[The complexity of chronic pelvic pain exemplified by the condition currently called interstitial cystitis. Part 2: Treatment]. / Die Komplexität chronischer Beckenschmerzen am Beispiel der Interstitiellen Zystitis. Teil 2: Therapie.

The so-called interstitial cystitis is a chronic pain syndrome rather than a purely end organ disease of the urinary bladder. New suggestions for definitions and nomenclature take this into consideration. Since aetiology and pathogenesis are still unknown a treatment of the cause is still not possible. There are neither evidence-based treatment algorithms nor a so-called standard therapy. Numerous therapeutic approaches have been tried up to now. These attempts can be divided into oral, intravesical, surgical and physical procedures. There are also meaningful supplementary therapy procedures beyond the boundaries of classical school medicine. The WHO staging scheme provides the basis for every pain therapy. For the oral therapeutic procedures in current use the following medications with differing levels of evidence have been recommended: amitriptylin, hydroxyzin, pentosan polysulfate. Many other orally administered drugs have also been used although in many cases evidence of efficacy is lacking, these included anticonvulsants, L-arginine and various immunomodulators and immunosuppressants. Among the intravesical therapeutic procedures botulinum toxin A, dimethyl sulfoxide, heparin and glycosaminoglycan substitutes have been used. For the physical procedures, besides bladder distension, hyperbaric oxygen therapy shows efficacy. When the conventional therapeutic methods fail, surgical (partial) removal of the urinary bladder or urinary diversion procedures represent the therapeutic ultimo ratio. There are hardly any controlled studies on alternative curative procedures although rather good results have been obtained in chronic pelvic pain syndrome with acupuncture as an additional therapeutic modality.

Amylase activity of parotid saliva in acute and chronic pancreatitis.

The activity of the alpha-amylase was estimated in the parotid resting saliva of 17 subjects without evidence of pancreatic disease, 17 patients with chronic relapsing pancreatitis in the intervals between acute attacks, and also in 4 patients with acute pancreatitis and 3 patients with an acute attack of chronic relapsing pancreatitis. In the patients with chronic relapsing pancreatitis between attacks the concentration, output and specific activity of the salivary amylase were significantly lowered. The patients with acute pancreatitis exhibited salivary amylase concentrations in the uppper normal to grossly supranormal range, whereas those of the patients with acute attacks of chronic relapsing pancreatitis were distinctly reduced. Unlike the amylase output, the amylase concentration was independent of the rate of salivary flow. Simultaneous infusion of secretin and pancreozymin produced a significant increase in the parotid salivary amylase levels in both the patients without pancreatic disease and in those with chronic relapsing pancreatitis between acute attacks.