Month: June 2015

How should I interpret a positive Treponema serology by enzyme immunoassay (EIA) in my elderly patient with dementia?

FA Manian MD, MPH, , , , Leave a comment

A positive EIA treponema-specific test (e.g. Trep-Sure) suggests either current or prior syphilis.  It should be followed by an RPR to better assess disease activity (1).  If the RPR is positive, syphilis can be assumed and further evaluation for neurosyphilis with lumbar puncture may be necessary in this elderly patient with neurological symptoms.

If the RPR is negative, a more specific treponema test (e.g. fluorescent tryponemal antibody [FTA], or  Treponema pallidum particle agglutination [TP-PA]) should be performed for confirmation of the treponema-specific test (1). 

Recall that the treponema-specific antibody tests by EIA  are much more sensitive and specific than RPR, especially during the primary and late stages of syphilis.   Also remember that serum RPR may be negative in about 30% of patients with neurosyphilis (2); so a negative serum RPR should not rule out neurosyphilis.

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 References

1. Binnicker MJ, Jespersen DJ, Rollins LO. Treponema-specific tests for serodiagnosis of syphilis: comparative evaluation of seven assays 2011;49:1313-1317. https://www.ncbi.nlm.nih.gov/pubmed/21346050

2. Whitefield SG, Everett As, Rein MF. Case 32-1991;tests for neurosyphilis. N Engl J Med 1992;326:1434. https://www.ncbi.nlm.nih.gov/pubmed/1569992

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

How should I interpret a positive Treponema serology by enzyme immunoassay (EIA) in my elderly patient with dementia?

Is there anyway to predict a significant rise in INR from antibiotic use in patients who are also on warfarin?

FA Manian MD, MPH, , , , , , , , , , , , , , 1 Comment

Not really!  Many of the commonly used antibiotics have the potential for increasing the risk of major bleeding through disruption of intestinal flora that synthesize vitamin K-2 with or without interference with the metabolism of warfarin through cytochrome p450 isozymes inhibition.

Although there may be some inconsistencies in the reports, generally quinolones (e.g. ciprofloxacin, levofloxacin), sulonamides (e.g. trimethoprim-sulfamethoxazole), macrolides  (e.g. azithromycin), and azole antifungals (e.g. fluconazole) are thought to carry the highest risk of warfarin toxicity, while amoxacillin and cephalexin may be associated with a more modest risk (1,2).  Metronidazole can also be a culprit (2).

References

1. Baillargeon J, Holmes HM, Lin Y, et al. Concurrent use of warfarin and antibiotics and the risk of bleeding in older adults. Am J Med. 2012 February ; 125(2): 183–189. https://www.ncbi.nlm.nih.gov/pubmed/22269622

2. Juurlink DN. Drug interactions with warfarin: what every physician should know. CMAJ, 2007;177: 369-371. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1942100/pdf/20070814s00018p369.pdf

Is there anyway to predict a significant rise in INR from antibiotic use in patients who are also on warfarin?

What is the role of direct oral anticoagulant (DOAC) agents in preventing venous thromboembolism (VTE) in patients who undergo hip or knee arthroplasties?

FA Manian MD, MPH, , , , , , , , , , , , , , , Leave a comment

DOACs (eg, rivaroxaban, apixaban,and dabigatran) are increasingly considered for use after hip and knee arthroplasties due to their demonstrated efficacy against VTE prophylaxis and an acceptable safety profile. 

In a meta-analysis involving 16 trials in over 38,000 patients, when compared to enoxaparin, the risk of symptomatic VTE appeared to be significantly lower with rivaroxaban (relative risk 0.48, 95% C.I. 0.3-0.75), and similar with dabigatran and apixaban (1).

In the same study, compared to enoxaparin, the relative risk of clinically relevant bleeding was significantly higher with rivaroxaban (1.25, 95% C.I. 1.1-1.5), similar with dabigatran , but lower with apixaban (0.82, 95% C.I. 0.7-0.98) (1). The authors concluded that new anticoagulants did not differ significantly for efficacy and safety.

Of course, the decision to use a DOAC vs enoxaparin should be made on an individual basis taking into account a variety of factors,  such as patient preferences, cost, comorbidities, patient compliance with medications, etc…  

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 Reference

1.  Gomez-Outes, Suarez-Gea L, Vargas-Castrillon E.  Dabigatran, rivaroxaban, or apixaban versus enoxaparin for thromboprophylaxis after total hip or knee replacement: systematic review, meta-analysis, and indirect treatment. BMJ 2012;344:e3675. https://pubmed.ncbi.nlm.nih.gov/22700784/ 

 

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

What is the role of direct oral anticoagulant (DOAC) agents in preventing venous thromboembolism (VTE) in patients who undergo hip or knee arthroplasties?

