Discrepancies of MRI findings between recumbent and upright positions in atlantoaxial lesion. Report of two cases

Two cases of atlantoaxial (A-A) instability that showed different MRI findings between supine and upright positions are presented. The upright MRI represented the findings corresponding to their symptoms. In A-A lesions, conventional MR images taken in the supine position do not always explain the pathophysiological consequences. The MR images taken in the upright position disclose the actual spinal pathophysiology with gravitational effects.

     

Atlantoaxial transarticular screw fixation and posterior fusion using ultra-high-molecular-weight polyethylene cable

This article attempts to evaluate the effectiveness of the ultra-high-molecular-weight polyethylene (UHMW-PE) cable system in atlantoaxial transarticular screw fixation and posterior fusion through the clinical results of 10 postoperative patients with atlantoaxial subluxation secondary to rheumatoid arthritis. Among them, one patient with only one screw placed owing to an anomalous vertebral artery had the correction loss of the 3-mm atlas-dens interval after surgery. Another patient had a second operation to remove the screw and cable after 2 years 11 months because a unilateral transarticular screw had come to protrude through the lateral mass of the atlas ventrally. All patients had achieved C1-C2 osseous fusion without any complications associated with this cable system. The UHMW-PE cable is a very useful material as sublaminar wiring in atlantoaxial transarticular screw fixation and posterior fusion.     

Analysis of ischemia-reperfusion injury in a microcirculatory model of pressure ulcers

The aim of this study was to establish a pressure ulcer model that visualizes the microcirculation, and to examine the participation of ischemia-reperfusion injury in the pathophysiology of pressure ulcers. An original system composed of a new skin fold chamber and compression device allowed loading quantitative vertical stress to the skin. An intravital microscopic technique enabled direct visualization of the microcirculation in the physiological condition and in response to pressure application. To estimate the effect of ischemia-reperfusion injury, animals were divided into two groups: the compression-release group (n = 8), in which the animals received four cycles of compression-release which consisted of 2 hours of compression followed by 1 hour of pressure release; and the compression alone group (n = 8) in which the animals underwent continuous compression for 8 hours. Functional capillary density was quantified before the compression procedure and on day 1 (35 hours) after the first evaluation. The cyclic compression-release procedure significantly decreased functional capillary density as compared to continuous compression, indicating that in our experimental setting repetition of ischemia-reperfusion cycle more severely damaged the microcirculation than single prolonged ischemic insult. This finding supports the significant contribution of ischemia-reperfusion injury to the pathophysiology of pressure ulcers at the level of dynamic in vivo microcirculation.     

Pathogenic implication of epidermal scratch injury in psoriasis and atopic dermatitis

Mechanical scratching, a common external stress affecting the skin, is induced by various causes, such as pruritus. Scratch injury to epidermal keratinocytes upregulates the production and release of chemokine (C-C motif) ligand 20 (CCL20) in vitro, which selectively chemoattracts interleukin (IL)-17A-producing immune cells that express chemokine (C-C motif) receptor 6 (CCR6). In IL-17A-dominant psoriasis, scratch-induced CCL20 upregulation and subsequent accumulation of IL-17A-producing immune cells and CCR6⁺ mature dendritic cells may trigger the development of psoriatic lesions, a process known as the Koebner phenomenon. In IL-4/IL-13-dominant atopic dermatitis, pruritus and subsequent scratching are the primary symptoms. Scratch-induced CCL20 production from keratinocytes may explain why IL-17A levels are also elevated in atopic dermatitis. In contrast, mechanical scratching is likely to negatively regulate IL-13 signaling by upregulating the expression of IL-13 receptor α2, which serves as a decoy receptor for IL-13 in keratinocytes. In this review, we summarize current reports on topics related to the pathogenic role of epidermal scratch injury in psoriasis and atopic dermatitis.     

Plasma trough levels of adalimumab and infliximab in terms of clinical efficacy during the treatment of psoriasis

We examined the relation between adalimumab and infliximab plasma trough levels, anti‐adalimumab and anti‐infliximab antibody formation. We analyzed plasma from 32 adalimumab‐treated and 20 infliximab‐treated psoriasis patients for evaluating trough levels of each drug. The presence of anti‐adalimumab and anti‐infliximab antibodies was analyzed and the severity of psoriasis was evaluated. At week 28, 25 out of 32 and at week 48, 21 out of 30 adalimumab‐treated patients maintained as more than PASI 75. At week 28, 12 out of 20 and at week 48, nine out of 18 infliximab‐treated patients were evaluated as more than PASI 75. In patients treated with 40 mg adalimumab every other week, the mean trough level was 7.62 μg/mL (range, 0.05–10.6) at week 48. In patients treated with 80 mg adalimumab every other week, the mean trough level was 8.61 μg/mL (range, 0.08–13.5) at week 48. Mean trough level of infliximab‐treated cases (4.1–5.2 mg/kg; mean, 4.6) was 4.64 μg/mL (range, 0.03–16.9) at week 48. Anti‐adalimumab antibody was detected in five out of 32 cases and anti‐infliximab antibody was detected in six out of 20 cases, respectively, at weeks 24 and 48. The optimal cut‐off values of adalimumab and infliximab concentration for more than PASI 75 were more than 7.84 μg/mL and more than 0.92 μg/mL, respectively. The trough levels of adalimumab and infliximab in psoriasis patients were positively associated with clinical response and were significantly lower in cases having anti‐adalimumab or anti‐infliximab antibodies.     

