Blood Bank Case Study: Transfusion Transmitted Malaria

Case Study

A 26 year old African American female with sickle cell anemia presented to a New York emergency room with cough, chest pain, fever and shortness of breath. Laboratory results showed an increased white blood cell count, slightly decreased platelet count and a hemoglobin of 6.2 g/dl. Her reticulocyte count was 7%, considerably below her baseline of 13%. Consulting the patient’s medical records revealed history of stroke as a child and subsequent treatment with chronic blood transfusions. She was admitted to the hospital for acute chest syndrome and aplastic crisis and care was transferred to her hematologist. Two units of RBCs were ordered for transfusion.

The blood bank technologists checked the patient’s blood bank history and noted her blood type was A, Rh(D) positive, with a history of a warm autoantibody and anti-E. The current blood bank sample confirmed the patient was blood type A, RH(D) positive with a negative DAT but the antibody screen was positive. Anti-E was identified. Per request of the hematologist, phenotypically similar units were found and the patient was transfused with 2 units of A RH(negative), C/E/K negative, HgS negative, irradiated blood. The patient’s hemoglobin rose to 8g/dl and she was discharged from the hospital 3 days after transfusion.

Ten days after discharge the patient returned to the emergency room with symptoms including aching muscles, fever and chills. A delayed transfusion reaction was suspected. A type and screen was immediately sent to the blood bank. The post transfusion type and screen remained positive for anti-E, DAT was negative. No additional antibodies were identified. However, a CBC sent to the lab at the same time revealed malarial parasites on the peripheral smear. The patient was consulted for a more complete medical history and reported that she had never traveled outside of the country. A pathology review was ordered and the patient was started on treatment for Plasmodium falciparum.

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Discussion

Red Blood cell transfusions can be life saving for patients with sickle cells anemia. These patients are frequently transfused by either simple transfusion of red cell units or by exchange transfusion. Because of this, alloimmunization is reported to occur in 20% to 40% of sickle cell patients.1 Blood bank technologists are very diligent in adhering to strict procedures and follow a standard of practice aimed to prevent transfusion reactions. While preventing immune transfusion reactions may be the most forefront in our minds when transfusing the alloimmunized patient, it is important to consider transfusion transmitted diseases as a potential complication of blood transfusions.

Malaria is caused by a red blood cell parasite of any of the Plasmodium species. Mosquito transmitted infection is transmitted to humans through the bite of an infected mosquito. Transfusion-transmitted malaria is an accidental Plasmodium infection caused by a blood transfusion from a malaria infected donor to a recipient.

Donors, especially those from malarial endemic countries who may have partial immunity, may have very low subclinical levels of Plasmodium in their blood for years. Even these very low levels of parasites are sufficient to transmit malaria to a recipient of a blood donation. Though very rare, transfusion-transmitted malaria remains a serious concern for transfusion recipients. These transfusion-transmitted malaria cases can cause high percent parisitemia because the transfused blood releases malarial parasites directly into the recipient’s blood stream.

Blood is considered a medication in the United States, and, as such, is closely regulated by the FDA. Blood banks test a sample of blood from each donation to identify any potential infectious agents. Blood donations in the US are carefully screened for 8 infectious diseases, but malaria remains one infectious disease for which there is no FDA-approved screening test available. For this reason, screening is accomplished solely by donor questioning.2 A donor is deferred from donating if they have had possible exposure to malaria or have had a malarial infection. Deferral is 12 months after travel to an endemic region, and 3 years after living in an endemic region. In addition, a donor is deferred from donating for 3 years after recovering from malaria. It is important, therefore, for careful screening to take place by questionnaire and in person, to make sure that the potential donor understands and responds appropriately to questions concerning travel and past infection.

Malaria was eliminated from the United States in the early 1950’s. Currently, about 1700 cases of malaria are reported in the US each year, almost all of them in recent travelers to endemic areas. From 1963-2015, there have been 97 cases of accidental transfusion-transmitted malaria reported in the United States. The estimated incidence of transfusion-transmitted malaria is less than 1 case in 1 million units.4 Approximately two thirds of these cases could have been prevented if the implicated donors had been deferred according to the above established guidelines.3 While the risk of catching a virus or any other blood-borne infection from a blood transfusion is very low, a blood supply with zero risk of transmitting infectious disease may be unattainable. With that being said, the blood supply in the United Sates today is the safest it has ever been and continues to become safer as screening tests are added and improved. Careful screening of donors according to the recommended exclusion guidelines remains the best way to prevent transfusion-transmitted malaria.

