependent reaction required for the formation of clotting factors. Thankfully, most of the MTT-containing cephalosporins (cefotetan, cefoperazone, cefmetazole, cefamandole, moxalactam) are gone from the market (at least the US market).

      3) Impairment of vitamin K production by gut flora. This is a commonly invoked explanation with a striking lack of supportive data. We know that the typical diet contains about 300-500 mcg/day of vitamin K, and it has been estimated that a chronic change in intake of about 250 mcg/day would be required to alter one’s response to warfarin. But we have not quantified the contribution of vitamin K production by gut flora, nor do we know the reduction that might be expected from anti-infective therapy (or the extent to which it would vary depending on the drug).

      4) Alteration in dietary vitamin K intake as a consequence of infection. In other words, sick people may eat less leafy green vegetables.

      5) Reduced warfarin metabolism resulting from the infection itself, i.e. proinflammatory cytokines released during infection acting as inhibitors of drug metabolism by downregulating enzymes such as CYP2C9 (Clin Pharmacol Ther 85:434, 2009). Thus an anti-infective that appears to inhibit warfarin metabolism is simply acting as a marker for the true culprit, and the disappearance of the interaction is due to resolution of the infection, not withdrawal of the drug.

      The fifth listed reason may be most likely with a possible (lesser) contribution from the third and fourth reasons. Many anti-infectives have been associated with elevated INR in patients taking warfarin, but it is important to note that case reports from infected patients make up the bulk of the positive interaction data whereas controlled, prospective, randomized trials in healthy subjects usually fail to demonstrate the interaction. An interesting observational case-control and case-crossover study of warfarin users using US Medicaid data was published in 2008. Exposure to all seven antimicrobials examined in the study (ciprofloxacin, levofloxacin, gatifloxacin, TMP/SMX, fluconazole, amoxicillin, cephalexin) was associated with GI bleeding. But here’s the best part. After adjusting the risk for confounders including the use of cephalexin as a reference group, only the odds ratios for TMP/SMX and fluconazole were still significantly elevated (predictable since they are both 2C9 inhibitors). Because cephalexin (they could have used amoxicillin) is a drug known to be devoid of effect on warfarin metabolism, this study is the first to control for infection in assessing the interaction. Obviously it’s not the best way to control for infection but it is ethically challenging to have a group of infected warfarin-treated patients who are not administered anti-infective treatment (Clin Pharmacol Ther 84:581, 2008).

      In summary, the interaction of warfarin with anti-infectives, except for known inhibitors of CYP2C9, may be more a disease-drug (infection-warfarin) interaction than anything else (Pharmacy Times June:27, 2009).

 

    • Trimethoprim (TMP), which is structurally related to the potassium-sparing diuretic amiloride, interferes with sodium reabsorption by the kidney. Hyperkalemia secondary to TMP-SMX is well known, but hyponatremia is less commonly appreciated. In a retrospective single-center review of hospitalized patients who received high-dose TMP-SMX* (defined as TMP ≥8 mg/kg/day for ≥3 consecutive days), the incidence of hyponatremia (defined as serum sodium <136 mEq/L) was 72.3% (55 of 76 patients). Patients with comorbid conditions and those receiving other drugs that lower serum sodium concentrations were excluded from the cohort. Mean starting sodium concentration was 138.4 mEq/L, and mean sodium concentration at nadir was 131.6 mEq/L. Mean time to nadir development was 5.5 days. 43.6% of the patients had sodium concentrations <130 mEq/L at nadir, and the lowest concentration observed was 117 mEq/L. Male patients and African-American patients had a higher overall incidence of hyponatremia, and lower serum sodium concentrations were associated with longer duration of TMP-SMX therapy and higher cumulative doses. 32.9% of patients in the cohort also developed hyperkalemia (more commonly in those receiving concomitant corticosteroids). In those patients who had serum sodium concentrations measured within 1-3 weeks after discontinuation of TMP-SMX, hyponatremia had resolved in 57.9% (38 of 58 patients). Although most patients in this retrospective review had pneumonia, the observed incidence of hyponatremia was higher than that described in other pneumonia studies (Am J Med 129:1322, 2016).

