Fitz-Hugh–Curtis syndrome is a rare complication of pelvic inflammatory disease (PID) involving liver capsule inflammation leading to the creation of adhesions. The condition is named after the two physicians, Thomas Fitz-Hugh, Jr and Arthur Hale Curtis who first reported this condition in 1934 and 1930 respectively. Signs and symptoms
The major symptom and signs include an acute onset of right upper quadrant (RUQ) abdominal pain aggravated by breathing, coughing or laughing, which may be referred to the right shoulder. There is usually also tenderness on palpation of the right upper abdomen and tenderness to percussion of the lower ribs which protect the liver. Surprisingly there is often no or only minimal pelvic pain, vaginal discharge or cervical motion tenderness, which may lead to the diagnosis being missed. This may be due to infectious bacteria bypassing pelvic structures on the way to the liver capsule. Pathophysiology
Fitz-Hugh–Curtis syndrome occurs almost exclusively in women. It is usually caused by Chlamydia trachomatis (Chlamydia) or Neisseria gonorrhoeae (Gonorrhea) though other bacteria such as Bacteroides, Gardnerella, E. coli and Streptococcus have also been found to cause Fitz-Hugh-Curtis syndrome on occasion. These bacterial pathogens  cause a thinning of cervical mucus and allow bacteria from the vagina into the uterus and fallopian tubes, causing infection and inflammation. Occasionally, this inflammation can cause scar tissue to form on Glissons capsule, a thin layer of connective tissue surrounding the liver. (Bailey&Love)

Diagnosis
Abdominal ultrasound will typically be normal.
Both substances are structurally different but have the same mechanism of action. Cyclosporin binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase A (known as cyclophilin), while tacrolimus binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase FKBP12. These complexes inhibit calcineurin, block dephosphorylation of the transcription factor NFAT of activated T-cells and its translocation into the nucleus. Standard prophylaxis involves the use of cyclosporine for six months with methotrexate. Cyclosporin levels should be maintained above 200 ng/ml. Other substances that have been studied for GvHD treatment include, for example: sirolimus, pentostatin, etanercept, and alemtuzumab.In August 2017 the US FDA approved ibrutinib to treat chronic GvHD after failure of one or more other systemic treatments. Clinical research
There are a large number of clinical trials either ongoing or recently completed in the investigation of graft-versus-host disease treatment and prevention.On May 17, 2012, Osiris Therapeutics announced that Canadian health regulators approved Prochymal, its drug for acute graft-versus-host disease in children who have failed to respond to steroid treatment. Prochymal is the first stem cell drug to be approved for a systemic disease.In January 2016, Mesoblast released results of a  phase 2 clinical trial on 241 children with acute Graft-versus-host disease, that was not responsive to steroids. The trial was of a mesenchymal stem cell therapy known as remestemcel-L or MSC-100-IV. Survival rate was 82% (vs 39% of controls) for those who showed some improvement after 1 month, and in the long term  72% (vs 18% of controls) for those that showed little effect after 1 month.