References

  1. LabQ, Clinical laboratory 2014 No.8, Transfusion Medicine. Jeanne E. Hendrickson, MD, Christopher Tormey, MD, Department of Laboratory Medicine, Yale University School of Medicine
  2. Technical Manual, editor Mark K. Fung-18th edition, AABB. 2014. P 201-202
  3. https://www.cdc.gov/malaria/about/facts.html. Accessed April 2018
  4. The New England Journal of Medicine. Transfusion-Transmitted Malaria in the United States from 1963 through 1999. Mary Mungai, MD, Gary Tegtmeier, Ph.D., Mary Chamberland, M.D., M.P.H., June 28, 2001. Accessed April 2018
  5. Malaria Journal. A systematic review of transfusion-transmitted malaria in non-endemic areas. 2018; 17: 36. Published online 2018 Jan 16. doi: 1186/s12936-018-2181-0. Accessed April 2018
  6. http://www.aabb.org/advocacy/regulatorygovernment/donoreligibility/malaria/Pages/default.aspx

 

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-Becky Socha, MS, MLS(ASCP)CM BB CM graduated from Merrimack College in N. Andover, Massachusetts with a BS in Medical Technology and completed her MS in Clinical Laboratory Sciences at the University of Massachusetts, Lowell. She has worked as a Medical Technologist for over 30 years. She’s worked in all areas of the clinical laboratory, but has a special interest in Hematology and Blood Banking. When she’s not busy being a mad scientist, she can be found outside riding her bicycle.

Is It Possible to Have Coexistence of Hepatitis B Surface Antigen and Antibody?

Hepatitis B surface antigen (HBsAg) is the serologic hallmark of acute Hepatitis B virus (HBV) infection. It can be detected in serum using immunoassays a few weeks after HBV infection, and normally disappears after 4-6 months in recovered patients (1). Antibodies against HBsAg (anti-HBs) appears as a response from the host immune system, and these antibodies neutralize HBV infectivity and clear circulating HBsAg (2). Anti-HBs generally persist in life, indicating recovery and immunity from HBV infection.

Some of us may simply assume that the presence of anti-HBs should always associated with the loss of HBsAg. However, it is possible to see concurrent anti-HBs and HBsAg in patients. In fact, coexistence of HBsAg and anti-HBs is not rare, and has been reported in 10 to 25 percent of HBV chronic carriers in previous studies (3-4).  The underlying mechanism is not fully understood but several reports explained it as HBsAg mutants escaping the immune system (2-4). HBsAg mutants are believed to arise under the selective pressure from the host immune system, or from vaccinations (4-6).

“a” determinant in HBsAg is one of the main target of anti-HBs. It has been reported that mutations in the “a” determinant of the surface gene (S-gene) result in amino acid substitutions in HBsAg, and reduce the binding of anti-HBs to HBsAg, leading to immune escape (4). The first HBV mutant was reported by Zanetti et al in 1988 as G145R mutation. In their report, infants born to HBsAg carrier mothers developed breakthrough infections despite receiving HBIG and HBV vaccine at birth (5). Since this report, several other HBsAg mutations have been reported (4, 6).

Currently, there is no easily available assay to diagnose individuals who are suspected of harboring HBsAg escape mutants. Moreover, mutated HBsAg may leads to false negativity in some serologic assays, leading to a missed diagnosis of chronic HBV infection (6). Another concern is the potential risk of transmission to others, as vaccination does not provide protection from these mutated viruses (8); this is especially important in liver transplant recipient and newborns from HBsAg positive mothers.