Patulous eustachian tube following otitis media

Loss of weight, dehydration, pregnancy, fatigue, and otitis media are among the factors proposed as causes of a patulous eustachian tube, but true details remain obscure. We studied patients who developed a patulous eustachian tube following otitis media and discuss the relationship between these 2 conditions. Subjects were 12 patients diagnosed with otitis media at our department who later developed a patulous eustachian tube. The initial middle ear disease progressed from acute otitis media to otitis media with effusion in 2, acute otitis media in or acute mastoiditis in 1 each, and otitis media with effusion in the remaining 8 patients. Seven patients evidenced a low body mass index (BMI), weight loss, and underlying disease, but 5 with a patulous eustachian tube following otitis media did not. We retrospectively analyzed 119 patients diagnosed with a patulous eustachian tube in our department for whether they had been diagnosed by an ENT physician as having otitis media, i.e., acute otitis media or otitis media with effusion. Some 42 (35.3%) had a history of otitis media. At acute otitis media or otitis media with effusion, the tympanic cavity becomes inflamed, accompanied by inflammation of the eustachian tube mucosa and a stenotic tendency. Healing from otitis media is accompanied by decreased eustachian tube mucosa inflammation. We surmise that, depending on how inflammation disappears, fibrosis of the eustachian tube mucosa occurs, leading to a pathologically patulous eustachian tube. Many aspects of the causation of this condition remain unclear, but we surmised that in patients with earlier otitis media, a pathological patulous eustachian tube develops during resolution of inflammation. Our findings indicate the involvement of otitis media as a causative factors in a patulous eustacian tube.     

CELL PROLIFERATION AND CYTOKINE INDUCTION BY TNF-�� OF PSORIATIC KERATINOCYTES ARE NOT DIFFERENT FROM NORMAL KERATINOCYTES IN VITRO

Background:

Recent studies indicate that various cytokines including tumor necrosis factor-α (TNF-α) play an essential role in the induction and maintenance of psoriatic lesion.

Aims:

To compare the cell proliferation of keratinocytes by various cytokines and TNF-α-induced cytokine secretion among normal keratinocytes, uninvolved, and involved keratinocytes.

Methods:

The keratinocytes from normal skin, uninvolved, and involved psoriasis were cultured in the presence of IL-6, IL-8, epidermal growth factor (EGF), hepatocyte growth factor (HGF), transforming growth factor-α (TGF-α) epiregulin, amphiregulin, and TNF-α and then MTT assay for keratinocytes proliferation was performed. Furthermore, TNF-α-induced secretion of IL-6, IL-8, EGF, HGF, TGF-α, epiregulin, and amphiregulin were compared among these keratinocytes.

Results:

IL-6, IL-8, EFG, TGF-α, epiregulin, and amphiregulin, but not TNF-α increased keratinocyte proliferation of normal, psoriatic uninvolved, and involved skin. The increased cell proliferation by these cytokines and growth factors were not different among the keratinocytes derived from normal skin, uninvolved, and involved psoriasis. The significant induction of TNF-α increased IL-6, IL-8, EGF, HGF, TGF-α, epiregulin, and amphiregulin, but the increase in these cytokines and growth factors were not different among normal skin, uninvolved, and involved psoriasis.

Conclusion:

Cell proliferation by various cytokines and growth factors and TNF-α-induced cytokine secretion are not different between normal and psoriatic keratinocytes.     

Effect of epidural analgesia on postoperative insulin resistance as evaluated by insulin clamp technique

The influence of epidural neural blockade on postoperative insulin resistance was studied using the euglycaemic insulin clamp technique. Eighteen patients undergoing elective upper abdominal surgery of moderate severity were allocated to two groups: group G patients underwent operation under general anaesthesia, and postoperative pain was relieved by systemic administration of analgesia; and group E patients received epidural analgesia during surgery and epidural morphine postoperatively. In each patient the euglycaemic insulin clamp test was performed twice: several days before surgery and on postoperative day 1. Peroperative catecholamine and cortisol responses were also measured to investigate possible endocrine mechanisms of the insulin resistance. Glucose disposal (M) decreased in both groups on postoperative day 1 at plasma insulin concentrations ranging from 1.2 to 10.0 milliunits ml-1, resulting in the downward shift of dose-response curves. However, this downward shift was significantly smaller in group E than in group G patients. Urinary adrenaline excretion increased markedly on the day of operation in group G, but was significantly inhibited in group E. Urinary noradrenaline excretion increased mainly on postoperative day 1 in group G, but was significantly inhibited in group E. Plasma cortisol response was lower in group E than in group G during and shortly after operation, and was significantly inhibited in group E on postoperative day 1. These results indicate that insulin resistance after elective abdominal surgery is due to a postreceptor deficit in glucose utilization, as indicated by the downward shift of the dose-response curves. This disturbance in glucose metabolism was reduced by epidural analgesia, the results being associated with inhibited catecholamine and cortisol responses.