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ID PMID Title PublicationDate abstract
18250973 Modulating the immune response by oral zinc supplementation: a single approach for multipl 2008 Jan Zinc is required for multiple cellular tasks, and especially the immune system depends on a sufficient availability of this essential trace element. During the last decades, many studies attempted to affect the outcome of various diseases by zinc supplementation. These efforts either aimed at supporting immunity by zinc administration or at correcting a loss of zinc secondary to the disease to restore the zinc-dependent functions of the immune system. This review aims to summarize the respective findings and to discuss possible molecular mechanisms by which zinc could influence viral, bacterial, and parasitic infections, autoimmune diseases, and the response to vaccination. Zinc supplementation in diseases such as diarrhea, chronic hepatitis C, shigellosis, leprosy, tuberculosis, pneumonia, acute lower respiratory infection, and leishmaniasis seems beneficial. In contrast, the results for the common cold and malaria are still not conclusive, and zinc was ineffective in most vaccination and rheumatoid arthritis studies. For AIDS and type 1 diabetes, zinc supplementation may even be a risk factor for increased mortality or deterioration of the glucose metabolism, respectively. In these cases, zinc supplementation should be used with care and limited to clearly zinc-deficient individuals.
18211497 Pyoderma gangrenosum--rebel without a cure? 2008 Feb BACKGROUND: Pyoderma gangrenosum (PG) is a rare neutrophilic, ulcerating dermatosis that is frequently difficult to diagnose and often a diagnosis of exclusion. It is hypothesized that PG may be caused by an abnormal T-cell and neutrophil response, which correlates with its common link to other disorders, such as inflammatory bowel disease, rheumatoid arthritis, and malignancies. Several treatments have been used successfully for PG, but none has proven to be universally effective. METHODS: We present three cases of PG treated with adalimumab after failed courses of steroids (orally and parenterally), thalidomide, cyclosporine, and mycophenolate mofetil. RESULTS: Patients 2 and 3, who had previously responded to infliximab, albeit with recurrence, were successfully treated with adalimumab at a dose of 40 mg once a week. Patient 1 initially responded to adalimumab, but after 7.5 months failed to show wound bed improvement at a dose of 80 mg/week subcutaneously. This patient had not previously been treated with infliximab. CONCLUSION: We believe adalimumab to be a valuable alternative for the treatment of PG, with comparable efficacy to infliximab.
18177271 Chemokines and cancer: migration, intracellular signalling and intercellular communication 2008 Feb 1 Inappropriate chemokine/receptor expression or regulation is linked to many diseases, especially those characterized by an excessive cellular infiltrate, such as rheumatoid arthritis and other inflammatory disorders. There is now overwhelming evidence that chemokines are also involved in the progression of cancer, where they function in several capacities. First, specific chemokine-receptor pairs are involved in tumour metastasis. This is not surprising, in view of their role as chemoattractants in cell migration. Secondly, chemokines help to shape the tumour microenvironment, often in favour of tumour growth and metastasis, by recruitment of leucocytes and activation of pro-inflammatory mediators. Emerging evidence suggests that chemokine receptor signalling also contributes to survival and proliferation, which may be particularly important for metastasized cells to adapt to foreign environments. However, there is considerable diversity and complexity in the chemokine network, both at the chemokine/receptor level and in the downstream signalling pathways they couple into, which may be key to a better understanding of how and why particular chemokines contribute to cancer growth and metastasis. Further investigation into these areas may identify targets that, if inhibited, could render cancer cells more susceptible to chemotherapy.
18175051 New advances in renal amyloidosis. 2008 Apr Renal amyloidosis is a rare and intractable disease that accounts for 0.2% of the original kidney diseases of dialysis patients in Japan. However, the number of patients with renal amyloidosis seems to be increasing in recent years. There have been some new concepts focusing on the mechanism of amyloidogenesis, such as molecular chaperones, seeding mechanism, and genetic polymorphisms of precursor protein. Clinical and histological features of renal amyloidosis vary according to the type. Significantly higher levels of urinary protein excretion are seen in the AL type, whereas microscopic haematuria is more prominent in the AA type. Histologically, amyloid deposition of AL type has stronger predilection for GBM than mesangium, and spicule formation is more frequently observed. In contrast, AA type has a higher affinity to TBM and interstitial area. For the histological diagnosis of renal amyloidosis, plural staining methods including Congo-red, Daylon and thioflavin-T stains are available. Combinations of these staining methods are necessary for establishing the precise diagnosis. The more recent and intensive treatments for renal amyloidosis are expected to improve patient outcome. For AL amyloidosis, high-dose melphalan plus high-dose dexamethasone or VAD, in conjunction with bone marrow stem cells transplantation, have shown a definitive effect on reducing urinary protein excretion. The biological agent, tumor necrosis factor (TNF alpha) blocker, improves the renal function in AA-type renal amyloidosis, as well as suppresses the inflammatory reactions in patients with rheumatoid arthritis. Clinical advances have been made in various aspects of renal amyloidosis.
