Internal quality control of histological diagnosis in pathology. A nine-year experience

Internal quality control (IQC) is a necessary component of total quality management. We report our experience with an internal audit scheme focusing on the histological diagnosis. We outline other strategies of IQC and analyze the causes of errors and ways to prevent them. Some practical guidelines to initiate this type of procedure are presented. Our audit was designed to check the accuracy of diagnosis, the clarity and completeness of the report, the quality of the documents leading to the diagnosis, and the turn-around time. It consisted of a retrospective analysis of 4185 randomly selected cases (representing 2% of all cases), over nine years. The control took place once a week and was done by two pathologists working as a team. The mean time spent by each pathologist was 45 minutes per week. Errors were scored using a 3-level grading scheme depending on their potential harm or impact on patient care. The overall rate of errors was 1.1%, and 0.1% of errors were potentially harmful to the patients. A single case (0.02%), in which a cancer was missed, had a real impact on patient care. Retrospective analysis of randomly selected cases mirrors the overall activity of a surgical pathology department. Nevertheless, each lab has to develop its own strategy of IQC, based on its size, its functioning, and its objectives. Although it may be difficult to initiate quality assurance when medical time is already limited, it is a helpful procedure in a more and more demanding medical and societal context and a pragmatic step towards "culture of quality".     

Obstetric consequences of uncontrolled gestational diabetes--a case study

This paper presents a case of a pregnant woman who was admitted to the obstetrics and gynecology department because of a new onset of uncontrolled diabetes in 27 weeks gestation. The maternal and fetal diabetic complications suggested a chronic character of the disease which must have been undiagnosed before pregnancy. Many of the co-existing infections caused a life-threatening ketoacidosis. Fortunately with the adequate treatment it was possible to ensure appropriate birth weight of the newborn baby despite the ultrasound markers for LGA (Large For Gestational Age) observed during pregnancy. Intensive insulin therapy was obligatorily continued by the mother after the delivery.     

Volumetric growth of the lungs in human fetuses: an anatomical,hydrostatic and statistical study

Purpose

The prenatal assessment of lung volume is becoming increasingly important in determining survival in both preterm infants and newborns affected by pulmonary hypoplasia. This study aimed to examine the lung volumes in the human fetus at varying gestational ages.

Materials and methods

Using anatomical, hydrostatic (water displacement according to Archimedes’ patent) and statistical methods (one-way ANOVA test for paired data and post-hoc Bonferroni test, Kolmogorov–Smirnov test, Levene’s test, Student’s t test, regression analysis), volumes of the right and left lungs were measured in 67 human fetuses of both sexes (35 males, 32 females) aged 16–25 weeks, derived from spontaneous abortions and stillbirths.

Results

No male–female differences concerning the right and left pulmonary volumes were found. The mean volume of the right lung increased from 1.43 ± 0.25 to 8.45 ± 2.66 cm³, according to the cubic function y = –1.592 + 0.0007 × age³ ± 0.851 (R ² = 0.84). The volumetric growth of the left lung, from 1.24 ± 0.22 to 6.78 ± 3.03 cm³, followed the cubic model y = –1.110 + 0.0005 × age³ ± 0.794 (R ² = 0.78). The total pulmonary volume increased from 2.67 ± 0.47 to 15.22 ± 5.58 cm³, in accordance with the cubic model y = –2.729 + 0.0012 × age³ ± 1.598 (R ² = 0.83). The mean volumes of the right and left lungs accounted for 54.9 ± 2.0 and 45.1 ± 2.0 %, respectively, of the total lung volume.

Conclusions

No sex differences are found between the lung volumes in the fetus. The growth of fetal lung volume follows a three-degree polynomial function. Throughout the analyzed period the two lungs grow proportionately to each other, with the volumetric predominance of the right lung. The lung volumes in the fetus are of great relevance in the evaluation of the normal pulmonary growth and the diagnosis of pulmonary hypoplasia.     

Detection of human bocavirus in hospitalised children

Aim:   The objectives of this study are to assess the frequency of human bocavirus (HBoV) infection in hospitalised children and to study the clinical symptoms associated with the detection of HBoV.
Methods:   Two groups of hospitalised children were included in this study: group 1 consisted of 1946 children hospitalised from 1st September 2004 to 30th May 2005, and group 2 consisted of 448 children hospitalised from 1st November 2003 to 30th March 2004. The respiratory specimens were tested by polymerase chain reaction.
Results:   In the first group, HBoV was detected by polymerise chain reaction in 11/828 (1.3%) of nasal specimens that tested negative for other respiratory viruses. One child tested positive for HBoV in both a nasal aspirate and stool sample. In the second group, nasal specimens were tested for all respiratory viruses, including HBoV. The presence of HBoV infection was detected in seven children (1.6%). Detection of a mixed viral population was observed in four of these children. The main symptoms in children infected with HBoV were rhinitis (50%), cough (45%), dyspnoea (28%), wheezing (28%), fever (23%) and diarrhoea (22%). The final clinical diagnoses were bronchiolitis (seven children), rhinopharyngitis (five children), the exacerbation of asthma (two children) and pneumonia (one child). Moreover, four children have associated gastroenteritis.
Conclusion:   These results contribute to the interest in the HBoV detection in children. HBoV detection in hospitalised children with or without any other respiratory virus detection was essentially associated with lower respiratory tract infection and in a lower score with upper respiratory tract infection and gastroenteritis.     

