Leukocytapheresis (LCAP), performed with a leukocyte removal filter, was administered five times, at 1-week intervals, for 5 weeks of intensive therapy and five times, at approximately 1-month intervals, for approximately 5 months of maintenance therapy, to 13 patients with inflammatory bowel disease (IBD) diagnosed as ulcerative colitis (UC) in 8 and Crohn's disease (CD) in 5. Clinical and blood examinations showed no side effects in any of the patients. During the intensive therapy, excellent or moderate clinical response was recognized in 11 of the 13 patients (84.6%), of whom 6 had a dramatic response; the excellent or moderate clinical response continued throughout the maintenance therapy in 8 of the patients (61.5%). Flow cytometry showed that the patients who had improved generally had high values for percentages of HLADR+, HLADR+CD3+, and HLADR+CD8+ cells before the first LCAP, and that these values and the C-reactive protein levels and erythrocyte sedimentation rates had decreased to the normal range by the end of both intensive and maintenance therapy. In the patients who showed poor response, in contrast, all the above values had been at or near normal before the initial LCAP administration. The clinical improvement in the absence of any additional medical treatment suggests that LCAP has the capacity to influence the causal mechanism(s) of IBD and that IBD is strongly associated with the cell-mediated immune response.

The importance of tumor necrosis factor (TNF)-alpha and the TNF receptor gene polymorphisms in the etipathogenesis of inflammatory bowel disease (IBD) has not been elucidated. DNA from peripheral blood samples was obtained from 124 patients with Crohn's disease (CD), 106 patients with ulcerative colitis (UC), and 111 unrelated healthy controls. We examined two single nucleotide polymorphisms (SNPs) of the TNF-alpha gene, TNF (-308 G/A and -238 G/A), an SNP of the TNF receptor superfamily member 1A gene, TNFRSF1A(also known as TNFR1), at codon 12 in exon 1 (CCA/CCG), and two SNPs of the 1B gene, TNFRSF1B (also known as TNFR2), (1466 A/G and 1493 C/T). There was a difference in the carrier frequency for haplotype AG (-308 A, -238 G) between UC patients and the controls (OR=4.76, 95% CI=1.53-14.74, P<0.01). We found a significant difference in carrier frequency for haplotype AT (1466 A, 1493 T) of the TNFRSF1B gene between CD patients and the controls (OR=2.13, 95% CI=1.08-4.21, P<0.05). The significance proved to be greater in CD patients with both internal and external fistula (OR=4.8, 95% CI=1.73-13.33, P<0.01), and in those who were poor responders ( n=22) to our treatments, which consisted of nutritional therapy, medical therapy and surgical therapy (OR=9.24, 95% CI=3.37-25.36, P<0.001). This study suggests that one of the genes responsible for UC may be the TNF gene, or an adjacent gene, and that TNFRSF1B gene polymorphisms contribute greatly to the increased onset risk of CD and to the disease behavior.

A total of 71 joints and 91 medial branches were studied in 48 patients. The distribution of referred pain from the L1/2 to L5/S1 zygapophyseal joints, and the medial branches of the dorsal rami from L1 to L5 were similar for each level stimulated, and the overlap of referred pain between each level was considerable.

The purpose of this study was to determine the distribution of referred pain from the cervical zygapophyseal joints (C0/1 to C7/Th1) and the cervical dorsal rami (C3 to C7). The subjects were 61 patients who had occipital, neck, and shoulder pain of suspected zygapophyseal origin in whom pain was reproduced by injection of contrast medium into the joints or by electrical stimulation of the dorsal rami. Under fluoroscopic control, the zygapophyseal joints from C0/1 to C7/Th1 were stimulated by the injection of contrast medium and while electrical stimulation of the cervical zygapophyseal dorsal rami at segments C3 to C7 was performed during facet denervation. If injection or electrical stimulation reproduced the patient's usual pain, the distribution of referred pain was determined and the sites of referred pain were divided into 10 areas. A total of 181 joints and 62 segments were studied. Each joint and dorsal ramus produced referred pain with a characteristic distribution. The main distribution of referred pain was as follows. Pain in the occipital region was referred from C2/3 and C3, while pain in the upper posterolateral cervical region was referred from C0/1, C1/2, and C2/3. Pain in the upper posterior cervical region was referred from C2/3, C3/4, and C3, that in the middle posterior cervical region from C3/4, C4/5, and C4, and that in the lower posterior cervical region from C4/5, C5/6, C4, and C5. In addition, pain in the suprascapular region was referred from C4/5, C5/6, and C4, that in the superior angle of the scapula from C6/7, C6, and C7, and that in the mid-scapular region from C7/Th1 and C7.

IL18 is probably one of several genes that determine susceptibility to Crohn's disease.

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Neuropathic pain has a substantial effect on quality of life (QOL). The Japanese Society of Pain Clinicians (JSPC) has developed clinical guidelines of pharmacotherapy for neuropathic pain. These guidelines offer clarity on recommendations based on both the most recent scientific evidence and expert opinions. Understanding the concept, disease entity, and burden of neuropathic pain, as well as its screening and diagnosis are important steps before starting pharmacotherapy. As well as other guidelines, the guidelines propose several lines of pharmacotherapies in a step-wise manner. To name a few different points, our guidelines propose an extract from inflamed cutaneous tissue of rabbits inoculated with vaccinia virus, which has been found to be effective for post-herpetic neuralgia in Japan, as one of the second-line drugs. When prescribing opioid analgesics, proposed as the third-line drugs, for neuropathic pain, the guidelines recommend physicians continue evaluations on either abuse or addiction. The guidelines do not recommend concomitant use of nonsteroidal anti-inflammatory drugs and acetaminophen because of lack of clinical evidence of their efficacy. If patients do not respond well to pharmacotherapy, which is prescribed in a step-wise manner, other treatment strategies should be considered to improve patients’ activities of daily living and QOL.