References

  1. Lok A, Esteban R, Mitty J. Hepatitis B virus: Screening and diagnosis. UpToDate. Retrieved Feb 2018 from https://www.uptodate.com/contents/hepatitis-b-virus-screening-and-diagnosis#H3
  2. Liu W, Hu T, Wang X, Chen Y, Huang M, Yuan C, Guan M. Coexistence of hepatitis B surface antigen and anti-HBs in Chinese chronic hepatitis B virus patients relating to genotype C and mutations in the S and P gene reverse transcriptase region. Arch Virol 2012;157:627–34.
  3. Colson P, Borentain P, Motte A, Henry M, Moal V, Botta-Fridlund D, Tamalet C, Gérolami R. Clinical and virological significance of the co-existence of HBsAg and anti-HBs antibodies in hepatitis B chronic carriers. Virology 2007;367:30–40.
  4. Lada O, Benhamou Y, Poynard T, Thibault V. Coexistence of hepatitis B surface antigen (HBs Ag) and anti-HBs antibodies in chronic hepatitis B virus carriers: influence of “a” determinant variants. J Virol. 2006 Mar;80(6):2968-75.
  5. Zanetti AR, Tanzi E, Manzillo G, Maio G, Sbreglia C, Caporaso N, Thomas H, Zuckerman AJ. Hepatitis B variant in Europe. 1988 Nov 12; 2(8620):1132-3.
  6. Leong J, Lin D, Nguyen M. Hepatitis B surface antigen escape mutations: Indications for initiation of antiviral therapy revisited. World J Clin Cases 2016;4:71.
  7. Colson P, Borentain P, Motte A, Henry M, Moal V, Botta-Fridlund D, Tamalet C, Gérolami R. Clinical and virological significance of the co-existence of HBsAg and anti-HBs antibodies in hepatitis B chronic carriers. 2007;367:30–40.
  8. Thakur V, Kazim S, Guptan R, Hasnain S, Bartholomeusz A, Malhotra V, Sarin S. Transmission of G145R mutant of HBV to an unrelated contact. J Med Virol 2005;76:40–6.

 

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-Xin Yi, PhD, DABCC, FACB, is a board-certified clinical chemist, currently serving as the Co-director of Clinical Chemistry at Houston Methodist Hospital in Houston, TX and an Assistant Professor of Clinical Pathology and Laboratory Medicine at Weill Cornell Medical College.

Critical Care, Critical Labs

Sepsis is a medical emergency and a global public health concern. The Surviving Sepsis Campaign started in 2012 and has since issued International Guidelines for Management of Sepsis and Septic Shock. These Guidelines have been updated several times, and the 4th edition of the 2016 guideline have been issued. The Guidelines are written from the perspective of developed (“resource-rich”) countries, where critical care settings are equipped with tools for managing these patients. Yet, the developing world carries the greatest burden of sepsis-related mortality. Unfortunately, the developing world lacks access to many of the necessary tools for managing the critically ill patient – including basic laboratory testing.

Laboratory values are a significant part of the management of the septic patient. Take a look at the sepsis screening tool. Analytes and lab tests included in screening patients for sepsis include: lactate, creatinine, bilirubin, INR, and blood gases. The Surviving Sepsis bundles require a lactate concentration within 3 hours of presentation, and a subsequent lactate within 6 hours. The care bundle also requires a blood culture within 3 hours of presentation and prior to administration of antibiotics. Early-goal directed therapy for sepsis requires administration of crystalloid based on lactate concentrations. Basics of laboratories in the US, lactate and blood cultures are both difficult to obtain and far from routine in the resource-poor care settings.

Blood gases and lactate are particularly difficult to find and to maintain in the developing world. While there are a number of point-of-care or small benchtop devices – like the iStat (Abbott), the Piccolo (Abaxis), and the Stat Profile pHOx (Nova), it is often cost-prohibitive to maintain these devices.  The iStat and the Piccolo are examples of cartridge-based devices. All of the chemistry takes place in single-use cartridges and the device itself is basically a timer. In my experience, cartridge based devices hold up in environmental extremes better than open reagent systems. However, they are not cheap and this can be prohibitive. Cost of a single cartridge can range from $3-10 USD. In countries where patients and their families are expected to pay upfront or as they go for even inpatient medical care, and the income for a family is $2USD/day, routine monitoring of blood gases and lactate by cartridge is just not feasible. Reagent based devices like the Stat Profile use cartons of reagent for many uses. This is much cheaper – if all the reagent is used before it expires! Some healthcare settings can accommodate only 1-3 critical patients, and might not be able to use a whole carton before the expiry, even when adhering to Surviving Sepsis guidelines.

