Clinical trial NCT05051293: Comparison of the Concentration of Estrogen and Testosterone Ratio in Male Patients With Cirrhosis and Hypotension
Official title: Comparison of the Concentration of Estrogen and Testosterone Ratio in Male Patients With Cirrhosis and Hypotension Compared to Male Cirrhosis Patients Without Hypotension
Study type: OBSERVATIONAL
Overall status: WITHDRAWN
Conditions: Hypotension
Cirrhosis
Lead sponsor: Methodist Health System
Sponsor class: OTHER
First posted: 2021-09-21
Enrollment: 0
Sex: MALE
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Observational model: COHORT
Time perspective: RETROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Male patients attending the outpatient clinic of the Liver Institute at Methodist Dallas Medical Center, Dallas, Texas

Brief summary: Cirrhosis is an end stage in liver disease leading to replacement of normal liver tissue with regenerative nodules surrounded by fibrous bands in response to chronic liver injury. It is the eighth leading cause of death in the United States and the thirteenth leading cause of death globally. Patients with cirrhosis have decreased spontaneous vascular resistance leading to hypotension. The mechanism of hypotension in cirrhosis is thought to be a complex result of the presence of increased level of circulating vasodilators such a nitric oxide coupled with reduced resistance to vasoconstrictors and increased sensitivity to vasodilators.

Detailed description: Another potential contributor to the development of hypotension in cirrhosis is thought to be due to the increased production of estrogen in males especially the estrone (E1) and estradiol (E2) concentration. The concentration of estrogen in cirrhotic patients is thought to increase by fourfold compared to individuals without cirrhosis. The increased estrogen concentration in cirrhosis patients results, in large part, from an increased peripheral conversion from androgens including testosterone. Previous studies have shown that increased estrogen concentration can cause a significant decrease in blood pressure in various cell, animal, and human models. Of note, estrogen has also been shown to enhance nitric oxide production in human beings.

Eligibility criteria: Inclusion Criteria:

* Male cirrhotic patients \>18 years of age
* Patient must attend the outpatient clinic of the Liver Institute at Methodist Dallas Medical Center
* willing to provide informed consent to participate in the study

Exclusion Criteria:

* Patients with a history of cirrhosis \<18 years of age
* Cirrhosis patients with active infection
* Cirrhosis patients with active gastrointestinal bleeding
* Cirrhosis patients on hormone replacement therapy testosterone
* Cirrhosis patients on any antihypertensive medications

Primary outcomes:
measure: Serum estrogen (E1 and E2) levels
timeFrame: July to September 2021
measure: Serum testosterone levels
timeFrame: July to September 2021
Secondary outcomes:
Other outcomes:
Locations:
city: Dallas
country: United States
facility: Methodist Health System Clinical Research Institute
state: Texas
Study officials:
affiliation: Methodist
name: Mangesh Pagadala, MD
role: PRINCIPAL_INVESTIGATOR
References:
citation: Ge PS, Runyon BA. Treatment of Patients with Cirrhosis. N Engl J Med. 2016 Nov 24;375(21):2104-5. doi: 10.1056/NEJMc1612334. No abstract available.
citation: Iwakiri Y, Groszmann RJ. The hyperdynamic circulation of chronic liver diseases: from the patient to the molecule. Hepatology. 2006 Feb;43(2 Suppl 1):S121-31. doi: 10.1002/hep.20993.
citation: Cavanaugh J, Niewoehner CB, Nuttall FQ. Gynecomastia and cirrhosis of the liver. Arch Intern Med. 1990 Mar;150(3):563-5.
citation: Gordon GG, Olivo J, Rafil F, Southren AL. Conversion of androgens to estrogens in cirrhosis of the liver. J Clin Endocrinol Metab. 1975 Jun;40(6):1018-26. doi: 10.1210/jcem-40-6-1018.
citation: Seely EW, Walsh BW, Gerhard MD, Williams GH. Estradiol with or without progesterone and ambulatory blood pressure in postmenopausal women. Hypertension. 1999 May;33(5):1190-4. doi: 10.1161/01.hyp.33.5.1190.