Bunyamin Kisacik

Mean platelet volume (MPV) as an inflammatory marker in ankylosing spondylitis and rheumatoid arthritis

AIMS The aim of this retrospective study was to investigate the correlation between MPV and the clinical disease activity indices of rheumatoid arthritis and ankylosing spondylitis. METHODS The study consisted of 32 active RA patients (males/females: 7/25, mean age: 49+/-13) and 30 active AS patients (males/females: 15/15, mean age: 36+/-12) along with 26 osteoarthritis (OA) patients (males/females: 4/22, mean age: 52+/-8) and 29 age-matched healthy subjects (males/females: 5/24, mean age: 41+/-7) as control groups for RA and AS, respectively. RESULTS MPV was significantly lower in both AS patients and RA patients with active disease as compared to controls (RA vs OA p<0.001, AS vs healthy subjects p<0.001). After treatment MPV values significantly increased in AS and RA (p<0.001 for all). However, MPV values remained somewhat lower in RA patients than OA patients (p=0.019). There was a negative correlation between MPV values and BASDAI scores in AS patients after two months of treatment (r=-0.507; p=0.004). CONCLUSION Our results suggest that assessment of MPV may provide additional information about inflammation in AS and RA.

An unusual cause of acalculous cholecystitis during pregnancy: hepatitis A virus.

To the Editor: Acalculous cholecystitis accounts for 5–10% of all acute cholecystitis cases and is usually a complication of various other medical or surgical conditions. Acute cholecystitis due to hepatitis A infection is quite a rare entity and hydropic and wall-thickened gallbladder and sludge formation have been described (1, 2). We present a 19-yearold pregnant woman with acalculous cholecystitis induced by hepatitis A infection. The patient was initially admitted to the obstetrics clinic with complaints of nausea and malaise of 2 weeks duration. She was in the twelfth week of pregnancy and was discharged as the complaints pertained to pregnancy. One week after discharge she developed jaundice, fever, and severe right upper abdominal pain. On physical examination the patient was normal except for slight icterus and right upper quadrant tenderness (a positive Murphy’s sign). Laboratory studies showed the following: white blood cell count, 4100; hematocrit, 35%; platelets, 215,000; alanine aminotransferase (ALT), 1213 U/L (normal range, 0–40); aspartate transaminase (AST), 984 U/L (0–40); alkaline phosphatase (ALP), 296 U/L (38–155); γ -glutamyltranspeptidase (GGT), 124 U/L (15–60); total bilirubin, 11.6 mg/dL (0.1–2.0); direct bilirubin, 5.7 mg/dL (0.1–0.8); albumin, 3.4 g/dL; globulin, 2.7 g/dL; C-reactive protein, 17.5 mg/L (0– 5); erythrocyte sedimentation rate, 34 mm/hr; anti-HAV IgM, positive; HbsAg, negative; anti-HBc IgM, negative; and anti-HCV, negative. Abdominal ultrasonography revealed hepatomegaly, hydropic gallbladder with a thickened wall (8 mm), and 12-week intrauterine pregnancy. There was no calculus, pericholecystic, or intraabdominal fluid, however, a positive Murphy’s sign induced by ultrasound probe was present. After hospitalization and strict bedrest, the patient’s complaints regressed in the first week and her laboratory findings improved in the second week (ALT, 562 U/L; AST, 213 U/L; ALP, 194 U/L; GGT, 81 U/L). A month later, the patient was free of symptoms, biochemistry studies returned to normal, and the gallbladder was normal in sonographic examinations. Our case had hepatitis A infection proved by serological and biochemical tests and her clinical acalculous cholecystitis resolved without any medical or surgical intervention. To the best of our knowledge, only four cases of acalculous cholecystitis induced by hepatitis A infection have been reported in the literature to date. Two of them demonstrated a similar clinical course with conservative management (3); whereas one underwent surgery (4) and the other died of acute fulminant hepatitis (5). Pregnancy may have been a predisposing factor for cholecystitis in the present case. We recommend keeping hepatitis A infection in mind in the clinical approach to patients with acalculous cholecystitis.

Serum adenosine deaminase activities during acute attacks and attack-free periods of familial Mediterranean fever.

BACKGROUND Familial Mediterranean Fever (FMF) is a systemic relapsing autoinflammatory disorder. Adenosine deaminase (ADA) is an enzyme widely distribute in tissues and body fluids. Circulating levels of ADA have been shown to increase in several inflammatory conditions. This study was designed to evaluate the serum ADA in patients with FMF during acute attacks and attack-free periods. METHODS The study groups comprised 23 FMF patients in attack-free period (male/female: 11/12), 30 FMF patients in attack period (male/female: 11/19) and 20 healthy control (male/female:10/10). The groups were similar for age, gender and disease duration. RESULTS The mean age of FMF patients in attack-free period, patient with acute attack were 34.3+/-11.7 and 29.4+/-11.1 respectively. The disease durations were 13.1+/-10.2 and 8.2+/-7.6 years for patients in attack-free periods and patients with acute FMF attack, respectively. Patients with acute attack had significantly higher ADA levels than both patients with attack-free periods and healthy controls (for each, p<0.001). CONCLUSION In this study we demonstrated that FMF patients with acute attacks had higher serum ADA levels than attack-free periods and healthy controls. It is likely that ADA may have a role in the cytokine network of the inflammatory cascade of FMF. Also, elevated ADA levels may be a part of the activated Th1 response in the disease. ADA may be used as a supportive marker to differentiate FMF attacks from attack-free periods. Further larger-scale studies are needed to support this result.