Blood cultures and subsequent treatment with appropriate antibiotics is a large part of the surviving sepsis campaign. Microbiology in the developing world is often limited to a few reference laboratories in country. Also, the number of potential infectious agents is larger in the developing world where diseases like malaria and dengue fever are common. Multiplexed nucleic acid tests might fill the gap here. Again, the cost is a major factor. Just reagents alone for a single multiplexed NAT can be over $250 USD.

In short, if the surviving sepsis guidelines really do help decrease sepsis mortality, the developing world doesn’t have a chance unless it has a greater laboratory capacity. Basic labs that we don’t think twice about can be very hard to come by in resource-poor environments. The tests already exist in forms that can be used in resource-poor settings – they just need to be cheaper, at least for those in limited resource settings. Are you listening, Abbott?

 

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Sarah Riley, PhD, DABCC, is an Assistant Professor of Pediatrics and Pathology and Immunology at Washington University in St. Louis School of Medicine. She is passionate about bringing the lab out of the basement and into the forefront of global health.  

A Serious Aside

As an unscheduled post, I’d like to make a quick side note separate from public health, zika, and medical school. You may have seen a post I wrote last January about the potential stereotypes and stigmas we might face in laboratory medicine. But, just because we as laboratory professionals operate behind-the-scenes most of the time, we’re still healthcare professionals—and clinician burnout can affect any of us.

I recently watched a video of Dr. Zubin Damania, also known as “ZDoggMD,” a primary care physician and founder of Turntable Health in Las Vegas. He’s a brilliant and passionate doctor with great opinions and an even greater creative sense of humor. Among his many parodies, and “rounds” Q&A questions, ZDoggMD recently had a guest on one of his Facebook shows called “Against Medical Advice” to address the serious issue of suicide and depression in medicine. Janae Sharp was the guest on this episode speaking about her husband, John, a physician fresh into his residency who committed suicide. They go on to talk about her life after this tragedy and how if flipped her and their children’s’ lives upside down. Janae’s described John as a father, a writer, a musician, an idealist, who always wanted to become a doctor. My interest was definitely piqued by this—I tend not to miss most of Dr. Damania’s content—and this is something I’ve been hearing more and more about as my path through medical school continues. But, at one point in the interview my heart just stopped: John was a clinical pathologist. Too close to home, for me at least. I was admittedly surprised.

Pathologist’s don’t have that much stress to make depression and suicide part of that life, I thought. But that is a cold hard assumption. Depression affects so many people at large, and when you’re in healthcare it almost seems like a risk factor on top of issues one might be struggling with. Med school is touted as one of the hardest intellectually, physically, and emotionally grueling experiences you could go through—I will personally vouch for Dr. John and Dr. Damania’s statements about how much these experiences push you to your limits. No sleep, no recognition, no support, fear of failure, imposter syndrome, a wealth and breadth of knowledge that makes you feel like you’re drowning—not to mention that if you do ask for help you’re immediately “lesser” for doing so.

Video 1. ZDoggMD interviews Janae Sharp about her tragic loss, her husband John’s suicide, and the rampant problem of depression and burnout in medicine. Against Medical Advice, Dr. Damania.

Last month, I was fortunate enough to attend a grand rounds session at my current hospital about this very topic. Presented by Dr. Elisabeth Poorman, internal medicine attending physician, and clinical instructor at Harvard Medical School, who talked about how (because of stigmas) medical trainees don’t get the help they need. She demonstrated that prior to med school students are pretty much on-par with their peers with regard to depression. However, once medical school starts, those peers all plummet together as depression rates rise and fall dramatically throughout the various stages of their careers. (I’m just going to go ahead and vouch for this too.) Dr. Poorman shared several case studies that effectively conveyed just how hard it can be when it seems like you are a source of help for many, but no one is there to help you. Story and story recounted the same model of apparent—and often secretive—burnout which ultimately led to a decrease in the quality of care, and in some instances suicide. Dr. Poorman was also brave enough to share her own story. No stranger to depression, herself, it was something that she encountered first hand. She connected herself with this increasingly difficult picture of inadequate support for those of us spending our lives serving others.

docs-depression1
Figure 1. Dr. Poorman’s data reveals that depression rates for medical school classmates in a cohort generally rise and fall as their duties and responsibilities change during their career trajectory. I’m currently on the slope downward between the first 1-3 years of school’s peak and the 4th year trough.

