FIT screening

Dikkedarmkanker, ook wel colorectaal carcinoom, is een veelvoorkomende ziekte onder voornamelijk ouderen. Het detecteren van dikke darmkanker in een vroeg stadium kan de overlevingskans van een patiënt aanzienlijk vergroten. Door gebruik te maken van een fecale immunochemische test (FIT) worden kleine hoeveelheden bloed (met behulp van antilichamen voor humaan hemoglobine) opgespoord in ontlastingsmonsters.

Sysmex biedt FIT-tests aan voor twee hoofdgroepen: grootschalig tests voor nationale of regionale bevolkingsonderzoeken, en symptomatische tests die hoofdzakelijk plaatsvinden in ziekenhuizen of klinische omgevingen. Lees hier meer over op onze FIT screening microsite

HIV Infection under unsuccessful therapy

Pathogen:RNA viruses →retroviruses →human immunodeficiency virus
Transmission:Predominantly sexually and via contaminated needles or blood products
Geographical range:Worldwide
Incidence:2.6 million new infections per year

Case history

A young man infected with human immunodeficiency virus (HIV) 8 years ago recently started HIV treatment. The patient visited his HIV clinician for a regular blood check (complete blood count, CD4+ and CD8+ count and viral plasma load) 8 months after starting therapy. While under the HIV regimen the viral load in his blood dropped significantly. However, his immune system was not responding to anti-HIV medications (there was no CD4+ count rise). Therefore the clinician evaluated the options of changing the patient’s treatment regimen.

HIV pathophysiology and diagnosis

Human immunodeficiency virus (HIV) is a retrovirus that causes HIV infection and over time leads to acquired immunodeficiency syndrome (AIDS). Following the virus infection the patient is initially asymptomatic for a long period of time, but the first few weeks after the initial infection may experience a period of influenza-like symptoms including fever, headache, rash or sore throat. As the HIV infection progresses, the virus interferes more severely with the immune system and destroys and impairs the function of immune cells. As a result the person gradually becomes immunodeficient and much more susceptible to common infections (tuberculosis, opportunistic infections) and some cancer types, which becomes life-threatening. The average survival period after the HIV infection is 9-11 years (1). HIV can be transmitted via the exchange of many different body fluids – blood, semen, and vaginal fluid, ejaculate or breast milk. The virus is present in the body fluids as a free native virus as well as integrated in the infected host immune cells.

The HIV virion enters macrophages, dendritic cells and CD4+ T cells through glycoproteins on its surface, binding to receptors on the target cell. The anchoring process is followed by fusion of the viral envelope with the cell membrane and the release of the viral capsid into the cell (2,3). HIV can spread between CD4+ T cells by two routes: cell-free and cell-to-cell transmission, of which the latter was reported to be more efficient (4).

Once HIV has entered the host cells, the viral genome is transcribed and integrated with the host DNA and begins replicating for the first 3-6 weeks. Infection is further triggered when the virus and infected immune cells reach the lymph nodes, where activated CD4+ T cells are infected (5). In this way the immune system’s response spreads HIV by presenting infected cells to additional CD4+ memory T cells, resulting in the severe depletion of these cells. This is associated with the activation of CD8+ T cells, which kill CD4+ infected cells. The CD8+ T cell response is known to be important in controlling blood virus levels, which peak and then decline, as the CD4+ T cell counts increase. It has been shown that the level of CD8+ activation is able to predict the length of the period without treatment (8). The peak viral blood load is the period when clinically apparent flu-like symptoms often occur.

After the acute phase the immune system responds strongly in order to decrease the viral infection and increase the CD4+ T cells in the blood. However, the immune system is not able to combat the infection. The viral load decreases and the chronic stage of infection begins (5). The CD4+ cell blood count gradually decreases and when the count falls below 200 cells/µL, the clinical condition of the patient is classified as acquired immunodeficiency syndrome (AIDS).

Serological tests such as enzyme immunoassays detect antibodies against HIV antigens. These tests detect antibodies against HIV and not HIV itself. Since most individuals develop antibodies to HIV within one month, the antibodies may not be detectable in the early stage of infection. However, HIV transmission can occur even in this stage of the infection. According to the best practice patients are initially retested and after the second positive result diagnosed as HIV-positive. (6).

Laboratory results

Case interpretation

The complete blood count revealed that the patient had a normal-to-low absolute lymphocyte count (900 cells/µl) and an increased count of atypical lymphocytes RE-LYMP% = 7.4% (38% of the lymphocytes). The complete blood count did not show other pathologies. This can be interpreted as a continuation of the decrease in lymphocytes due to the unsuccessful therapy (mainly CD4+ T cells) and active cell-mediated immune response due to the high number of activated lymphocytes. Taking into consideration other laboratory results (HIV viral load = 100/ml, CD4+ cell count = 220/µl, activated CD8+ cell count = 400/µl) almost half of the lymphocyte count is cytotoxic CD8+ cells, which attack CD4+ cells. The presence of plasma HIV copies is low, but CD4+ cells are also low and still decreasing after the initiation of the therapy (initiated at CD4+ cell count = 350/µl). An increased number of activated cytotoxic cells (CD8+) indicates a persisting immune system response to virally infected CD4+ cells (8). These cells are attacked by CD8+ cells and a low ratio (CD4+/CD8+ = 0.55) indicates that the therapy is not successful and needs adjustment.


  1. World Health Organization (2007): AIDS epidemic update
  2. Chan DC, Kim PS (1998): HIV entry and its inhibition. Cell. May 29;93(5):681-4.
  3. Wyatt R, Sodroski J (1998): The HIV-1 envelope glycoproteins: fusogens, antigens, and immunogens. Science. Jun 19;280(5371):1884-8.
  4. Duncan CJ, Russell RA, Sattentau QJ (2013): High multiplicity HIV-1 cell-to-cell transmission from macrophages to CD4+ T cells limits antiretroviral efficacy. AIDS. Sep 10;27(14):2201-6.
  5. Mogensen TH, Melchjorsen J, Larsen CS, Paludan SR (2010): Innate immune recognition and activation during HIV infection. Retrovirology: 7:54.
  6. World Health Organization (2015): HIV/AIDS.
  7. Cossarizza A, Bertoncelli L, Nemes E, Lugli E, Pinti M, Nasi M, De Biasi S, Gibellini L, Montagna JP, Vecchia M, Manzini L, Meschiari M, Borghi V, Guaraldi G, Mussini C (2012): T cell activation but not polyfunctionality after primary HIV infection predicts control of viral load and length of the time without therapy. PLoS One. 7(12):e50728.

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