Qinjie Tian

Peking Union Medical College Hospital

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Fengxia Yao

Chinese Academy of Medical Sciences & Peking Union Medical College

Shan Deng

Fourth Affiliated Hospital of Guangxi Medical University

Min Luo

Chinese Academy of Medical Sciences & Peking Union Medical College

Duoduo Zhang

Huizhou University

Aijun Sun

Peking Union Medical College Hospital

Rong Chen

Peking Union Medical College Hospital

Hung Tseng

National Taiwan University of Science and Technology

Chunqing Wang

Southwest University

He Huang

West China Hospital of Sichuan University

Zhaolin Lu

University of Chinese Academy of Sciences

Cooperative Institutions

Chinese Academy of Medical Sciences & Peking Union Medical College

Peking Union Medical College Hospital

Capital Medical University

Peking University

Sun Yat-sen University

Beijing Obstetrics and Gynecology Hospital

Chinese Academy of Sciences

Academy of Medical Sciences

Central South University

Shanghai Jiao Tong University

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Use and knowledge of the two FIGO systems for nongestational abnormal uterine bleeding in the reproductive years: A multinational survey

International Journal of Gynecology & Obstetrics (2025)

Francisco J. Ruiloba Ally Murji Qinjie Tian Sarah Maheux‐Lacroix Elif Göknur Topçu

Uterine bleeding

10.1002/ijgo.16138

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Citations (0)

MYRF mutation leads to a single manifestation of sexual development and mimics partial androgen insensitivity syndrome: a case report and literature review

Gynecological Endocrinology (2024)

Duoduo Zhang Qinjie Tian

To highlight the challenges in diagnosing 46, XY disorder of sex development related to

Clitoris

Gonadal dysgenesis

10.1080/09513590.2024.2331072

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Citations (1)

Genotyping of a Chinese family with 46,XX and 46,XY 17-hydroxylase deficiency

Gynecological Endocrinology (2009)

Qinjie Tian Fengxia Yao Guihua Sha Shangzhi Huang Hung Tseng

Background. 17-Hydroxylase deficiency is a rare form of congenital adrenal hyperplasia caused by CYP17A1 gene mutations.Method. A 46,XY and a 46,XX Chinese patients with 17-hydroxylase deficiency in a family and their four generations family members were genotyped by PCR-sequencing method.Results. Two CYP17 gene mutations were identified from these patients. Among them, IVS1-1G > A was a novel splicing mutation which disrupted the acceptor signal of exon 2 and might create a new exon after exon 1. The indel mutation of TAC329AA was a one-base deletion mutation and one-base change at codon 329 in exon 6.Conclusion. The results confirmed the diagnosis of 17-hydroxylase deficiency in these two patients and their autosome recessive heritage mode. The TAC329AA indel mutation had been identified in several reports of Chinese and Asian, suggesting that codon 329 was an unstable point of the CYP17 gene and this mutation was a prevalent CYP17 mutation in the Asian population. Although the noval mutation IVS1-1G > A founded in this family need more study to know its machinism of interrupting P450c17 function.

INDEL Mutation

Indel

10.1080/09513590902898239

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Citations (15)

Partial 17alpha-hydroxylase/17,20-lyase deficiency–clinical report of five Chinese 46,XX cases

Gynecological Endocrinology (2008)

Qinjie Tian Yiwen Zhang Zhaolin Lu

Objectives. To summarize the clinical characteristics of partial 17α-hydroxylase/17,20-lyase deficiency (17OHD) in 46,XX Chinese patients.

Alpha (finance)

10.1080/09513590802194051

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Citations (26)

Gonadal Dominance and Internal Genitalia Phenotypes of Patients with Ovotesticular Disorders of Sex Development: Report of 22 Cases and Literature Review

Sexual Development (2019)