Ocena skuteczności Lactobacillus rhamnosus ATC A07FA w zapobieganiu martwiczego zapalenia jelit wcześniaków z bardzo małą urodzeniową masą ciała: badanie z randomizacją (wstępne wyniki)

BackgroundEvidence suggests that probiotics, as a group, are reducing the risk of necrotizing enterocolitis (NEC). The efficacy of each probiotic strain needs to be evaluated separately.ObjectiveTo evaluate the efficacy of administering Lactobacillus rhamnosus ATC A07FA (L. rhamnosus) for the prevention of necrotizing enterocolitis (NEC) ≥2 by the criteria of Bell in very low-birth-weight preterm infants.MethodPreterm infants children fulfillingthe inclusion criteria (gestational age <32 weeks and birth weight <1500 g and partial orfull enteral feeding) were enrolled in a randomized, double-blind, placebo-controlled trial. They received L. rhamnosus (commercially available as Lakcid) at a dose of 1.2 × 10¹⁰ CFU or a placebo orally, twice daily, for the duration of the hospital stay. The primary outcome measures were NEC ≥2 by the criteria of Beli, sepsis and death.ResultsThe study was stopped prematurely because of slow recruitment. Data from 55 preterm infants were included in the fina? analysis. In the experimental group, compared with the placebo group, the risk of developing NEC ≥2 by the criteria of Beli was reduced, however the difference was not statistically significant (1/30; 3.3% versus A/25; 16%, RR 0.2, 95% Cl 0.02 do 1.75). L. rhamnosus did not significantly affect the risk of developing sepsis or death. There was also no difference between the probiotic and placebo groups for any of the other secondary outcomes. No adverse events were reported.ConclusionThe administration of L. rhamnosus ATC A07FA compared with placebo had no effect on the incidence of NEC. Further studies with sufficient sample size are warranted.     

Germinal center and activated b-cell profiles separate Burkitt lymphoma and diffuse large B-cell lymphoma in AIDS and non-AIDS cases

Morphologic features of Burkitt lymphoma (BL) and diffuse large B-cell lymphoma (DLBCL) overlap. No single phenotypic marker or molecular abnormality is pathognomonic. We tested a panel of 8 germinal center (GC) and activated B-cell (ABC) markers for their ability to separate BL and DLBCL. We diagnosed 16 BL and 39 DLBCL cases from 21 patients with AIDS and 34 without AIDS based on traditional morphologic criteria, Ki-67 proliferative index, and c-myc rearrangement (fluorescence in situ hybridization). After immunohistochemically staining tissue microarrays of BL and DLBCL for markers of GC (bcl-6, CD10, cyclin H) and ABC (MUM1, CD138, PAK1, CD44, bcl-2), we scored each case for the percentage of positive cells. Hierarchical clustering yielded 2 major clusters significantly associated with morphologic diagnosis (P < .001). For comparison, we plotted the sum of the GC scores and ABC scores for each case as x and y data points. This revealed a high-GC/low-ABC group and a low-GC/high-ABC group that were associated significantly with morphologic diagnosis (P < .001). Protein expression of multiple GC and ABC markers can separate BL and DLBCL.     

Characterization of FimH adhesins expressed by Salmonella enterica serovar Gallinarum biovars Gallinarum and Pullorum: reconstitution of mannose-binding properties by single amino acid substitution

Recombinant FimH adhesins of type 1 fimbriae from Salmonella enterica serovar Gallinarum biovars Gallinarum and Pullorum, in contrast to those of Salmonella enterica serovar Typhimurium, did not bind to high-mannose oligosaccharides or to human colon carcinoma HT-29 cells. However, mutated FimH proteins from biovar Gallinarum and biovar Pullorum, in which the isoleucine at position 78 was replaced by the threonine found in S. enterica serovar Typhimurium, bound well to glycoproteins carrying high-mannose oligosaccharides and colon carcinoma cells. The loss of sugar-binding properties by biovar Gallinarum and biovar Pullorum FimH adhesins, which are a part of the type 1 fimbriae, is most probably the result of a single T78I mutation, as was proven by site-directed mutagenesis of FimH proteins.