Low-dose naltrexone therapy improves active Crohn’s disease.

 
Am J Gastroenterol. 2007 Apr;102(4):820-8. Epub 2007 Jan 11. Related Articles, Links
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Low-dose naltrexone therapy improves active Crohn’s disease.

Smith JP, Stock H, Bingaman S, Mauger D, Rogosnitzky M, Zagon IS.

Department of Medicine, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033, USA.

OBJECTIVES: Endogenous opioids and opioid antagonists have been shown to play a role in healing and repair of tissues. In an open-labeled pilot prospective trial, the safety and efficacy of low-dose naltrexone (LDN), an opioid antagonist, were tested in patients with active Crohn’s disease. METHODS: Eligible subjects with histologically and endoscopically confirmed active Crohn’s disease activity index (CDAI) score of 220-450 were enrolled in a study using 4.5 mg naltrexone/day. Infliximab was not allowed for a minimum of 8 wk prior to study initiation. Other therapy for Crohn’s disease that was at a stable dose for 4 wk prior to enrollment was continued at the same doses. Patients completed the inflammatory bowel disease questionnaire (IBDQ) and the short-form (SF-36) quality of life surveys and CDAI scores were assessed pretreatment, every 4 wk on therapy and 4 wk after completion of the study drug. Drug was administered by mouth each evening for a 12-wk period. RESULTS: Seventeen patients with a mean CDAI score of 356 +/- 27 were enrolled. CDAI scores decreased significantly (P= 0.01) with LDN, and remained lower than baseline 4 wk after completing therapy. Eighty-nine percent of patients exhibited a response to therapy and 67% achieved a remission (P < 0.001). Improvement was recorded in both quality of life surveys with LDN compared with baseline. No laboratory abnormalities were noted. The most common side effect was sleep disturbances, occurring in seven patients. CONCLUSIONS: LDN therapy appears effective and safe in subjects with active Crohn’s disease. Further studies are needed to explore the use of this compound.

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PMID: 17222320 [PubMed – in process]

Posted in Psychiatry/Neurology |

Protection of endogenous enkephalin catabolism as natural approach to novel analgesic and antidepressant drugs.

 
Expert Opin Ther Targets. 2007 Feb;11(2):145-59. Related Articles, Links
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Protection of endogenous enkephalin catabolism as natural approach to novel analgesic and antidepressant drugs.

Noble F, Roques BP.

CNRS UMR 7157, Paris F-75006, France.

The most efficient drugs to alleviate severe pain are opioid compounds. However, their chronic use could be associated with serious drawbacks, such as tolerance, respiratory depression and constipation. Therefore, there is a need for compounds able to efficiently alleviate inflammatory and neurogenic pain following chronic treatment. The discovery that the endogenous opioid peptides, enkephalins, are inactivated by two metallopeptidases, neutral endopeptidase and aminopeptidase N, which can be blocked by synthetic dual inhibitors, represents a promising way to develop ‘physiological’ analgesics devoid of morphine side effects. These dual inhibitors also have antidepressant-like properties through enkephalin-related activation of delta-opioid receptors. This is expected to reduce the emotional component of pain in humans. This article reviews the promising data obtained for future development of a new class of analgesic that could be of major interest in a number of severe and chronic pain syndromes.

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PMID: 17227231 [PubMed – indexed for MEDLINE]

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The distinctive effects of acute and chronic psychological stress on airway inflammation in a murine model of allergic asthma.

 
Allergol Int. 2007 Mar;56(1):29-35. Epub 2007 Jan 29.
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The distinctive effects of acute and chronic psychological stress on airway inflammation in a murine model of allergic asthma.

Okuyama K, Ohwada K, Sakurada S, Sato N, Sora I, Tamura G, Takayanagi M, Ohno I.

Department of Pathophysiology, Tohoku Pharmaceutical University, Miyagi, Japan.

