Article
Author(s):
Patients with cirrhosis had higher mortality rates, tophi, and gout flare.
Complications related to gout were more common in patients with cirrhosis, according to a study published in World Journal of Hepatology.1 Further, patients without cirrhosis reported higher rates of interventions, which may be due in part to hesitancy regarding performing these interventions given the higher complication risk in cirrhosis.
Gout, which affects 3.9% of adults in the United States, can cause chronic joint destruction, severe joint pain, difficulty walking, and in some cases, nephropathy, and urate nephrolithiasis. Flares can be triggered by alcohol consumption, fatty foods, trauma, dehydration, and certain medications.2
“A positive correlation between serum uric acid (UA) levels, cirrhosis-related complications and the incidence of nonalcoholic fatty liver disease has been established, but it is unknown whether hyperuricemia results in worsening cirrhosis outcomes,” wrote Ayham Khrais, DO, Division of Medicine, Rutgers New Jersey Medical School, and a team of investigators. “We hypothesize[d] that patients with cirrhosis will have poorer gout outcomes.”
The cross-sectional study used a national inpatient sample (NIS) to identify adult patients hospitalized with gout, which were then stratified based on a history of cirrhosis between 2001 and 2013. The NIS contains data on over 7 million hospital stays in the United States. Primary endpoints included joint interventions, gout complications, and mortality. Demographics, such as age, sex, and ethnicity were also collected and evaluated. Confounding variables were controlled via multiple logistic regression.
In total, 36,948 patients had cirrhosis and 1,491,829 did not have a cirrhosis diagnosis. Most patients were male, although patients in the cirrhosis cohort had a greater number of males compared with the non-cirrhosis group (74.63% vs 66.83%). Patients without cirrhosis were older when compared with those with cirrhosis (70.37 ± 13.53 years vs 66.21 ± 12.325 years; P <.05).
Those in the cirrhosis group had higher mortality rates (5.49% vs 2.03%; adjusted P <.05), tophi (0.97% vs 0.75%; adjusted P = .677), and gout flare (2.89% vs 2.77%; adjusted P <.05). Patients without cirrhosis reported higher rates of joint injections (0.72% vs 0.52%; adjusted P <.05) and arthrocentesis (2.45% vs 2.21%; adjusted P <.05).
Rates of UA nephrolithiasis (.025 in both groups), nephropathy (.02% in the non-cirrhosis group and .01% in the cirrhosis group), and septic arthritis (.31% in both groups) were similar among all patients.
Investigators noted that risk factors for cirrhosis, such as chronic alcohol use, are independently associated with gout and elevated serum UA levels. As patients in the study had both alcoholic and nonalcoholic etiologies of cirrhosis, alcohol use disorder may be a significant confounding variable. Another limitation was that investigators could not determine whether interventions designed to treat gout may have led to any bleeding complications. Lastly, patients were not categorized by the subtype of cirrhosis, such as nonalcoholic fatty liver disease (NAFLD), alcoholic, and viral.
Investigators suggested a retrospective chart review of patients with gout flares and a history of cirrhosis further categorizing patients into alcoholic or NAFLD cirrhosis to determine the relationship between cirrhosis and gout. It could also analyze gout rates in this patient population, as a history of significant alcohol use is an independent risk factor for gout.
“Patients with cirrhosis may have differential rates of gout exacerbations and potential therapeutic options due to a combination of pathophysiology, cirrhosis-related comorbidities and clinical decision making,” investigators concluded. “As there are few studies connecting both disease states, more investigation is required to further delineate the relationship between liver disease and gout.”