Chronic pain is nowadays considered not only the mainstay symptom of rheumatic diseases but also “a disease itself.” Pain is a multidimensional phenomenon, and in inflammatory arthritis, it derives from multiple mechanisms, involving both synovitis (release of a great number of cytokines) and peripheral and central pain-processing mechanisms (sensitization). In the last years, the JAK-STAT pathway has been recognized as a pivotal component both in the inflammatory process and in pain amplification in the central nervous system. This paper provides a summary on pain in inflammatory arthritis, from pathogenesis to clinimetric instruments and treatment, with a focus on the JAK-STAT pathway.

Lactose malabsorption was studied, by hydrogen breath test, in 72 adults suffering from irritable bowel syndrome, in 20 ulcerative colitis patients, and in 69 healthy subjects. The minimum dose of lactose required to cause a positive breath test was determined, and the symptoms caused and the resulting hydrogen eliminated quantified. A high incidence of lactose malabsorption was shown at standard doses (up to 50 g) in both the healthy subjects (70%) and the patients (86% and 85%, respectively). In the irritable bowel syndrome and the ulcerative colitis groups, symptoms occurred with a smaller quantity of breath hydrogen, presumably in association with a greater individual sensitivity of the colon to distension. The threshold lactose dose was notably lower in the diseased subjects who registered as evidence a prevalence of malabsorption at a 20-g lactose load. The pathogenetic role of lactose malabsorption in the irritable bowel syndrome is emphasized, as is the importance of the personal lactose tolerance.

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The inhibitory activity of gallbladder bile on in vitro calcium carbonate crystallization was investigated in 12 normal subjects, 18 patients with radiolucent gallstones, and 18 patients with radiopaque or mixed gallstones, all of whom had functioning gallbladders. Inhibitory activity, expressed as CIT (crystallization inhibition time), was notably higher in the normal subjects and only slightly greater than the effect of water in the gallstone patients; the extrapolation of the results suggests that the difference in the method used to obtain the bile, by duodenal probe or during surgery, had little effect on the inhibitory activity. No significant correlation was found with the CSI (cholesterol saturation index) and the biliary lipid variables. In view of the frequent appearance of calcium carbonate in the composition of gallstones, the possibility is emphasized that the reduced inhibitory effect of bile in the crystallisation of CaCO3 plays a part in gallstone growth or formation.