BACKGROUND: Psychological stress has long been recognized to be associated with asthma symptoms. There appear to be individual differences in the susceptibility to even the same kind of stress, and furthermore, stress responses are different between the types of the stress, acute and chronic, even in the same person. However, the mechanisms linking stress to asthma are not well defined. Psychological stress upregulates the expression of endogenous opioids. The opioids stimulate the hypothalamus-pituitary-adrenal axis and sympathetic and adrenomedullary system, through the activation of mu-opioid receptor (MOR) to release stress hormones, such as cortisol and catecholamines, respectively. These hormones can modulate immune responses via the induction of Th1 immunity. METHODS: Female BALB/c and C57BL/6, wild and MOR-deficient, mice sensitized with ovalbumin (OVA) were exposed to OVA with or without either acute or chronic restraint stress. Airway inflammation was evaluated by the measurement of the number of inflammatory cells and cytokine contents in bronchoalveolar lavage fluids. RESULTS: In BALB/c mice, but not in C57BL/6 mice, the number of total cells, eosinophils and lymphocytes in the acute stress group were significantly decreased compared with those in the non-acute stress group. In contrast, chronic stress significantly increased the cell numbers and the contents of IL-4 and IL-5 in both mouse strains. Furthermore, these exacerbations were abolished in MOR-deficient mice. CONCLUSIONS: These results suggest that acute stress modifies the allergic airway responses distinctively depending on the genetic background, and MOR is involved in the chronic psychological stress-induced exacerbation of allergic airway inflammation.

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PMID: 17259807 [PubMed – in process]

Posted in Uncategorized |

Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides.

 
Am J Physiol Endocrinol Metab. 2007 Feb;292(2):E561-70.
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Dietary fat stimulates endogenous enkephalin and dynorphin in the paraventricular nucleus: role of circulating triglycerides.

Chang GQ, Karatayev O, Ahsan R, Gaysinskaya V, Marwil Z, Leibowitz SF.

The Rockefeller University, 1230 York Ave., New York, NY 10021, USA.

The opioid peptides enkephalin (ENK) and dynorphin (DYN), when injected into the hypothalamus, are known to stimulate feeding behavior and preferentially increase the ingestion of a high-fat diet. Studies of another peptide, galanin (GAL), with similar effects on feeding demonstrate that a high-fat diet, in turn, can stimulate the expression of this peptide in the hypothalamus. The present study tested different diets and variable periods of high- vs. low-fat diet consumption to determine whether the opioid peptides respond in a similar manner as GAL. In six experiments, the effects of dietary fat on ENK and DYN were examined in three hypothalamic areas: the paraventricular nucleus (PVN), perifornical hypothalamus (PFH), and arcuate nucleus (ARC). The results demonstrated that the ingestion of a high-fat diet increases gene expression and peptide levels of both ENK and DYN in the hypothalamus. The strongest and most consistent effect is seen in the PVN. In this nucleus, ENK and DYN are increased by 50-100% after 1 wk, 1 day, 60 min, and even 15 min of high-fat diet consumption. While showing some effect in the PFH, these peptides in the ARC are considerably less responsive, exhibiting no change in response to the briefer periods of diet intake. This effect of dietary fat on PVN opioids can be observed with diets equal in caloric density and palatability and without a change in caloric intake, body weight, fat pad weight, or levels of insulin or leptin. The data reveal a strong and consistent association between these peptides and a rise in circulating levels of triglycerides, supporting a role for these lipids in the fat-induced stimulation of opioid peptides in the PVN, similar to GAL.

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PMID: 17283367 [PubMed – indexed for MEDLINE]

Posted in Psychiatry/Neurology |

Upregulation of opioid receptor binding following spontaneous epileptic seizures.

 
Brain. 2007 Apr;130(Pt 4):1009-16. Epub 2007 Feb 14. Related Articles, Links
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Upregulation of opioid receptor binding following spontaneous epileptic seizures.

Hammers A, Asselin MC, Hinz R, Kitchen I, Brooks DJ, Duncan JS, Koepp MJ.

MRC Clinical Sciences Centre and Division of Neuroscience, Faculty of Medicine, Imperial College, Hammersmith Hospital, London, UK.

Animal and limited human data suggest an important anticonvulsant role for opioid peptides and their receptors. We aimed to provide direct human in vivo evidence for changes in opioid receptor availability following spontaneous seizures. We scanned nine patients within hours of spontaneous temporal lobe seizures and compared their postictal binding of the non-subtype selective opioid receptor PET radioligand [11C]diprenorphine (DPN), quantified as a volume-of-distribution (VD), with interictal binding and with binding changes in 14 healthy controls, controlling for a range of behavioural variables associated with opioid action. A regionally specific increase of opioid receptor availability was evident in the temporal pole and fusiform gyrus ipsilateral to the seizure focus following seizures (Z 5.01, P < 0.001, 16 432 mm3). Within this region, there was a negative correlation between VD and log10 time since last seizure (r = -0.53, P < 0.03), compatible with an early increase and gradual return to baseline. [11C]DPN VD did not undergo systematic changes between time points in controls. This study provides direct human in vivo evidence for changes in opioid receptor availability over a time course of hours following spontaneous seizures, emphasizing an important role of the opioid system in seizure control.

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PMID: 17301080 [PubMed – in process]

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