There are clear problems facing those of us in healthcare jobs. An ironic consequence, however, of modern scientific advancement is the “doubling time” of medical knowledge. While not necessarily a problem, this refers to the amount, depth, and scope of knowledge physicians and medical scientists are expected to master in order to effectively treat, make critical clinical decisions, and educate our patients. While in 1980 it took 7 years for all medical knowledge to double in volume, it only took 3.5 years in 2010, and in 2020 it’s expected to double every 73 days!1. The problems come as a result of this knowledge because more data means more to do. More time on the computer, higher critical responsibility, and less time to focus on your own mental health all lend themselves to a cyclic trap of burnout. Physicians commit suicide at a rate of 1.5 – 2.3 times higher than the average population.1

Physicians, nurses, clinical scientists, lab techs, administrators, phlebotomists, PCTs—we’re all over worked, under-supported, fall victim to emotional fatigue, and have some of the highest rates for depression, substance abuse, PTSD, and suicide.1 Sometimes, reports from Medscape or other entities will report that burnout is a phenomenon of specialty, hypothesizing that critical nature specialties have more depression than lesser ones2 (the assumption that a trauma surgeon might burn out before a hematopathologist). But truthfully, this is just part of the landscape for all providers. A May 2017 Medscape piece wrote “33% chose professional help, 27% self-care, 14% self-destructive behaviors, 10% nothing, 6% changed jobs, 5% self-prescribed medication, 4% other, 1% pray.”3

So I’m talking about this. To get your attention. So that people reading know they’re not alone. So that  people with friends going through something can lend a hand. I’m talking about this. ZDoggMD is talking about this. Jamie Katuna, another prolific medical student advocate, is talking about this. Dr. Elisabeth Poorman is talking about this. This is definitely something we should come together to address and ultimately solve.

What will you do to help?

This was a heavy topic. So in a lighter spirit, I have to share this with all of my laboratory family. If you haven’t heard or seen Dr. Damania’s videos yet, this is the one for you:

Thanks! See you next time!

References

  1. Poorman, Elisabeth. “The Stigma We Live In: Why medical trainees don’t get the mental health care they need.” Cambridge Health Alliance, Harvard Medical School. Grand rounds presentation, Feb 2018. Bronx-Lebanon Hospital Center, New York, NY.
  2. Larkin, Mailynn. “Physician burnout takes a toll on U.S. patients.” Reuters. January 2018. Link: https://www.reuters.com/article/us-health-physicians-burnout/physician-burnout-takes-a-toll-on-u-s-patients-idUSKBN1F621U
  3. Wible, Pamela L. “Doctors and Depression: Suffering in Silence.” Medscape. May, 2017. Link: https://www.medscape.com/viewarticle/879379

 

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Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola University Chicago with a BS in Molecular Biology and Bioethics and then Rush University with an MS in Medical Laboratory Science. He is currently a medical student at the American University of the Caribbean and actively involved with local public health.

The “C” in HCV Stands for “Curable”

Hi everyone! It has felt so good to find myself back in the throes of hospital life. My time in the classroom during the first half of medical school was great—but this new chapter is what makes medical school very worth it. As with any new hospital, orientation was pretty run-of-the-mill: administrative paperwork, employee/student health clearance, and yet another Mantoux PPD (despite having a current QuantiFERON—lab family, you get me).

However, after all the introductory logistics, I finally reported to my first rotation. It is an elective clerkship in primary care focused primarily on patients with HIV and/or Hepatitis. My familiarity with hospital life made the transition back easy enough as I made my way to the nurses’ station looking for my attending. Being forwarded in the direction I had to go, I knocked on the door and started to introduce myself—but was abruptly interrupted. There were already two fellow student colleagues in that room with my attending and a patient. I was enthusiastically included in the process right away, and it has been non-stop since then. I am told this is a “different” rotation where I’m going to feel lucky to have so much hands-on experience, and so far, I agree. While I reminisce on these past few weeks, it’s not a specific patient or case that has stuck with me, but an overall theme I’ve noticed in this rotation. With heavy utilization of the right test at the right time (I’m sure we’re all familiar with ASCP’s Choosing Wisely campaign) and proper interpretations of lab data, patients’ chronic illnesses are being managed well and even cured.

