Prolonged release oxycodone and naloxone treatment counteracts opioid-induced constipation in patients with severe pain compared to previous analgesic treatment.

Objective: Treatment with prolonged-release oxycodone/naloxone (PR OXN) has been shown to improve opioid induced constipation (OIC) in constipated patients. This publication reports on a real-life observational study investigating the efficacy of PR OXN with regard to bowel function in patients switching to PR OXN from WHO step 1, step 2 and step 3 opioids.

Methods: Patients with chronic pain experiencing insufficient pain relief and/or unacceptable side effects were switched to PR OXN and monitored in this observational study with respect to efficacy regarding bowel function and efficacy regarding pain relief in comparison with previous analgesic therapy.

Treatment with prolonged-release oxycodone/naloxone improves pain relief and opioid-induced constipation compared with prolonged-release oxycodone in patients with chronic severe pain and laxative-refractory constipation.

Purpose: Laxative-refractory opioid-induced constipation (OIC) is defined as OIC despite using 2 laxatives with a different mechanism of action (based on the Anatomical Therapeutic Chemical Classification System level 4 term [contact laxatives, osmotically acting laxatives, softeners/emollients, enemas, and others]). OIC has a significant impact on the treatment and quality of life of patients with severe chronic pain. This noninterventional, observational, real-life study in Belgium investigated the efficacy of prolonged-release oxycodone/naloxone combination (PR OXN) treatment regarding pain relief and OIC compared with previous prolonged-release oxycodone (PR OXY) treatment for laxative-refractory OIC in daily clinical practice.

Somatostatin modulates mast cell-induced responses in murine spinal neurons and satellite cells.

The course of intestinal inflammatory responses is tightly coordinated by the extensive communication between the immune system and the enteric nervous system, among which the bidirectional mast cell-neuron interaction within the intestinal wall plays a prominent role. Recent research suggests that somatostatin (SOM) is able to inhibit this self-reinforcing network by simultaneously suppressing the inflammatory activities of both neurons and mast cells. Therefore, we assessed the modulatory effects of SOM on both the short-term and long-term effects induced by the main mast cell mediators histamine (HIS) and 5-HT on spinal sensory neurons.

Effect of genetic SSTR4 ablation on inflammatory peptide and receptor expression in the non-inflamed and inflamed murine intestine.

The recently suggested pivotal role of somatostatin (SOM) receptor 4 (SSTR4) in inflammation and nociception in several non-intestinal organs and in gastrointestinal (GI) physiology, necessitates exploration of the role of SSTR4 in GI pathophysiology. Therefore, the role of SSTR4 in GI activity was explored by investigating the effects of SSTR4 deficiency on intestinal motility, smooth muscle contractility and on the expression of SSTRs and neuropeptides in the healthy and Schistosoma mansoni-infected murine small intestine. Functional experiments revealed no differences in intestinal motility or smooth muscle cell contractility between wild-type and SSTR4 knockout (SSTR4(-/-)) mice in physiological conditions.

The role(s) of somatostatin, structurally related peptides and somatostatin receptors in the gastrointestinal tract: a review.

Extensive functional and morphological research has demonstrated the pivotal role of somatostatin (SOM) in the regulation of a wide variety of gastrointestinal activities. In addition to its profound inhibitory effects on gastrointestinal motility and exocrine and endocrine secretion processes along the entire gastrointestinal tract, SOM modulates several organ-specific activities. In contrast to these well-known SOM-dependent effects, knowledge on the SOM receptors (SSTR) involved in these effects is much less conclusive.

Schistosomicidal activity of the antimalarial drug, mefloquine, in Schistosoma mansoni-infected mice.

Therapeutic effects of racemic mefloquine were assessed in Schistosoma mansoni-infected mice, and evaluated by recording worm burden, the status of egg maturation and viability, and intestinal mast cell recruitment. Age-matched mice were divided into four groups, of which two were infected. At 8 weeks postinfection, one group of infected and one group of uninfected mice were treated with a single dose of mefloquine (150 mg/kg).

Region-specific distribution of the P2Y4 receptor in enteric glial cells and interstitial cells of Cajal within the guinea-pig gastrointestinal tract.

Although there is pharmacological evidence to assume that the P2Y4 receptor is a regulator of epithelial ion transport, no detailed data about its distribution within the gut are available. Therefore, this study, using whole mounts and cryosections, aimed to reveal the expression pattern of P2Y4 along the entire guinea-pig gastrointestinal tract. P2Y4 immunoreactivity was absent from enteric neurons but present in enteric glial cells of the stomach, small and large intestine.