 

  • Central nervous system toxicity is the second most common toxicity of fluoroquinolones* (gastrointestinal toxicity is most common) but the vast majority of reports are in adult patients (reflecting the typical usage of the drugs). Only two case reports of levofloxacin neurotoxicity in pediatric patients have been published. In the first case, a previously healthy 13-year-old girl was treated with oral levofloxacin for acute bronchitis and developed delirium two hours after her first dose. The drug was immediately discontinued and she recovered gradually over the next four days (Med J Armed Forces India 69:404, 2013). More recently, a 2-year-old girl with neuroblastoma was begun on levofloxacin prophylaxis prior to stem cell transplantation. Drug administration late in the evening was consistently associated with agitation, confusion, and hallucinations. Altering the time of administration to earlier in the evening resulted in disappearance of symptoms, while incidental rechallenge with a dose late in the evening led to symptom recurrence (J Clin Psychopharmacol 36:737, 2016).

    CNS side effects of fluoroquinolones are poorly understood. Symptoms range from headache, dizziness, and insomnia to delirium, psychosis, and seizures. Among the fluoroquinolones the relative potential for CNS toxicity seems to be:

    Norfloxacin > ciprofloxacin > ofloxacin > gemifloxacin > levofloxacin > moxifloxacin

    One proposed mechanism is inhibition of the binding of GABA (gamma-aminobutyric acid), an inhibitory neurotransmitter, to its receptors (the same mechanism associated with beta-lactam neurotoxicity). The drugs may also activate excitatory N-methyl-D-aspartate receptors. Coadministration of fluoroquinolones with certain NSAIDs may potentiate seizure risk, and the ability of some fluoroquinolones to inhibit CYP450 enzymes can result in toxic concentrations of certain epileptogenic drugs. As fluoroquinolone usage in pediatrics increases, it is important for clinicians caring for younger patients to be aware of this potential toxicity (Clin Infect Dis 41(suppl 2):S144, 2005; Br J Clin Pharmacol 72:381, 2011).

Drug Shortages (US)

    • Antimicrobial drugs or vaccines in reduced supply due to increased demand, manufacturing delays, product discontinuation by a specific manufacturer, or unspecified reasons:
      • [New on the list]: Hepatitis A Virus Vaccine Inactivated, Tetanus and Diphtheria Toxoids Adsorbed
      • [Continue to be in reduced supply]: Amikacin, Ampicillin injection, Ampicillin/sulbactam, Cefepime, Cefotetan, Cefoxitin, Ceftazidime, Ceftriaxone, Cefuroxime injection, Ciprofloxacin oral suspension, Clindamycin injection, Erythromycin lactobionate injection, Gentamicin injection, Meningococcal vaccines (various), Mupirocin calcium 2% cream, Ofloxacin 0.3% ophthalmic solution, Oxacillin injection, Penicillin G benzathine, Penicillin G benzathine 900,000 units/Penicillin G procaine 300,000 units (Bicillin C-R 900/300), Piperacillin/tazobactam, Tigecycline, Tobramycin injection, Vancomycin injection, Yellow Fever vaccine
      • [Shortage recently resolved]: Ceftazidime/avibactam injection, Chloroquine tablets (250, 500 mg), Diphtheria, Tetanus Toxoid, and Acellular Pertussis vaccine (DTaP), Diphtheria, Tetanus Toxoid, and Acellular Pertussis and Inactivated Poliovirus and Haemophilus B Conjugate Vaccine (DTaP-IPV/HiB), Haemophilus B conjugate vaccine, Poliovirus vaccine inactivated

 

  • Antimicrobial drugs currently unavailable due to manufacturing delays or product discontinuation:
    • [New on the list]: Amoxicillin/clavulanate 1000 mg/62.5 mg ER tablets
    • [Continue to be unavailable]: Cefotaxime injection, Mupirocin calcium 2% nasal ointment, Penicillin G benzathine/Penicillin G procaine 1.2 million units (Bicillin C-R), Penicillin G procaine injection
  • Antimicrobial drugs discontinued: Elvitegravir (Vitekta, in December 2016), Peginterferon alfa-2b (in February 2016; 50 mcg vials still available in limited quantities), Boceprevir (in December 2015), Permethrin 1% topical lotion (in September 2015)
December 15, 2016

December ID Update

Sign up here to receive monthly ID Updates by e-mail.
Links marked with an asterisk (*) provide details to Sanford Guide Web Edition subscribers, while all other links are universal.

