scholarly journals An idiopathic hypogonadotropic hypogonadism patient with metabolic disorder and diabetes: case report

2015 ◽  
Vol 17 (2) ◽  
pp. 341 ◽  
Author(s):  
Shen Qu ◽  
Man-Na Zhang ◽  
Bin Su ◽  
Chun-Hua Qian ◽  
Le Bu ◽  
...  
Medicine ◽  
2021 ◽  
Vol 100 (5) ◽  
pp. e24007
Author(s):  
Liping Wang ◽  
Weisheng Lin ◽  
Xiaohong Li ◽  
Lijuan Zhang ◽  
Kai Wang ◽  
...  

2013 ◽  
Author(s):  
Yui Watanabe ◽  
Takeshi Hayashi ◽  
Hiroyuki Yamazaki ◽  
Katsuyoshi Tojo ◽  
Kazunori Utsunomiya

2015 ◽  
Author(s):  
Sasha Howard ◽  
Ariel Poliandri ◽  
Helen Storr ◽  
Louise Metherell ◽  
Claudia Cabrera ◽  
...  

2018 ◽  
Author(s):  
A Emile J Hendriks ◽  
Ross L Ewen ◽  
Yoke Sin Hoh ◽  
Nazia Bhatti ◽  
Rachel M Williams ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ting Ting Zhu ◽  
Jin Wu ◽  
Li Yuan Wang ◽  
Xiao Mei Sun

Abstract Background Phenylketonuria (PKU) is a genetic metabolic disorder in which patients have no ability to convert phenylalanine to tyrosine. Several autoimmune diseases have been reported to combine with PKU, co-existent of PKU and Juvenile Idiopathic Arthritis (JIA) has not been presented. Case presentation The girl was diagnosed with PKU at the age of 1 month confirmed by molecular data. At the age of 3.5 years, she presented with pain and swelling of her right ankle, right knee, and right hip joint. After a serial of examinations, she was diagnosed with JIA and treated with a nonsteroidal anti-inflammatory drug. Conclusions We report a rare case of a 4-year-old girl with PKU and JIA, which supports a possible interaction between PKU and JIA. Long-term metabolic disturbance may increase the susceptibility to JIA. Further chronic inflammation could alter the metabolism of tryptophan and tyrosine to increase blood Phe concentration. In addition, corticosteroid and methotrexate therapy for JIA may increase blood Phe concentration.


1991 ◽  
Vol 124 (4) ◽  
pp. 399-404 ◽  
Author(s):  
Wieland Kiess ◽  
Linda L. Liu ◽  
Nicholas R. Hall

Abstract. Sex-related differences in immune responsiveness are mediated at least in part by sex steroid hormones. Lymphocyte subset distribution in peripheral blood and natural killer cell function both have been reported to be under hormonal control. In order to gain more insight into sex steroid hormone action on the immune system, we have measured the lymphocyte subset distribution and natural killer cell activity in 18 men with idiopathic hypogonadotropic hypogonadism before treatment, and after hormonal treatment had normalized plasma testosterone levels. In untreated patients, the mean plasma testosterone concentrations were significantly lower than those in the treated men (3.0 ± 0.5 nmol/l vs 16 ± 1.7 nmol/l, p < 0.001). The percentage of peripheral CD3+ lymphocytes, CD8+ cells, the CD4+/CD8+ ratio, and the natural killer cell activity of peripheral mononuclear cells measured in a 51Cr release assay against target K 562 cells did not differ between patients with idiopathic hypogonadotropic hypogonadism and healthy adults, and most importantly, did not change during hormonal treatment which normalized plasma testosterone levels in the patients. In contrast, the percentage of peripheral CD4+ cells was significantly higher in untreated patients compared with normal adult subjects or patients with idiopathic hypogonadotropic hypogonadism after hormonal treatment that resulted in normal plasma testosterone levels (53 ± 2 vs 47 ± 2, p < 0.05). It should be noted that the percentage of peripheral CD 16+ cells was significantly lower in untreated men with low plasma testosterone levels than in normal controls. The percentage of CD16+ cells in peripheral venous blood rose significantly after hormonal treatment restored plasma testosterone levels to normal (6 ± 1 vs 11 ± 1, p < 0.001). In addition, the percentage of peripheral CD16+ cells correlated significantly with the plasma testosterone levels measured in men with idiopathic hypogonadotropic hypogonadism (r = 0.534, p < 0.001). In conclusion, both the percentage of peripheral CD4+ cells (T-helper lymphocytes) and peripheral CD16+ cells (non-T-non-B cells) are related to the plasma testosterone levels in men with idiopathic hypogonadotropic hypogonadism. These data suggest that in vivo human immune cells are under the regulatory influence of endogenous sex steroids.


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