scholarly journals Allo-Anti-D vs. Auto-Anti-D in Females of Child Bearing Years: The Critical Role of Rh Genotyping

2021 ◽  
Vol 156 (Supplement_1) ◽  
pp. S164-S164
Author(s):  
J T Keith ◽  
H Hastings

Abstract Introduction/Objective In females of child-bearing years, establishing accurate D-antigen identification is critical; this can be further complicated when a D+ patient seemingly develops an allo-anti-D. We present a unique case series highlighting the critical role of genotyping in distinguishing allo-anti-D vs. auto-anti-D. Methods/Case Report Case 1: An African American, 21-year-old, nulliparous female with a history of sickle cell disease presented for transfusion. The patient’s blood type was O, Rh Positive on multiple testing platforms (ORTHO VISION® Analyzer, 1001 US Highway 202, Raritan, NJ 08869, and Immucor, Inc., 3130 Gateway Drive, Norcross, GA 30071). On type and screen performed by manual tube testing, anti-D was identified. DAT IgG was weakly positive. The patient’s phenotype had been performed previously, and she was negative for both the C and E antigens. Genotyping results: RhD homozygote. RHD*DAU0 and RHD*DIVa type 3. The patient was determined to have auto-anti-D formation. Case 2 A 42-year-old female presented for routine prenatal care. At a previous facility, the patient tested as D+ and typed as O, Rh Positive (ORTHO VISION® Analyzer). An anti-D pattern was identified. Due to the patient’s Rh+ history and early pregnancy status, no Rh immune globulin was administered. A sample was sent to the reference laboratory which confirmed D+ status and a pattern of anti-D. The current titer was 8. Genotyping results RhD hemizyote. Positive for hybrid Rhesus box associated with deletion of RhD and RHD*DIVa, Go(a+). The patient was determined to have an allo-anti-D. Results (if a Case Study enter NA) NA Conclusion These two cases highlight the importance of RhD genotyping for resolutions of anti-D. In case 1, the patient had two altered alleles. While DIVa, type 3, is associated with anti-D formation, she also expressed RhD*DAU0 which is not considered to lack D proteins. We report the rare association between DAU0 expression and auto-anti-D formation.

2014 ◽  
Vol 114 ◽  
pp. 70-80 ◽  
Author(s):  
Zhi Wang ◽  
Sang-Hon Park ◽  
Huijuan Zhao ◽  
Shuling Peng ◽  
Zhiyi Zuo

Endocrinology ◽  
2012 ◽  
Vol 153 (6) ◽  
pp. 2919-2928 ◽  
Author(s):  
Arturo Hernandez ◽  
Beatriz Morte ◽  
Mónica M. Belinchón ◽  
Ainhoa Ceballos ◽  
Juan Bernal

Thyroid hormones regulate brain development and function through the control of gene expression, mediated by binding of T3 to nuclear receptors. Brain T3 concentration is tightly controlled by homeostatic mechanisms regulating transport and metabolism of T4 and T3. We have examined the role of the inactivating enzyme type 3 deiodinase (D3) in the regulation of 43 thyroid hormone-dependent genes in the cerebral cortex of 30-d-old mice. D3 inactivation increased slightly the expression of two of 22 positively regulated genes and significantly decreased the expression of seven of 21 negatively regulated genes. Administration of high doses of T3 led to significant changes in the expression of 12 positive genes and three negative genes in wild-type mice. The response to T3 treatment was enhanced in D3-deficient mice, both in the number of genes and in the amplitude of the response, demonstrating the role of D3 in modulating T3 action. Comparison of the effects on gene expression observed in D3 deficiency with those in hypothyroidism, hyperthyroidism, and type 2 deiodinase (D2) deficiency revealed that the negative genes are more sensitive to D2 and D3 deficiencies than the positive genes. This observation indicates that, in normal physiological conditions, D2 and D3 play critical roles in maintaining local T3 concentrations within a very narrow range. It also suggests that negatively and positively regulated genes do not have the same physiological significance or that their regulation by thyroid hormone obeys different paradigms at the molecular or cellular levels.