Essentially, pharmaceuticals have been advancing so well in the last 5-10 years that treatment regimens for chronic diseases like HIV and HCV are now being actively controlled and cured, respectively. Why does this pique my interest enough to share it with all of you? As I try my best each month to provide you a window into the life of a medical lab scientist/medical student, I do so while focusing on the lab details that seem to be present in every aspect of my journey. The cures and treatments I’m currently working with are tied to lab tests like CD4 counts, viral loads, liver and kidney function tests, and many other routine values. Diagnostic criteria for different patients’ stages of hepatic damage are classified using a Child-Pugh (CTP) score from clinical information such as ascites and encephalopathy along with lab data like INR, bilirubin, and albumin. Patients with chronic conditions come back for follow up week in and week out for lab tests that let us as care providers adjust therapy accordingly. The clinic I currently rotate in provides its patients with the most up to date treatment protocols based on current literature. For example, The American Association for the Study of Liver Diseases (AASLD) and the Infectious Diseases Society of America (IDSA) regularly publish their recommendations for patients with Hepatitis C. It’s heavy reading, and anyone who goes through literature on standards of care knows it’s dense, so I’ll leave the link to the most recent guidelines on HCV testing, management, and treatment here (https://www.hcvguidelines.org/sites/default/files/full-guidance-pdf/HCVGuidance_September_21_2017_g.pdf). Actively and accurately incorporating these treatment protocols into the patient care algorithms works and demonstrates great utilization of lab driven data with new available therapies.

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Figure 1. AASLD and IDSA HCV Recommendations Standards, 2018.

As a baseline it is critical to understand that patients with positive HCV antibodies will always test positive; once exposed at any point patients will remain positive. While 20% of patients can clear the infection on their own, the remaining majority develop a chronic HCV infection. There is no vaccine for HCV currently; however, there is potential to cure patients—assuming the lab values are interpreted correctly. So, we’ve established that positive HCV antibodies don’t necessarily provide diagnostic data, so the next logical step is to examine a patient’s HCV viral load. Since 2015, the New York State Department of Health established a mandate and protocol for reflex testing HCV Ab positive patients with HCV RNA viral loads. Read the public letter here (https://www.health.ny.gov/diseases/communicable/hepatitis/hepatitis_c/docs/reflex_testing_letter.pdf). While it makes logical sense, it’s still taking some time to get off the ground as I have seen patient records of different clinics’ providers ordering repeat HCV Ab testing for in-house confirmation—not the best use of resources or lab data. A clear example here of Choosing Wisely for the appropriate lab test. However, so long as HCV viral load stays undetectable by a validated testing method, patients with chronic HCV are promoted to a status of “cured HCV” and need no further testing or follow-up unless new clinical reasons appear to add testing as needed.

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Figure 2. HCV Infection testing and treatment algorithm seen in literature from the Centers for Disease Control and Prevention (CDC), the NYS Health Department, the AASLD, and the IDSA.

Protocols for treatment are based on things like genotype, cirrhosis, and naïve vs. previously failed treatment; treatment schedules last from 8 weeks up to 24 weeks. So, what does a patient’s first visit for HCV treatment therapy look like? Right away (assuming a positive HCV Ab has been obtained) a Hepatitis C RNA viral load is ordered, along with genotype (older treatments are dependent on genotype due to potential for resistance, while newer treatments are pangenotypic), hepatic fibrosis scans (because cirrhosis status determines length of treatment), PT/INR, CBC, CMP, HIV, RPR/CG and other STI screening, and urine drug testing. New generation therapies allow us to proceed despite any comorbid conditions, while maintaining upwards of 95% or greater cure rates. Coinfected patients with HIV or otherwise compromised immune systems are no longer contraindicated to receive HCV treatment. The only significant contraindication in the standards of care currently is that patients not be terminal (i.e. they must have a general prognosis of greater than 6 months).

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Figure 3. Calculated FIB-4 and APRI scores are useful in prognostic and treatment decision-making, demonstrating how crucial laboratory-driven data is in managing chronic illness.