Is the “8 day rule” for treatment of healthcare-associated pneumonia (HAP) appropriate irrespective of etiologic agent?

FA Manian MD, MPH, , Leave a comment

Not necessarily.  In fact, an often-quoted study showed more relapses among patients with Pseudomonas aeruginosa nosocomial pneumonia treated for 8 days compared to 15 days, and concluded that the results did not apply to “non-fermenting gram negative bacilli” (1).

For methicillin-resistant Staphylococcus aureus (MRSA) pneumonia, the data on the effectiveness of the shorter course therapy is also quite limited (1,2) .  So for patients with pneumonia due to organisms such as P. aeruginosa or MRSA I decide on the duration of therapy on case-by-case basis depending on the overall stability of the patient and their progress in recovery.

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References

1. Chastre J, Wolff M, Fagon JY. Comparison of 8 vs 15 days of antibiotic therapy for ventilator-associated pneumonia in adults: a randomized trial. JAMA 2003;290:2588-98. 

2. Rubinstein E, Kollef MH, Nathwani D. Pneumonia caused by methicillin-resistant Staphylococcus aureus. Clin Infect Dis 2008;46 (Suppl5):S378-385.

Is the “8 day rule” for treatment of healthcare-associated pneumonia (HAP) appropriate irrespective of etiologic agent?

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?

FA Manian MD, MPH, , , , , , , , , , , Leave a comment

Yes!  Although we often associate oral candidiasis with thrush or pseudomembranous white plaques, another common form of oral candidiasis seen in hospitalized patients is “acute atrophic candidiasis” (AAC), also referred to as “antibiotic sore mouth” because of its association with use of broad spectrum antibiotics (1,2). 

Despite the absence of thrush, patients with AAC often have erythematous patches on the palate, buccal mucosa and dorsum of the tongue. Common symptoms include burning sensation in the mouth (especially with carbonated drinks in my experience), dry mouth and taste buds “being off” (2).  

Aside from antibiotics, other predisposing factors for AAC include corticosteroids, HIV disease, uncontrolled diabetes mellitus, iron deficiency anemia, and vitamin B12 deficiency.

So next time you see a hospitalized patient with new onset sore, burning mouth that wasn’t present on admission, think of antibiotic sore mouth!

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References

1. Stoopler ET, Sollecito TP. Oral mucosal diseases. Med Clin N Am 2014;98:1323-1352. https://www.ncbi.nlm.nih.gov/pubmed/25443679

2. Millsop JW, Fazel N. Oral candidiasis. Clin Derm 2016;34:487-94. https://www.ncbi.nlm.nih.gov/pubmed/27343964

Can oral candidiasis be symptomatic without actual pseudomembranes or “thrush”?

Is there a connection between cirrhosis and elevated CK or rhabdomyolysis?

FA Manian MD, MPH, , , , , , , Leave a comment

Besides the usual causes of rhabdomyolysis such as trauma, drugs, alcohol, sepsis, etc…, cirrhotic patients may also have what some have called “hepatic myopathy”.  

One study involving 99 patients with cirrhosis and myopathy (all with elevated serum myoglobin) found “infections” as the most common cause (47%),  followed by “idiopathic” (27%) sources as well as ETOH, herbal medicine, and trauma-related causes (<10% each) (1).  Whether this is truly an entity  or just a non-causal association is unclear.

Another study reported that ~60% of rhabdomyolysis cases in cirrhosis had no apparent cause (2), with mortality among patient with cirrhosis and rhabdomyolysis significantly higher than that of controls without cirrhosis (27.5% vs 14.5%).

So perhaps we should lower our threshold for checking serum CK in our patients with cirrhosis and weakness.

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Reference

1. Lee O-J, Yoon J-H, Lee E-J, et al. Acute myopathy associated with liver cirrhosis. World J Gastroenterol 2006;12:2254-2258.  https://www.ncbi.nlm.nih.gov/pubmed/16610032 .

2. Baek JE, Park DJ, Kim HJ, et al. The clinical characteristics of rhabdomyolysis in patients with liver cirrhosis. J Clin Gastroenterol 2007;41:317-21.

 

Is there a connection between cirrhosis and elevated CK or rhabdomyolysis?

What is the connection between cirrhosis and hyperkalemia?

FA Manian MD, MPH1 Comment

Although, many of the familiar causes of hyperkalemia, including K-sparing diuretics, renal dysfunction, and adrenal insufficieny may be present in our cirrhotic patients as well, a poorly-functioning liver itself may be the culprit.