Nature ◽  
1983 ◽  
Vol 304 (5925) ◽  
pp. 459-462 ◽  
Author(s):  
D. M. A. Evans ◽  
P. D. Minor ◽  
G. S. Schild ◽  
J. W. Almond

2021 ◽  
Vol 13 (1) ◽  
pp. 41-49
Author(s):  
M. Deenadayal ◽  
V. Günther ◽  
I. Alkatout ◽  
D. Freytag ◽  
A. Deenadayal-Mettler ◽  
...  

A septate uterus with a non-communicating hemicavity was first described by Robert in 1969/70 as a specific malformation of the uterus. The condition is commonly associated with a blind uterine hemicavity, unilateral haematometra, a contralateral unicornuate uterine cavity and a normal external uterine fundus. The main symptoms are repetitive attacks of pain at four-weekly intervals around menarche, repeated dysmenorrhea, recurrent pregnancy loss and infertility. In this report, we review the disease, its diagnosis and treatment, and describe five cases of Robert’s uterus. Three dimensional (3D) ultrasound (US) imaging was performed by the transvaginal route in four cases. In the fifth case of a 13-year-old girl, we avoided the vaginal route and magnetic resonance imaging (MRI) and 3D transrectal US yielded the correct diagnosis. The following treatment procedures were undertaken: laparoscopic endometrectomy, hysteroscopic septum resection, laparoscopic uterine hemicavity resection and total laparoscopic hysterectomy (TLH). The diagnosis and optimum treatment of Robert’s uterus remains difficult for clinicians because of its rarity. A detailed and careful assessment by 3D US should be performed, followed by hysteroscopy in combination with laparoscopy, to confirm the diagnosis.


2009 ◽  
Vol 119 (9) ◽  
pp. 1419-1428 ◽  
Author(s):  
Hee Jung Baik ◽  
Yueming Huang ◽  
Jacqueline M. Washington ◽  
Zhiyi Zuo

2021 ◽  
Vol 22 (3) ◽  
pp. 1250
Author(s):  
Hyun Jung Park ◽  
Sung Won Lee ◽  
Luc Van Kaer ◽  
Seokmann Hong

We have previously shown that CD1d-restricted iNKT cells suppress dysregulated IFNγ expression and intestinal inflammation in Yeti mice on the C57BL/6 background. Since type 3 innate lymphoid cells (ILC3s) in mesenteric lymph nodes (MLN) protect against intestinal inflammation in a CD1d-associated manner, we investigated whether crosstalk between iNKT cells and MLN ILC3s controls IFNγ-mediated intestinal inflammation in Yeti mice. We found that Yeti mice display increased levels of ILC3s and that iNKT cell deficiency in Yeti/CD1d KO mice decreases levels of IL22-producing ILC3s during DSS-induced colitis. This finding indicates that iNKT cells and ILC3s cooperate to regulate intestinal inflammation in Yeti mice. Yeti iNKT cells displayed a pronounced anti-inflammatory (IL4- or IL9-producing) phenotype during colitis. Their adoptive transfer to iNKT cell-deficient animals induced a significant increase in IL22 production by ILC3s, indicating that crosstalk between iNKT cells and ILC3s plays a critical role in modulating colitis in Yeti mice. Moreover, we showed that the IL9-producing subset of iNKT cells potently enhances IL22-producing ILC3s in vivo. Taken together, our results identify a central role of the iNKT cell-ILC3 axis in ameliorating IFNγ-mediated intestinal inflammation.


2006 ◽  
Vol 281 (50) ◽  
pp. 38133-38138 ◽  
Author(s):  
Yueming Huang ◽  
Xiaorong Feng ◽  
Julianne J. Sando ◽  
Zhiyi Zuo

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