Being able to watch these treatment protocols in action is great, but one patient in particular will stay with me beyond this clerkship. We received lab results back for a male in his 60s. It was his final HCV viral load based on his treatment schedule. His chart had a box at the end of his schedule labeled “test for cure” and it had remained non-detectable the whole time through treatment. The staff at this clinic does painstaking follow-up with their patients via telephone with impressive results in patient adherence and treatment success. My task one day was to call this patient and inform him that, unless he needed any medical treatment outside of his annual physical, he no longer needed to come in for therapy or testing—his Hep C was cured. He was extremely delighted to hear this news, and I was happy to give it to him. He had been on therapy for less than a few months but had lived with HCV for years. It was an excellent experience! And even more excellent—being part of the connection between lab tests, clinics, and patients. When I started I was just excited to wear that white coat and go visit the hospital’s lab, but I was pleasantly surprised to see the impact on patients’ treatments. Especially considering using the right test at the right time, and truly making a visible difference with excellent data.

See you next time!

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Image 1. Me (center) and my medical student colleagues Ahmad M. Khan (right) and Emeka Ajufo (left).

 Post script: listen to a new podcast my colleagues and I are in where we discuss clinical stories and pearls of wisdom through medical school. As they relate to my posts here on Lablogatory I’ll include a link—this post will focus more in depth on what I presented here regarding HCV cures and lab data.

 

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Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola University Chicago with a BS in Molecular Biology and Bioethics and then Rush University with an MS in Medical Laboratory Science. He is currently a medical student at the American University of the Caribbean and actively involved with local public health.

A Primer on HIV, Hepatitis, and Clinicals: A Bronx Tale

Hello again everyone! Last time on Lablogatory, I discussed the importance of patient advocacy and how it was especially poignant around the recent holiday season. We all have families, and sometimes those families and our medical professions intersect. Since then, I hope you’re all having a good start to the new year!

For me, the new year means a new start in medical school with clinical clerkships in New York City. Building off the theme I started last year, I hope to continue a message of patient advocacy through a laboratorian’s lens as I learn and navigate the clinical side of our field. My first such rotation is in a clinic serving a population with very significant statistics, both from the standpoint of laboratory data and epidemiology: HIV, hepatitis, and chronic infectious disease. As such, let me use this as a primer and explore what that really means for the patients in that community.

Now it’s no surprise that laboratory professionals like ourselves are deeply involved with public health efforts aimed at mitigating chronic/infectious diseases through screening, collaborating, and advancing technology. Last year I was fortunate enough to be part of the 2017 ASCP Annual Meeting in Chicago. Participating in sessions, and roundtable discussions, I was also able to listen to US Global AIDS Coordinator, Deborah L. Birx, MD had to say regarding ASCP’s global contributions to HIV/AIDS research and public health efforts. She spoke about resource limited laboratories and how ASCP has been an active and longstanding partner to the President’s Emergency Plan for AIDS Relief (PEPFAR), a global health initiative to address HIV/AIDS.

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Image 1. My wife Kathryn C. Booth, RN, MSN, CNL, and I, take part in a roundtable discussion at ASCP Chicago 2017. From Critical Values: 2017;11(1):34-39. doi:10.1093/crival/vax040
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Image 2. US Global AIDS Coordinator Deborah Birx, MD, delivers the scientific general session at ASCP 2017 in Chicago. From Critical Values: 2017;11(1):34-39. doi:10.1093/crival/vax040

The relationship between laboratory data and epidemiology is evident, as results from screening and routine testing demonstrates both snapshots of evolving health statistics as well as progress in public health initiatives like PEPFAR. ASCP’s global initiatives reach all the way to Africa as those resource-limited laboratories gain support from telecommunications and shared materials. From rapid HIV tests with Western Blots, to Zika seroprevalence research, laboratory data and public health are dependent on each other. So how does this manifest in a place like New York, specifically the Bronx where my clinical rotations are located?

First, let me illustrate a snap shot of the scene in this New York borough. Something that demonstrates important data are a region’s social determinants of health—something I have found in my research and experience to be invaluable pieces of information when trying to address health concerns and influence outcomes with particular patient populations.

