ABSTRACT
OBJECTIVE: Coronavirus disease-2019 (COVID-19) disease can cause asymptomatic and mild flu-like symptoms as well as severe symptoms ranging from respiratory failure and death. Growth hormone (GH) is produced in the anterior pituitary and plays an important role in the immune system. COVID-19 is severe in the elderly, men, obese, diabetics, and people with immune deficiency. The probability of GH deficiency is high in these patient groups. In this study, we aimed to investigate the relationship between the severity of COVID-19 infection and GH level. METHODS: A total of 456 patients, between 45 and 80-years-old, who were hospitalized with the diagnosis of COVID-19 disease were evaluated in the study. Our study was a retrospective study. Demographic data of the patients, GH, insulin-like growth factor-I (IGF-1), and biochemical parameters and thorax tomography results were evaluated. Patients with chronic diseases that would affect GH levels and those in need of intensive care were excluded from the study. RESULTS: 456 patients were included in the study, 168 female, 288 male, mean age 67.57±12.60 years. Patients were divided into two groups according to thorax tomography findings, patients with lung involvement in Group-1:352 (77%) and those without pulmonary involvement in Group-2:104 (23%). While the GH of Group-1 was 0.125 ng/ml, the GH of Group-2 was 0.238 ng/ml, the difference between them was statistically significant (p=0.000). IGF-1 in Group-1 was: 55.05 ng/ml, while IGF-1 in Group-2 was: 104.08 ng/ml, the difference between them was statistically significant (p=0.000). In multivariate regression analysis, low IGF-1 (p=<0,01, OR:1,06 [1028-1093]) level was found to be significantly effective in lung involvement in COVID-19 disease. CONCLUSION: In our study, we found GH and IGF-1 deficiency in COVID-19 cases with lung involvement, regardless of age and gender. We can say that COVID-19 infection progresses worse in GH and IGF-1 deficiency.
ABSTRACT
Aromatase deficiency (AD) is a rare autosomal recessive inheritance syndrome. Its worldwide incidence is unknown, and there are few case reports in the literature. Aromatase dysfunction develops due to CYP19A1 gene mutation and a decrease in estrogen synthesis. Estrogen deficiency can induce delayed epiphyseal closure, eunuchoid body habitus, osteopenia, and osteoporosis in both genders. Our patient was a 27-year-old male who presented with bone pain, recurrent bone fractures associated with minimal trauma starting in puberty, and a progressive increase in height. Laboratory tests revealed that the blood levels of follicle-stimulating hormone and luteinizing hormone were above normal, testosterone level was normal, and estrogen was undetectable. Plain bone radiography of the left wrist and hand demonstrated that the epiphyses were still unfused. Lumbar osteoporosis was detected in bone densitometry. In the genetic analysis, homozygous R375H guanine-adenine (G-A) mutation was detected in the CYP19A1 gene, and a diagnosis of AD was reached. Treatment with 25 µg transdermal estradiol was started. All family members were examined. Homozygous R375H G-A mutation was detected in the patient's younger brother. Heterozygous R375H G-A mutation was found in his mother, father, and older brother. In conclusion, this AD patient requires lifetime estrogen replacement in order to provide sufficient bone mineralization, to reduce the risk of bone fractures, and to lead a healthy life. The best method to prevent the possible complications is to diagnose the AD syndrome at early ages and to provide adequate estrogen replacement starting at puberty.