17949557 Antikinectin autoantibody in Behçet's disease and several other autoimmune connective tis 2007 Jul OBJECTIVE: Antikinectin autoantibody has recently been identified as a potential biomarker in Behçet's disease (BD). Here, we established an enzyme-linked immunosorbent assay (ELISA) and an indirect immunofluorescent assay (IFA) for detecting this antibody. The clinical significance of antikinectin was investigated. METHODS: Partial or full-length cloning for human kinectin in prokaryotic or eukaryotic system was carried out. Three fragments covered kinectin coding sequence were used to establish ELISA. Full-length kinectin overexpressed HepG2 cells were used as a substrate for IFA. Serum samples from BD (n = 46), systemic lupus erythematosus SLE, n = 16), rheumatoid arthritis (RA, n = 160, ankylosing spondylitis (AS, n = 14), primary Sjörgen syndrome (pSS, n = 12), mixed connective tissue disease (MCTD, n = 8), and healthy donors (n = 51) were examined. RESULTS: Good measurement consistency between IFA and ELISA (p < 0.001) and previous immunoprecipitation assay (p = 0.011) was found. Antikinectin was found not only in 32.6% (IFA) to 41.3% (ELISA) BD patients but was also identified in pSS, SLE, MCTD, and RA with prevalence ranging from 12.5% to 25%. Nevertheless, the titer of antikinectin (ELISA) is statistically higher in BD compared to other autoimmune connective tissue diseases (p = 0.0286). Antikinectin was found exclusively among complete form of BD (p < 0.001), but there was no correlation with specific clinical manifestations. CONCLUSIONS: We confirmed the previous observation that antikinectin is related to BD, especially in the complete form of disease. The specificity and predictive values are moderate.
17911470 Safety of cyclosporin A in HCV-infected patients: experience with cyclosporin A in patient 2007 Sep Because of the relatively high prevalence of both hepatitis C virus (HCV) infection and autoimmune disorders (ADs), it is not rare to encounter in daily clinical practice patients with ADs also carrying HCV. Corticosteroids and/or immunosuppressant drugs are needed to treat ADs, but they place HCV-infected patients at risk of worsening the infection. So, rheumatologists have often refrained from using corticosteroids or immunosuppressants in AD when HCV-RNA is also present. Cyclosporin A (CsA) is an immunosuppressive agent used to treat a wide range of ADs, but there is a large evidences in the literature, both in vitro and in vivo, suggesting that CsA also exerts an inhibitory effect on HCV replication at standard therapeutic dose. Therefore, this evidence has opened new ways to improve the therapy and the prognosis in patients with HCV-related liver diseases, including those with transplants. Recent reports, although limited in number, also suggest the safety of CsA in the treatment of patients with AD and concomitant HCV infection. In this review we also report our personal experience on the combination treatment with CsA and anti-TNF-alpha agents in rheumatoid arthritis.
17870646 Cross-cultural development of a child health care questionnaire on satisfaction, utilizati 2007 Sep OBJECTIVE: The instrument Child Health Care-Satisfaction, Utilization and Needs (CHC-SUN) has been developed cross-culturally to evaluate pediatric health care services for children with special health care needs (CSHCN) from the proxy perspective of parents. METHODS: The children of the participating parents received treatment in pediatric specialty clinics in 7 European countries for asthma, cystic fibrosis, diabetes, epilepsy, cerebral palsy, rheumatoid arthritis, and atopic dermatitis. The instrument was developed through a process including literature review, expert consensus, and item generation through focus groups. The pilot instrument was extensively tested to assess psychometric properties, support item reduction, and evaluate clinical validity. The final field version was tested in a new sample of 795 parents in 7 countries. RESULTS: Pilot testing and item reduction resulted in a practical 40-item instrument with 14 single items related to provision of services (module 1), and 26 items related to 6 scales on satisfaction with care (module 2), and 1 item on general satisfaction with care. Satisfaction with care scales showed very good psychometric properties, both initially and in the field version, with Cronbach's alpha ranging between .80 and .95 in the revised scales. Both modules discriminated well between functional status and diagnosis across countries. CONCLUSIONS: A new instrument is available to measure provision of services and satisfaction with care for children with chronic conditions from the perspective of parents. Cross-cultural analysis reveals that the measure is useful in multinational studies evaluating health services against the background of different health systems.