 

New Treatment Guidelines

  • New clinical practice guidelines for the diagnosis of tuberculosis disease and latent tuberculosis infection in adults and children have been prepared by a task force supported by the ATS, CDC, and IDSA (Clin Infect Dis 2016 Dec 8 [Epub ahead of print]). The guidelines are available for download on the IDSA website.

Practice Pearls

  • Drug-induced photosensitivity is a general term referring to cutaneous disease that results from the interaction of a chemical agent and sunlight. There are two types, phototoxicity (inflammatory) and photoallergy (immunologic). Clinically distinguishing between the two can be difficult; diagnostic tools such as phototesting and photopatch testing may be useful. Here is how the two reactions compare:

     

       Phototoxicity  Photoallergy
     Frequency  More common  Less common
     Typical presentation  Exaggerated sunburn  Pruritic, eczematous eruption
     Location  Sun-exposed skin  Sun-exposed skin and beyond
     Prior sensitization required  No  Yes
     Onset after initial exposure  Minutes to hours  >24 hours
     Mechanism  Direct tissue injury  T-cell mediated hypersensitivity
     Dose dependence  Yes  No

    The essential characteristic of a photosensitizing drug is its ability to absorb ultraviolet (UV) and/or visible electromagnetic radiation. The wavelength of UV (<400 nm) is shorter than visible light. UVA (black light) is 320-400 nm; UVB (the sunburn region) is 280-320 nm; UVC (germicidal) is 200-280 nm. UVA, which penetrates skin deeply, does not damage directly DNA but is capable of generating highly reactive radicals that do have that ability. UVB is capable of directly damaging DNA, as is UVC. UVC is the highest energy and most dangerous type of UV radiation. Most photosensitivity reactions are caused by UVA.
     
    The typical photosensitizing drug is of low molecular weight (200-500 dalton) with a planar, tricyclic, or polycyclic chemical configuration; it often has heteroatoms in its structure. Photoactivation results in generation of free radicals and singlet oxygen species. More than 300 drugs (mainly antimicrobials, NSAIDs, and cardiovascular agents) have been characterized as photosensitizers. A photosensitivity reaction generally resolves with drug discontinuation and sun avoidance, although patients who are unable to stop the offending drug will require topical steroids and protective physical measures to lessen symptoms. The Sanford Guide maintains a list* of possible and probable antimicrobial offenders (Clin Dermatol 34:571, 2016).

  •  

  • Many of us were taught that administration of ampicillin* or amoxicillin* results in a pruritic, maculopapular rash in most patients (65-100%) with infectious mononucleosis* (IM), a viral disease primarily caused by Epstein-Barr virus (EBV). This belief dates back to the 1960s. However, newer data suggest that the likelihood of rash may be considerably lower. An extensive literature search of all English language case reports and relevant articles addressing antibiotic-induced rash published from 1964 through June 2016 was recently conducted. Seventeen case reports and six retrospective studies were identified. The most commonly implicated drugs were amoxicillin, ampicillin, and azithromycin*. In the two most recent studies (published in 2013) the rate of rash was only 15% and 33%. The explanation for the higher rates reported in earlier publications is not known, but there are theories; for instance, impurities known to be present in early antibiotic preparations may have played a role, although not all published data support this suggestion. There seem to be two groups of patients with IM who experience an antibiotic-induced rash: a predominant group in whom the rash is likely due to transient and reversible EBV-mediated loss of immune tolerance (not a true penicillin allergy), and a smaller group of patients who appear to develop a true, persistent antibiotic hypersensitivity. The issue is not settled. For now, one can reasonably conclude that while the likelihood of antibiotic-induced rash in patients with IM is probably lower than 65-100%, we do not know with certainty what the actual rate of rash is, nor what the precise pathophysiologic mechanism is (Ann Pharmacother 2016 Sep 12 [Epub ahead of print]).
  • Nicolau syndrome, first described in the 1920s, is a rare complication of an intramuscular (IM) injection that results in varying degrees of necrosis involving the skin and adipose tissue. Offending drugs include penicillins*, local anesthetics, steroids, and NSAIDs. Nicolau syndrome is more prevalent in children, especially those under three years of age. Patients typically experience intense pain at the injection site immediately after the injection (minutes to a few hours), followed by bluish discoloration of the skin with possible ulceration and necrosis. Ulcers usually heal in a few months with scarring, and there may be transient neurological complications. The pathogenesis of Nicolau syndrome is not well understood; possible explanations include sympathetic nerve stimulation, direct vascular damage, perivascular inflammation, and vasospasm. Obese patients are at increased risk because the needle tip may not reach the muscle due to the thickness of the fat layer, resulting in drug injected outside of the muscle (sometimes repeatedly). There is no specific treatment for Nicolau syndrome. Conservative measures including debridement, topical corticosteroids, and analgesics are generally effective; vasoactive agents such as pentoxifylline may be helpful, and surgery is occasionally required. Three cases of Nicolau syndrome in children (ages 2, 2 and 9) following IM injection of benzathine penicillin G were recently reported. Two of the patients were fully recovered within one month; the third was significantly improved at two months follow-up (J Family Community Med 19:52, 2012; Bosn J Basic Med Sci 15:57, 2015; Case Rep Infect Dis 2016 Nov 1 [Epub ahead of print]).

