Patient: Female, 22Final Diagnosis: Fitz-Hugh-Curtis syndrome – disseminated gonococcal infectionSymptoms: Abdominal pain • fever • polyarthritisMedication: —Clinical Procedure: —Specialty: Infectious DiseasesObjective:Rare co-existance of disease or pathologyBackground:Fitz-Hugh-Curtis (FHC) syndrome is a perihepatitis linked to inflammatory pelvic disease. It can be caused by Neisseria gonorrhoeae or Chlamydia trachomatis infections. FHC syndrome usually presents with pain in the right hypochondrium and fever, associated with symptoms and signs of pelvic infection in women.Case Report:We present the case of a 22-year-old woman with systemic lupus erythematous (SLE) who presented with polyarthritis, cutaneous lesions, and abdominal pain. The diagnosis of FHC syndrome was based on the findings of abdominal computerized tomography (CT) and the isolation of Neisseria gonorrhoeae (NG) in blood cultures. The association of arthritis and cutaneous lesions was diagnosed as a syndrome of arthritis-dermatitis, also caused by systemic NG infection. The patient had a favorable outcome with antibiotic treatment.Conclusions:FHC syndrome should be considered in sexually active young patients, mainly women, with pelvic infection and perihepatitis. It may be caused by disseminated gonococcal infection. An important risk factor is the serum complement deficit, which may predispose to severe forms. Low serum complement level is a frequent manifestation of active SLE. CT images showing the typical findings of perihepatitis allow making the correct diagnosis.

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that commonly complicates the course of patients with liver disease. Despite the fact that the syndrome was probably first recognized hundreds of years ago, the exact pathogenesis still remains unclear. Minimal hepatic encephalopathy (MHE) is the earliest form of HE and is estimated to affect more that 75% of patients with liver cirrhosis. It is characterized by cognitive impairment predominantly attention, reactiveness and integrative function with very subtle clinical manifestations. The development of MHE is associated with worsen in driving skills, daily activities and the increase of overall mortality. Skeletal muscle has the ability to shift from ammonia producer to ammonia detoxifying organ. Due to its large size, becomes the main ammonia detoxifying organ in case of chronic liver failure and muscular glutamine-synthase becomes important due to the failing liver and brain metabolic activity. Gut is the major glutamine consumer and ammonia producer organ in the body. Hepatocellular dysfunction due to liver disease, results in an impaired clearance of ammonium and in its inter-organ trafficking. Intestinal bacteria, can also represent an extra source of ammonia production and in cirrhosis, small intestinal bacterial overgrowth and symbiosis can be observed. In the study of HE, to get close to MHE is to get closer to its big bang; and from here, to travel less transited roads such as skeletal muscle and intestine, is to go even closer. The aim of this editorial is to expose this road for further and deeper work.

Although the pathophysiology of HE is not completely elucidated, ammonia plays a key role [11]. Hyperammonaemia alters the integrity of the blood-brain barrier (BBB) in rats, increasing the influx of toxic substances into the brain [12]. Norenberg et al. [13] described, in an in vitro model, mitochondrial dysfunction oxidative and nitrosative stress as the main source of free radicals in the CNS under hyperammonaemia conditions [13].The bacterial lipopolysaccharide (LPS), and the ammonia produced by the intestinal bacteria arrive through the portal vein, and