A study of the moving rate of positive results for use in a patient‐based real‐time quality control program on a procalcitonin point‐of‐care testing analyzer

ObjectiveTo establish an applicable and highly sensitive patient‐based real‐time quality control (PBRTQC) program based on a data model constructed with patients’ results of a procalcitonin point‐of‐care testing (POCT) analyzer.MethodsPatients’ results were retrospectively collected within one year. The Excel software was used to establish quality control (QC) programs of the moving average (MA) and the moving rate of positive results (MR). A Monte Carlo simulation was used to introduce positive and negative biases between 0.01 and 1 ng/ml at random points of the testing data set. Different parameters were used to detect the biases, and the detection efficiency was expressed using the median number of patient samples affected until error detection (MNPed). After comparing the MNPeds of different programs, MA and MR programs with appropriate parameters were selected, and validation plots were generated using MNPeds and maximum number of the patient samples affected (MAX). β curves were generated using the power function of the programs, the performances were compared with that of the conventional QC program.ResultsNeither the conventional QC nor MA program was sensitive to small bias, While MR program can detect the minimum positive bias of 0.06 ng/ml and negative of 0.4 ng/ml at an average daily run size of 10 specimens, with FRs < 1.0%, βs < 1%.ConclusionThe MR program, which is more sensitive to small biases than conventional QC and MA programs, with low FR and β. As such, it can be used as a PBRTQC program with high performance.     

Will killing the last HIV1 particle cure AIDS patients? II: Second part. Decrease of viral load and of T-suppressor cells, and increase of the cytotoxic cells, without effect on CD4, after the use of 10 virostatics applied in 3 or 4 drug combinations of different sequences. The time for CD4 immunotherapy?

We reported in the first part of this editorial [1] and in an article on AIDS therapy with five HIV₁ virostatics applied in two then three, or initially three, or initially four agent combinations, given in 3 week sequences differing from each other due to drug rotation [2], the contrast between: a) the decrease of viral load, possibly below the detectable level, b) the absence of effect on the helper CD4⁺, the CD8⁺ C57⁻ cytotoxics and the CD8⁺ C57⁺ suppressor cells. We proposed a thesis according to which the HIV₁-AIDS complex might have another pathogenic component other than HIV₁, ie, a microchimerism graft-versus-host reaction (GvH) or an autologous GvH-like reaction [1].Shifting from five to 10 virostatics owing to the availability of lamivudine or 3TC [3], stavudine or d4T [4] and three HIV₁ protease inhibitors, saquinavir [5], ritonavir [6] and indinavir [7], applied according to the same modality, we have enhanced the reduction of viral load, and significantly decreased the CD8⁺ C57⁺ suppressor cell counts, and increased those of the CD8⁺ C57⁻ cytotoxic cells.This result which indirectly shows the role of HIV₁ in the increase of suppressor CD8⁺ cells, hence in the late loss pf immune memory and of opportunistic infections [8], reinforces the thesis of a role, in AIDS pathogenesis, of a latent GvH reaction activated by HIV, primo-infection, and its evolution from the hyperplastic phase to the hypoplastic one, which, inducing severe immune suppression, is responsible for HIV₁ active infection relapse after the so-called latent phase [1].Hence the proposition we make, of an indication of CD4 modulation with non specific immunotherapy by bestatin [9], of which we showed the effect in another population of HIV₁-AIDS complex patients [10]. Its effect can be potentiated by tuftsin [11, 12]. When the suppressor cell number goes up over that of the cytotoxic one after the HIV, active infection relapse, Interferon y could be added, which, by amplifying the CD28 pathway [13] on CD8⁺ cytotoxics, while suppressor cells lack CD28 [14], which might reestablish a ratio of suppressor over cytotoxic cells nearer to normal.It remains that the role of the five secondarily included agents in the decrease of suppressor cells will only be attributed with certainty and entirely to their virostatic effect, if it is shown that none of them exerts a selective anti-suppressor cell action.