Drug Shortages (US)

  • Antimicrobial drugs or vaccines in reduced supply due to increased demand, manufacturing delays, product discontinuation by a specific manufacturer, or unspecified reasons:

    • [New on the list]: None
    • [Continue to be in reduced supply]: Amikacin, Ampicillin injection, Ampicillin/sulbactam, Cefepime, Cefotetan, Cefoxitin, Ceftazidime, Ceftriaxone, Cefuroxime injection, Ciprofloxacin oral suspension, Clindamycin injection, Erythromycin lactobionate injection, Gentamicin injection, Meningococcal vaccines (various), Mupirocin calcium 2% cream, Ofloxacin 0.3% ophthalmic solution, Oxacillin injection, Penicillin G benzathine, Penicillin G benzathine 900,000 units/Penicillin G procaine 300,000 units (Bicillin C-R 900/300), Piperacillin/tazobactam, Tigecycline, Tobramycin, Vancomycin injection, Yellow Fever vaccine
    • [Shortage recently resolved]: Ceftazidime/avibactam injection, Haemophilus B conjugate vaccine, Poliovirus vaccine inactivated
  •  

    Antimicrobial drugs currently unavailable due to manufacturing delays or product discontinuation:

    • [New on the list]: None
    • [Continue to be unavailable]: Cefotaxime injection, Chloroquine tablets (250, 500 mg), Mupirocin calcium 2% nasal ointment, Penicillin G benzathine/Penicillin G procaine 1.2 million units (Bicillin C-R), Penicillin G procaine injection
  •  

  • Antimicrobial drugs discontinued: Elvitegravir (Vitekta, in December 2016), Peginterferon alfa-2b (in February 2016; 50 mcg vials still available in limited quantities), Boceprevir (in December 2015), Permethrin 1% topical lotion (in September 2015)
  •  

  • For detailed information including estimated resupply dates, see http://www.ashp.org/menu/DrugShortages
December 3, 2016

Web Edition Now Updated Continually

The Sanford Guide Web Edition was recently updated to a new platform in order to better serve our users. In addition to a clean new theme, the new site also enables us to add new features and functionality for all of our Web Edition and All Access subscribers.
 
The first change that users will notice is that content will no longer be updated on a monthly basis, but will instead be updated continually. This means that as soon as content is edited and reviewed by our editorial board, users will have access to the new information, bringing the latest changes in best practices to our users in real time. As always, our content will remain peer-reviewed by leaders in the field of infectious disease, and will reflect the best available guidance from the literature.
 
Our monthly ID Update newsletter, available on the Web Edition site, the Sanford Guide News site, and through e-mail subscription, will now be published earlier in the month. Updates to our mobile app content will be released according to this new schedule as well.
 
In the coming months, Sanford Guide digital subscribers will notice additional improvements, including a new searchable Spectra of Activity, additional interactive tables, expanded content, and optional add-ons to assist antimicrobial stewardship programs. Contact our sales team for more information about Sanford Guide Digital products and stewardship tools.