Shan Deng Aijun Sun Rong Chen Qi Yu Qinjie Tian

This study aimed to delineate internal genitalia phenotypes in patients with ovotesticular disorders of sex development (OT-DSD). Therefore, a cohort of 22 OT-DSD patients admitted to the Peking Union Medical College Hospital from March 1977 to August 2019 was analyzed retrospectively. The characteristics of karyotype, gonad type and location, and internal genital organs were reviewed and compared to 242 pooled cases from the Chinese literature. As a result, the most common karyotype was 46,XX (68.2% in 22 cases of our hospital, 60.8% in the domestic literature). The combination of gonads was separated (ovary-testis, 45.1%), unilateral (ovotestis-ovary, 17.4%; ovotestis-testis, 13.0%), and bilateral (ovotestis-ovotestis, 24.5%). All the cases in our hospital had a uterus on the side of the ovary or ovotestis. Among the 19 female patients, 5 had a hysterectomy due to genital tract obstruction, 9 had vaginal dysplasia, 3 had premature ovarian failure, and only 2 women gave birth to a child. In conclusion, OT-DSD is a typical model of unilateral gonadal determinism: the uterus is present on the side of the ovotestis and ovary and the internal genital organs predominantly exhibit female characteristics. However, combined reproductive tract malformation and ovarian function of premature failure are not uncommon.

Ovotestis

True hermaphroditism

Sex organ

10.1159/000507036

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Citations (8)

Clinical features and management of 33 patients with 46,XX pure gonadal dysgenesis

Gynecological Endocrinology (2016)

He Huang Chunqing Wang Qinjie Tian

The objective of the study is to summarize the clinical characteristics of 33 patients' cohort (46,XX pure gonadal dysgenesis, 46,XX PGD), discuss the management, and propose treatment suggestions. Patients' information, medical history, and medical records were obtained. All patients were closely followed up. At the time of diagnosis, the patients presented 19.53 ± 3.60 years old, 165 ± 6.49 cm height, breast development of Tanner stage I, and infantile female genitalia. High level of follicle-stimulating hormone (87.41 ± 21.50 mIU/mL) and LH (27.10 ± 8.47 mIU/mL) and low level of E2 (8.85 ± 6.13 pg/mL) were observed. Individualized hormone replacement therapy (HRT) was initiated after diagnosis. After 2 years of treatment, all patients had obvious breast development; the uterus showed (2.38 ± 0.60) × (1.38 ± 0.70) × (1.38 ± 0.55) cm growth. The incidence of osteopenia changed from 69.70% to 22.22% and that of osteoporosis changed from 18.18% to 0. Dysgeminoma was found in one patient. We concluded that gonadal dysgenesis in 46,XX PGD causes secondary sexual characteristic absence, tendency of taller, osteoporosis, infertility, and sexual health problems. There is minor chance of tumor occurrence for the patients. Optimal care including HRT and close follow-up are required.

Gonadal dysgenesis

Dysgenesis

Breast development

Osteopenia

10.1080/09513590.2016.1190820

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Citations (11)

[Identification of potential neoplastic risk in gonadal development abnormality with Y chromosome of 79 cases].

PubMed (2008)

Xilai Ding Aijun Sun Yuanzheng Zhou Qinjie Tian Qi Yu

To identify the potential neoplastic risk in gonadal development abnormality with Y chromosome.Inquiries about the illness history were made. Lymphocyte chromosomal karyotype of peripheral blood was analyzed. Sex determining region Y gene and relative steroids and enzymes were detected. Gonadal site was examined through medical imaging. Gonadal excision was performed by laparotomy or laparoscopy. Pathological examinations were done on all of the specimens.Among 41 cases of androgen insensitive syndrome, spermatogenic cell neoplasm occurred in 1 patient, sertoli cell tumor in 2, and interstitial cell hyperplasia in 5. Among 14 cases of 17 alpha-hydroxylase deficiency (XY) syndrome, one was sertoli cell tumor, and one was sertoli cell hyperplasia. In 4 cases of XY pure gonadal dysgenesis, one was gonadoblastoma with dysgerminoma. One of 16 cases of XO/XY gonadal dysgenesis was spermatogenic cell neoplasm with agenda cell tumor. Four cases of testes degeneration were all with dysgenetic testes. All of the gonadoblastoma and germ-cell tumor were located in the pelvis. Tumors occurred mostly during 15 years of age to 32 years.The gonads of XY pure gonadal dysgenesis has high risks of gonadoblastoma and germ-cell tumor. The older the onset age after puberty, the higher the malignancy risk is. Once diagnosed, bilateral gonads should be excised as soon as possible.

Gonadoblastoma

Gonadal dysgenesis

Dysgerminoma

Androgen insensitivity syndrome

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Citations (2)

[How to look dialectically at the hormone replacement therapy on menopausal women].

PubMed (2008)

Qinjie Tian

Hormone Therapy

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