A Popular myth - low-histamine diet improves chronic spontaneous urticaria - fact or fiction?

BACKGROUND: Chronic spontaneous urticaria (CsU) is a frequent dermatological disease that might last for months or years with high impact on quality of life. Known causes are autoreactive phenomena, infections or intolerances, rarely IgE-mediated allergies. One-third of CsU patients benefit from a low-pseudoallergen diet. Additionally, it is often discussed, that reducing histamine ingestion alone might improve clinical symptoms and quality of life in CsU patients despite the uncertain role of the histamine-degrading enzyme diamine oxidase (DAO). OBJECTIVE: Aim of this study was to investigate the impact of low-histamine diet on symptoms and quality of life in patients with CsU. METHODS: Patients suffering from CsU accompanied by gastrointestinal symptoms were included in the study. They underwent low-histamine diet for at least 3 weeks. During the whole study, urticaria activity score (UAS) was recorded daily in a patient's diary. Quality of life was assessed during screening, baseline and post diet visits by completing questionnaires (DLQI and Cu-Q(2)oL). DAO activity was measured before and after elimination diet. RESULTS: A total of 75% of the patients had a benefit from the low-histamine diet. Thirty-four of 56 patients (61%) reached the primary endpoint of the study, an improvement of UAS 4 of ≥3. Overall, a significant reduction from 9.05 to 4.23 points (P = 0.004) was achieved; the average reduction in a strongly affected subgroup was 8.59 points (P < 0.001). DAO activity remained stable. CONCLUSION: Low-histamine diet is a therapeutically useful, simple and cost-free tool to decrease symptoms and increase quality of life in CsU patients with gastrointestinal involvement. Further research is needed to understand the role of diamine oxidase.

Cognitive performance and cerebrohemodynamics associated with the Persian Gulf Syndrome.

The Persian Gulf Syndrome generally manifests as a set of nonspecific complaints with emphasis on central nervous system impairment. The purpose of this study was to determine if cognitive performance and middle cerebral artery blood flow velocity (MCABFV) were altered in symptomatic Gulf War veterans (sGWVs) and asymptomatic Gulf War veterans (aGWVs) by exposure to low levels of acetone. MCABFV was assessed in male aGWVs (n = 8) and sGWVs (n = 8) during cognitive challenges while breathing 1) clean air, 2) a clean air placebo, and 3) a mixture of air and 40 parts per million (ppm) acetone. Pulmonary function was also evaluated. Pulmonary function tests showed no statistical differences between aGWVs and sGWVs while breathing clean air or 40 ppm acetone in air. Cognitive performance was similar during the clean air, placebo, and acetone test conditions for sGWVs and aGWVs. Data pooled across test conditions for each group indicated a statistically significant (P < 0.05) poorer performance primarily in memory and executive function tasks by sGWVs. sGWVs had a 34.2% higher baseline MCABFV than aGWVs (P < 0.05). Increases in MCABFV for aGWVs (averaged over all cognitive tasks for each test condition) ranged between 7.8% and 8.8%, and were not statistically significant. Increases for sGWVs ranged between 0.3% and 4.8%, averaged over all cognitive tasks for each test condition. No significant differences were noted between the clean air and placebo test conditions but both were significantly different to the acetone condition. Differences in MCABFV increases for each of the test conditions between aGWVs and sGWVs were also statistically significant. sGWV did not appear to demonstrate pulmonary dysfunction following exposure to acetone. They did, however, appear to have generally lower cognitive function as compared to aGWVs. sGWVs appeared to have a significant degree of autoregulatory disruption in cerebral perfusion, resulting in reduced cognitive reserve capacity and potentially impaired ability to handle complex cognitive tasks.

Chemical sensitivity attributed to pesticide exposure versus remodeling.

One hundred twelve individuals who reported onset of multiple chemical sensitivity following well-documented exposure to either (1) a cholinesterase-inhibiting organophosphate or carbamate pesticide or (2) remodeling of a building completed mail-out/mail-back questionnaires concerning their exposure, symptoms, sensitivity to ingestants and inhalants, utilization of health-care resources, and impact of their illness on lifestyle. It was hypothesized that if multiple chemical sensitivity resulted from neurotoxic exposure, then organophosphate-exposed respondents should report greater severity of illness resulting from the relatively greater neurotoxicity of this class of chemicals. Pesticide-exposed and remodeling-exposed multiple chemical sensitivity groups reported similar patterns of symptoms and identified similar inhalants and ingestants as triggers for their symptoms; these results suggested a common mechanism (biological and/or psychological) for their conditions. The pesticide-exposed group, however, reported significantly greater symptom severity than did the remodeling-exposed group, especially for neuromuscular, affective, airway, gastrointestinal, and cardiac symptoms. These findings provide evidence for (1) a possible biological basis for multiple chemical sensitivity and (2) a distinct pathophysiology or final common pathway for the condition that, while as yet undefined, appears to be shared by these two groups. Although subjective multisystem health complaints characterize both multiple chemical sensitivity and somatoform disorder, features of this multiple chemical sensitivity sample were inconsistent with somatoform disorder, i.e., onset after 30 y of age in 83%, the predominance of severe cognitive symptoms, and attributions of environmental causation. No group differences were found with respect to lifestyle impact. Eighty-one percent of respondents said they had been working full-time at the time they were exposed, yet at the time of the survey (on average, 7.7 y post exposure) only 12.5% were working full-time. The majority said they had quit their jobs, changed jobs, or changed careers because of their illness. Approximately 40% reported that they had consulted 10 or more medical practitioners. The persistent, disabling neuropsychological symptoms reported by these multiple chemical sensitivity groups are strikingly similar to those reported among individuals exposed occupationally to pesticides and solvents. These parallel findings suggest that the types and levels of exposures associated with extermination and remodeling may not be inconsequential, at least for a subset of the population. Further studies from a variety of perspectives, including human challenge studies and the development of animal models, are needed to define the pathophysiological and psychological mechanisms underlying this costly condition.

The effect of anesthetics on neurologic outcome during the recovery period of spinal cord injury in rats.

We evaluated the effects of anesthetics on neurologic outcome in a model of recoverable experimental spinal cord injury (SCI). Adult rats were implanted with various sizes of hygroscopic plastic material at the T12 spinal level to determine the dimensions that would produce a progressive neurologic deficit from which recovery could occur. Neurologic evaluation was conducted on an inclined plane, noting the maximum angle at which an animal was able to maintain orientation perpendicular to the longitudinal midline. Scores were statistically modeled for each group to develop profiles of neurologic deficits. Rats were subjected to a 4-h exposure to isoflurane, fentanyl/nitrous oxide, or ketamine 7 or 8 days postimplantation. Neurologic outcomes were compared to a SCI reference group which received no postimplant anesthesia. An animal weight/desiccated implant volume (Wa/Vi) ratio of 53 to 73 g/mm3 produced postimplant neurologic deficits which deteriorated to near maximum within 3 days, followed by a gradual improvement beginning at Day 8 and returning to near normal between 21 and 25 days. Final outcome was based on modeled ramp scores for each group and reported in degrees +/- SD: reference, 71.2 +/- 1.1; fentanyl/N2O, 70.4 +/- 0.3; isoflurane, 72.6 +/- 1.1; and ketamine, 64.9 +/- 0.6. The fentanyl group attained maximum recovery first (P > 0.05) but did not recover to a level different on the average from the reference group. The ketamine group demonstrated a poorer (P > 0.05) recovery level relative to the other anesthetic protocols.