November 28, 2016

November ID Update

Sign up here to receive monthly ID Updates by e-mail.
Links marked with an asterisk (*) provide details to Sanford Guide Web Edition subscribers, while all other links are universal.

 

New Drug Approval

  • Tenofovir alafenamide (Vemlidy)* has been approved by the FDA for the treatment of chronic hepatitis B in adults with compensated liver disease. The recommended dosage is 25 mg orally once daily with food. Product availability: 25 mg tablets.

 New Dosage Form Approval

  • The FDA has approved Maraviroc(Selzentry) 20 mg/mL oral solution, 25 mg tablets, and 75 mg tabletsThe prescribing information has been updated to include use in pediatric patients 2 years of age and older and weighing at least 10 kg.

New Treatment Guidelines

  •  New clinical practice guidelines for the management of leishmaniasis have been prepared by a panel of the Infectious Diseases Society of America (IDSA) and the American Society of Tropical Medicine and Hygiene (ASTMH). The guidelines are available for download on the IDSA website.

Practice Pearls

  • Candida auris, an emerging fungus capable of invasive infection, is associated with high mortality and possible resistance to multiple antifungal drugs. It was first isolated in 2009 from the external ear canal of an inpatient in a Japanese hospital and has since been reported in a number of countries. A recent report describes the first seven US cases of C. auris infection reported to CDC as of August 31. C. auris is a serious concern because accurate laboratory identification requires specialized methods, it tends to be resistant to two or even three antifungal drug classes (azoles, echinocandins, polyenes), and it has caused outbreaks in health care settings. The optimal treatment regimen is not known (MMWR 65:1234, 2016).
  •  

  • Drug interactions that result in prolongation of the QT interval (QT-DDI) are often discovered many years after the drugs are marketed, suggesting the need for a more efficient strategy. A group of investigators recently mined the FDA Adverse Event Reporting System (FAERS) for signals indicating a QT-DDI. They then combined those data with ECGs from their institutional electronic health records (EHR). An unexpected interaction between lansoprazole (a proton-pump inhibitor) and ceftriaxone* was identified. Mean prolongation of the QTc (corrected QT interval) was 12 ms in males and 9 ms in females; men taking the combination were 1.4 times as likely to have a QTc above 500 ms as men taking a single drug. The largest effects were observed in white males and black females. The investigators then used patch-clamp electrophysiology to show that, in combination, the drugs block the hERG channel (the main mechanism by which drugs prolong the QT interval). As a negative control, no evidence of a QT-DDI was identified in the FAERS or EHR data, or in the electrophysiologic experiments, for the combination of lansoprazole and cefuroxime*. Further class analysis found no evidence in the FAERS or EHR for an interaction between any other cephalosporin and proton-pump inhibitor. The mechanism for this intriguing drug interaction, identified using a novel approach of data mining followed by laboratory experimentation, is not known (J Am Coll Cardiol 68:1756, 2016).
  •  

  • Many clinical trials have evaluated the use of cranberry products for UTI prevention, with inconsistent results (often negative, or positive results with flawed methodology). A recent report in JAMA describes a well-designed randomized, double-blind, placebo-controlled trial in elderly female nursing home residents intended to evaluate the effect of cranberry capsules on clinical and microbiologic outcomes. Study participants were administered two oral cranberry capsules (each capsule containing 36 mg of the active ingredient proanthocyanidin) or placebo once a day for a year. There was no significant difference in the primary outcome of bacteriuria plus pyuria, and also no significant differences in any of the secondary outcomes of the study such as symptomatic UTI, rates of death, or hospitalizations. The results of this study are consistent with the view that cranberry products cannot, at this time, be recommended for UTI prevention on the basis of proven benefit (JAMA 316:1879, 2016).
  •  