The liver, just as the muscle tissue, plays an important role in K uptake and serves as a buffer against serum K fluctuations. In a really cool experiment involving subjects given oral K supplements under controlled conditions (1), patients with cirrhosis had much greater bump in their serum K levels than normal controls despite similar weight, renal excretion of K and a significant rise in C-peptide levels. 

So even in the absence of usual risk factors, our cirrhotic patients may be more susceptible to hyperkalemia.

1. Decaux G, Soupart A, Cauchie P, et al. Potassium homeostasis in liver cirrhosis. Arch Intern Med 1988;148:547-8.

What is the connection between cirrhosis and hyperkalemia?

What is the rationale for using N-acetylcysteine (NAC) in the treatment of non-acetaminophen-related liver failure (NALF)?

FA Manian MD, MPH, , , , , Leave a comment

Although  the evidence on the effectiveness of NAC in NALF has often been inconclusive, an 2021 meta-analysis and systematic review of the role of NAC in NALF concluded that NAC significantly improves overall survival, post-transplant survival and transplant-free survival while decreasing the overall length of hospital stay (1). 

This meta-analysis included 7 studies involving 883 patients with a mean age of 21 years in the NAC group. Significantly higher overall survival (O.R. 1.8), post-transplant survival (O.R. 2.4) and transplant-free survival (O.R. 2.9) were observed in the NAC group. 

Previously, a 2009 randomized-controlled study involving adults with NALF (including many due to drug toxicity, hepatitis B virus-HBV, and autoimmune causes) had found longer transplant-free survival—not overall survival—in the treatment group, especially among those with lower grade encephalopathy, or liver failure caused by drugs or HBV (2). 

Although it’s not clear how NAC might work in the setting of of NALF, possible effect on microcirculation or 02 delivery through interference with cytokines or other mechanisms have been suggested (2,3).  An interesting 2013 article reported lower serum levels of interleukin-17 among treated patients (3)!

Bonus Pearl: Did you know that acute liver failure affects 2000-3000 persons in the U.S. each year with a mortality as high as 30%? (3)

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References

  1. Walayat S, Shaoib H, Asghar M, et al. Role of N-acetylcysteine in non-acetominophen-related acute liver failure: an updated meta-analysis and systematic review. Ann Gastroenterol 2021;34, 1-6. http://www.annalsgastro.gr/files/journals/1/earlyview/2021/ev-01-2021-04-AG_5321-0571.pdf 
  2. Bass S, Zook N. Intravenous acetylcysteine for indications other than acetaminophen overdose. Am J Health-Syst Pharm 2013;70:1496-1501. https://www.ncbi.nlm.nih.gov/pubmed/23943180
  3. Stravitz RT, Sanyal AJ, Reisch J, et al. Effects of N-acetylcysteine on cytokines in non-acetaminophen acute liver failure: potential mechanism of improvement in transplant-free survival. Liver Int. 2013;33:1324-1331. https://utsouthwestern.pure.elsevier.com/en/publications/effects-of-n-acetylcysteine-on-cytokines-in-non-acetaminophen-acu

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Mercy Hospital-St. Louis or its affiliate healthcare centers, Mass General Hospital, Harvard Medical School or its affiliated institutions. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!

 

What is the rationale for using N-acetylcysteine (NAC) in the treatment of non-acetaminophen-related liver failure (NALF)?

How should follow-up serum C-reactive protein (CRP) in patients with community-acquired pneumonia (CAP) be interpreted?

FA Manian MD, MPH, , , Leave a comment
CRP level should drop to less than one-half of its value on admission after a couple of days of antibiotic therapy, since CRP half-life is less than a day following zero order elimination kinetics. 

 

Of interest, in a study of serial CRP in severe CAP (1), a CRP ratio >0.5 by day 3 was associated with non-resolving pneumonia ( sensitivity 91%, specificity 55%)   performing significantly better than body temperature or WBC count.  

 

So if there is any doubt about how a patient is doing clinically, a repeat CRP looking for a drop of greater than on-half after 3-4 days of therapy may be helpful.

 

Bonus Pearl: Did you know that the half-life of CRP is 19 h?

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Reference

1. Coelho L, Povoa P, Almenda E, et al. Usefulness of C-reactive protein in monitoring the severe community-acquired pneumonia clinical course.  Critical Care 2007;11:R92 https://ccforum.biomedcentral.com/articles/10.1186/cc6105

 

 

How should follow-up serum C-reactive protein (CRP) in patients with community-acquired pneumonia (CAP) be interpreted?