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Figure 1. A clear layout of New York’s Boroughs. I currently live in Manhattan and go to clinical sites in the Bronx for my clerkship rotations. (Alamy stock photo. Photo credit: http://www.alamy.com/stock-photo-new-york-city-5-boroughs-map-96927034.html)

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Figures 2-5. 2015 NYC Rates of Persons Living with Diagnosed HIV compared against variable social determinants of health including poverty, high school education, median income, and income inequality. Accessed through AIDSVu.org interactive map, visit it here: https://tinyurl.com/y8u9op8v

It’s clear to see here that the Bronx area has the most significant epidemiologic presence of active and new HIV cases. Parallel to this, the data demonstrates that the social determinants of health illustrated in Figures 2-5 are clearly correlative. More so, in the most recent report by the New York City Department of Health and Mental Hygiene (DOHMH) and the office of HIV Epidemiology and Field Services Program (HEFSP), data collected since 1981 from reported clinical encounters, viral loads, CD4 counts, and HIV genotypes reveal significant social health statistics. According to their 2016 NYC HIV/AIDS Annual Surveillance Statistics, the Bronx remains plighted with high numbers for HIV. It would appear as well, that regardless of HIV status, an overwhelming majority of the population (>71%) live in very high poverty—defined as >30% of the federal poverty line. According to data from Community Board 6, the local representation for the Bronx and specifically the zip code around my clinical site, the median household income is $24,537. A majority of this population is comprised of minorities as well, >40% Black and >40% Latino. The data differs slightly between men and women (including transgendered men and transgendered women) with regard to transmission risk. For men the highest risk factor continues to be sexual transmission between homosexual men, or men who have sex with men (MSM). For women, the risk stratifies to a high majority of heterosexual transmission (>70%). Read the full 2016 NYC DOHMH report here: https://tinyurl.com/ycf82xld. According to AIDSVu.org nearly 3,000 people out of 100,000 residing in the Bronx are living with active diagnosis of HIV/AIDS. The same source reports that between 2011 and 2015, the number of new cases approaches 200 annually.

Another valuable function of the AIDSVu.org website is their HepVu.org companion site which provides incidence and infographic data about Hepatitis infections. The Hepatitis B and C Annual Report for 2014 published by the NYC DOHMH in 2016 also provides information about this chronic condition and how it affects the population. The maps below demonstrate that chronic Hepatitis is a serious and prevalent problem, and at a slight majority directly affects patients proportional to age.

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Figures 6-8. Maps from the DOHMH NYC Hepatitis B and C Annual Report for 2014 published in 2016. (Source: https://www1.nyc.gov/assets/doh/downloads/pdf/cd/hepatitis-b-and-c-annual-report.pdf)
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Figure 9. Mortality rates of HepB, HepC, and HIV in New York City at large. Note the decrease in HIV and slight increase in HepC. (Source: https://www1.nyc.gov/assets/doh/downloads/pdf/cd/hepatitis-b-and-c-annual-report.pdf)

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Figures 10-11. Maps that demonstrate that even though New York State has a lower-than-average HepC prevalence rate, it has a relatively higher rate of mortality. Source: https://hepvu.org/resources/

But what does all this data mean? First and foremost it means progress. Progress for our patient populations because we’re busy tracking and keeping ahead of health statistics as they happen, and progress in our innovative ways to test earlier, screen better, and use the data wisely. None of this would be possible without the lab. From every hepatitis viral load, antigen immunoassay, and serology, lab data becomes translated to health data. And, all the while, clinical encounters with real patients experiencing real chronic illnesses are reported into epidemiologic data. Together we use those two sets of data to improve patient outcomes—I talked about that a lot with Zika in Sint Maarten.

I am honored to be at that bridge between the lab and the patient. Translating data back and forth from bedside to primary source is something that brings me a real sense of purpose. As part of this clinical rotation I will have to be involved in patient education, delivering presentations and conducting follow-up with those in the community who these public health messages are targeted to. So, instead of boring you some more with facts about lab science, testing/screening opportunities, and a promising future for those with chronic illness, I’ll go ahead and get a presentation ready for them!

Talk to you soon with some more in-depth clinical case-based blogging! Thanks for reading!

 

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Constantine E. Kanakis MSc, MLS (ASCP)CM graduated from Loyola University Chicago with a BS in Molecular Biology and Bioethics and then Rush University with an MS in Medical Laboratory Science. He is currently a medical student at the American University of the Caribbean and actively involved with local public health.