  • Vancomycin*-induced thrombocytopenia, first described in 1985, is uncommon, poorly characterized, and probably under-diagnosed. The mechanism appears to involve vancomycin-dependent, platelet-reactive antibodies (N Engl J Med 356:904, 2007). A group of researchers conducted a systematic search of the English-language literature using the PubMed, Scopus, and Web of Science databases; 29 case reports, five observational studies, two clinical trials, two letters, and one case series were identified for analysis and the results were recently published. In summary, the precise incidence of vancomycin-induced thrombocytopenia remains unclear. The reaction appears to be duration-dependent with a mean time to platelet nadir of eight days after the first exposure (and significantly shorter in cases of re-exposure). Nadir platelet counts ranged from 2,000 to 100,000 in patients who experienced bleeding. In the case reports, vancomycin-specific antibodies were detected in 13 of 17 patients who were tested. No conclusive association between vancomycin serum concentration and thrombocytopenia was observed. The platelet count returned to normal in a mean time of 5-6 days following discontinuation of vancomycin. Platelet transfusions were used in some patients with variable results; other measures such as corticosteroids, intravenous immunoglobulin, or rituximab were employed in a few patients with unclear benefit (Drug Safety 2016 Nov 15 [Epub ahead of print]).

Drug Shortages (US)

  •  Antimicrobial drugs or vaccines in reduced supply due to increased demand, manufacturing delays, product discontinuation by a specific manufacturer, or unspecified reasons:
    • [New on the list]: Cefoxitin injection, Cefuroxime injection
    • [Continue to be in reduced supply]: Amikacin, Ampicillin injection, Ampicillin/sulbactam, Cefepime, Cefotetan, Ceftazidime, Ceftriaxone, Chloroquine tablets (250, 500 mg), Ciprofloxacin oral suspension, Clindamycin injection, Erythromycin lactobionate injection, Gentamicin injection, Haemophilus B conjugate vaccine, Meningococcal vaccines (various), Mupirocin calcium 2% cream, Ofloxacin 0.3% ophthalmic solution, Oxacillin injection, Penicillin G benzathine, Piperacillin/tazobactam, Poliovirus vaccine inactivated, Tigecycline, Tobramycin, Vancomycin injection, Yellow Fever vaccine
    • [Shortage recently resolved]: DTaP (Daptacel) vaccine, DTaP-IPV/Hib (Pentacel) vaccine, Imipenem-cilastatin injection
  •  

  • Antimicrobial drugs currently unavailable due to manufacturing delays or product discontinuation:
    • [New on the list]: None
    • [Continue to be unavailable]: Cefotaxime injection, Ceftazidime/Avibactam injection, Mupirocin calcium 2% nasal ointment, Penicillin G benzathine/Penicillin G Procaine (Bicillin C-R), Penicillin G procaine injection, Penicillin G benzathine 900,000 units/Penicillin G Procaine 300,000 units (Bicillin C-R 900/300)
  •  

  • Antimicrobial drugs discontinued: Peginterferon alfa-2b (in February 2016; 50 mcg vials still available in limited quantities), Boceprevir (in December 2015), Permethrin 1% topical lotion (in September 2015)
  •  

  • For detailed information including estimated resupply dates, see http://www.ashp.org/menu/DrugShortages
November 23, 2016

Guide to HIV/AIDS Therapy 2016-2017 Release

The Sanford Guide to HIV/AIDS Therapy

 

The Sanford Guide to HIV/AIDS Therapy 2016-2017 print guides are now available! The 24th edition of our Guide to HIV/AIDS Therapy provides practical clinical guidance for the treatment of HIV and AIDS, based on the latest available evidence. Popular with physicians, pharmacists, physician assistants, nurse practitioners, and other clinicians, the Sanford Guide to HIV/AIDS Therapy provides information that is convenient, concise, and reliable.

 

Featuring numerous updates, including the latest generation of combination formulations of ARV drugs and new formulations containing tenofovir alafenamide (TAF), the guide is available in both pocket-size and larger print “library” editions. Sections on differential diagnosis of HIV/AIDS-related clinical syndromes and opportunistic infections, immune reconstitution and treatment of specific OIs have been refined and updated to reflect current trends.

 

Coverage includes:

  • Risk assessment and recommendations for HIV testing
  • Initial evaluation of HIV-infected adults
  • Diagnostic tests
  • Antiretroviral resistance testing
  • Antiretroviral therapy in adults
  • Antiretroviral drugs
  • Pharmacologic features
  • Renal impairment dose adjustments
  • Drug-drug interactions
  • Drugs used for HIV/AIDS-related infections
  • Drug generic and trade names
  • Considerations for HIV-HCV co-infection
  • Opportunistic infections
  • HIV exposure management
  • Immunizations and travel
  • HIV/AIDS in women, newborns, and children