Prevalence of myeloperoxidase deficiency determined using an ADVIA 2120i

2020 ◽  
Vol 42 (5) ◽  
Author(s):  
Daniel Mark Gleghorn ◽  
Will Thomas
Keyword(s):  
Myeloperoxidase Deficiency

Genetic characterization of myeloperoxidase deficiency in Italy

2004 ◽  
Vol 23 (5) ◽  
pp. 496-505 ◽  
Author(s):  
Caterina Marchetti ◽  
Pierluigi Patriarca ◽  
G. Pietro Solero ◽  
Francisco E. Baralle ◽  
Maurizio Romano
Keyword(s):  
Genetic Characterization ◽  
Myeloperoxidase Deficiency

Partial Myeloperoxidase Deficiency in a Case of Preleukaemia.

1975 ◽  
Vol 30 (3) ◽  
pp. 279-288 ◽  
Author(s):  
J. Breton-Gorius ◽  
D. Houssay ◽  
J. L. Vilde ◽  
B. Dreyfus
Keyword(s):  
Myeloperoxidase Deficiency

Acquired Myeloperoxidase Deficiency of Neutrophils in a Patient with Aplastic Anemia (Idiopathic Marrow Aplasia)

1988 ◽  
Vol 80 (2) ◽  
pp. 71-73 ◽  
Author(s):  
Nicola Bizzaro ◽  
Giuseppe Briani ◽  
Paolo Boccato
Keyword(s):  
Aplastic Anemia ◽  
Myeloperoxidase Deficiency

Further evaluation of luminol-enhanced luminescence in the diagnosis of disorders of leukocyte oxidative metabolism: role of myeloperoxidase.

1983 ◽  
Vol 29 (3) ◽  
pp. 513-515 ◽  
Author(s):  
M S Cohen ◽  
P S Shirley ◽  
L R DeChatelet
Keyword(s):  
Chronic Granulomatous Disease ◽  
Oxidative Metabolism ◽  
Clinical Consequence ◽  
Granulomatous Disease ◽  
Myeloperoxidase Deficiency ◽  
Luminescence Assay ◽  
Diagnostic Confusion ◽  
Enhanced Luminescence ◽  
Hereditary Nature

Abstract Chemiluminescence can be used to identify defects in the oxidative metabolism of granulocytes. This procedure has recently been adopted for use with microliter quantities of whole blood, appropriate for prenatal or neonatal study. Although the contribution of myeloperoxidase to the chemiluminescence assay has been noted, the possible diagnostic confusion between chronic granulomatous disease of childhood (which is rare and severe) and myeloperoxidase deficiency (which is common and of little clinical consequence) has not been stressed. We report a father and his infant daughter whose cells emitted no light in the luminol-enhanced luminescence assay; both patients are totally peroxidase deficient. These results emphasize the hereditary nature of myeloperoxidase deficiency, and the possibility for erroneous diagnosis of chronic granulomatous disease of childhood based on the luminol-enhanced luminescence test.

scholarly journals Phagocytic Activity and Oxidative Burst of Granulocytes in Persons with Myeloperoxidase Deficiency

1996 ◽  
Vol 34 (11) ◽  
Author(s):  
Claudia E. Gerber ◽  
Selim Kuçi ◽  
Matthias Zipfel ◽  
Dietrich Niethammer ◽  
Gernot Bruchelt
Keyword(s):  
Oxidative Burst ◽  
Phagocytic Activity ◽  
Myeloperoxidase Deficiency

Myeloperoxidase deficiency in dogs observed with the ADVIA®120

2010 ◽  
Vol 38 (03) ◽  
pp. 139-146 ◽  
Author(s):  
J. Richartz ◽  
N. Bauer ◽  
A. Moritz ◽  
S. Klenner
Keyword(s):  
Screening Tool ◽  
High Standard ◽  
Pancreatic Abscess ◽  
High Standard Deviation ◽  
Diagnostic Use ◽  
Cellular Volume ◽  
Myeloperoxidase Deficiency ◽  
Scatter Plots ◽  
The Mean

Summary Objective: In contrast to humans, neutrophil myeloperoxidase deficiency (MPOD) has been rarely investigated in dogs. The hematology analyzer ADVIA®120 differentiates leukocytes based on the cellular volume and their myeloperoxidase concentration. The aim of this study was the characterization of myeloperoxidase deficiency in dogs and the evaluation of the diagnostic use of the ADVIA®120 Myeloperoxidase Index (MPXI). Material and methods: ADVIA® peroxidase scatter plots indicative of MPOD were reviewed. Severity of MPOD was classified semiquantitatively in three groups (MPOD grade 1–3): MPOD grade 1 (MPOD-1): neutrophils showing an abnormal shift of the population, < 25% extending in the monocyte cluster and therefore misclassified, MPOD-2: ~25–50% of neutrophils misclassified, MPOD-3: 50–100% of the neutrophils misclassified due to their location in the monocyte cluster. Sex, age, and breed of the dogs as well as diagnosis, and MPXI were recorded. Results: 29 dogs (nine females and 20 males belonging to 23 breeds) with 38 analyses consistent with MPOD were found. Diseases were characterized by severe leukocyte consumption and included mainly parvovirosis (8/29), DIC/sepsis (3/29), pyometra, pyothorax, pneumonia, pancreatic abscess, and cystitis. A significantly lower mean MPXI in MPOD-3 was present in comparison to the mean MPXI of MPOD-1 (p < 0.05), however, there was a great overlap between the groups. Conclusion: Diseases associated with neutrophil consumption may show an acquired MPOD in dogs. High standard deviation limits the diagnostic use of the MPXI for detection of MPOD. Clinical relevance: The ADVIA®120 cytograms are a good screening tool for detection of MPOD in dogs, but the use of the MPXI is impaired in this species.

scholarly journals Unexpected combination: DiGeorge syndrome and myeloperoxidase deficiency

2020 ◽  
Vol 13 (2) ◽  
pp. e232741
Author(s):  
Simona Abraitytė ◽  
Elisabeth Kotsi ◽  
Lisa Anne Devlin ◽  
John David Moore Edgar
Keyword(s):  
T Cell ◽  
Digeorge Syndrome ◽  
Fungal Infections ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
22Q11.2 Deletion Syndrome ◽  
Deletion Syndrome ◽  
22Q11.2 Deletion ◽  
Cell Counts ◽  
Myeloperoxidase Deficiency ◽  
Rare Diagnosis

We report a case of a 3-year-old boy who presented with recurrent bacterial and fungal infections and a known diagnosis of partial DiGeorge (22q11.2 deletion) syndrome. The nature and severity of his infections were more than normally expected in partial DiGeorge syndrome with normal T-cell counts and T-cell proliferative response to phytohaemagglutinin. This prompted further investigation of the immune system. An abnormal neutrophil respiratory oxidative burst, but normal protein expression of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase system, led to the identification of myeloperoxidase deficiency. DiGeorge syndrome has a heterogeneous clinical phenotype and may not be an isolated diagnosis. It raises awareness of the possibility of two rare diseases occurring in a single patient and emphasises that even when a rare diagnosis is confirmed, if the clinical features remain atypical or unresponsive, then further investigation for additional cofactors is warranted.

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