17868256 PTPN22 gene polymorphism in Behçet's disease. 2007 Nov A functional single nucleotide polymorphism (SNP) of PTPN22 gene encoding the protein tyrosine phosphatase has been reported to be associated with autoimmune disorders such as rheumatoid arthritis, systemic lupus erythematosus and type I diabetes. PTPN22 R620W polymorphism has a wide variation of allelic frequencies among different populations. This polymorphism is investigated in Turkish patients with Behçet's disease (BD), a systemic vasculitis with immune activation. DNA samples from 134 patients with BD and 177 healthy controls are genotyped by polymerase chain reaction (PCR)-restriction fragment length polymorphism method for the SNP (rs2476601, A/G) of PTPN22 gene. Polymorphic region was amplified by PCR and digested with XcmI enzyme. The frequency of heterozygous genotype (AG) was 5.1% (9/177) in control group, whereas polymorphic allele was not present in the whole BD group (P = 0.012, OR 0.65, 95% confidence interval 0.0-1.1). Both the lower prevalence in the general population and the absence in BD show the limited role of PTPN22 polymorphism in the pathogenesis of autoimmunity in Turkey.
17854744 Potential target of infliximab in autoimmune and inflammatory diseases. 2007 Sep Tumour necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine produced by many cell types (blood monocytes, macrophages, mast cells and endothelial cells), that play a key role in the pathogenesis of multiple autoimmune and nonautoimmune disorders. A number of large placebo-controlled trials have shown that infliximab, a chimeric monoclonal antibody against TNF-alpha, is effective and well tolerated in patients with Crohn's disease, rheumatoid arthritis and spondiloarthritides and has become a widely used treatment for these diseases. Preliminary data suggest that several forms of vasculitis appear responsive to TNF antagonists: Behçet's disease, Churg-Strauss vasculitis, polyarteritis nodosa, and giant cell arteritis, among others. Wegener's granulomatosis and sarcoidosis have been shown to improve with infliximab. Polymyositis/dermatomyositis may also be responsive to TNF blockade. TNF likely plays little role in Sjögren's syndrome as evidenced by the lack of efficacy of TNF antagonists. There is a rationale for using TNF blockade even in systemic lupus erythematosus, a prototype of autoantibody-mediated disease, and a pilot study seems to confirm this potential effective approach. A number of other more rare disorders also may be responsive to TNF blockade. We here review the current and prospective roles of infliximab in the treatment of autoimmune diseases and other conditions.
17804533 Chronic inflammatory autoimmune disorders and atherosclerosis. 2007 Jun Rheumatoid arthritis (RA), periodontal disease (PD), and coronary artery disease (CAD) are common chronic inflammatory diseases. RA is associated with accelerated vascular risk resulting in an increased prevalence of CAD with attendant early mortality and excess morbidity. RA and PD have a common pathobiology. Accordingly, the aim of this study was to evaluate the association between RA, PD, and CAD and the influence of systemic inflammatory factors. A total of 100 active RA patients of which 50 had established CAD and 50 had no CAD were assessed for PD. All subjects underwent a clinical, cardiac, dental, laboratory, and radiological evaluation. Blood samples were obtained and the level of high-sensitivity C-reactive protein (hs-CRP), total white blood counts (WBC), erythrocyte sedimentation rate (ESR), fibrinogen and tumor necrosis alpha (TNF-alpha), total cholesterol (TC), and high-density lipoprotein (HDL) were assayed. The findings of this study demonstrated an association between RA, PD, and CAD. The RA patients with CAD had significantly more PD than RA patients without CAD, P < 0.001. The inflammatory markers hs-CRP, ESR, WBC, fibrinogen, and TNF-alpha were raised in all patients but were significantly higher in RA patients with CAD who also had PD, that is, in those with more inflammatory disease burden. HDL levels were lower in RA patients with CAD when compared to RA patients without CAD, P < 0.005. Evidence from this study shows an association between RA, PD, CAD, and systemic levels of the inflammatory mediators. The implication is that inflammation may be the central link between the chronic inflammatory autoimmune disorders and atherosclerosis.
17712153 Advanced glycation and lipoxidation end products--amplifiers of inflammation: the role of 2007 Sep BACKGROUND: High levels of glycated and lipoxidated proteins and peptides in the body are repeatedly associated with chronic diseases. These molecules are strongly associated with activation of a specific receptor called RAGE and a long-lasting exaggerated level of inflammation in the body. METHODS: PubMed reports over 5000 papers plus >13,500 articles about the related HbA(1c), most of them published in the past 5 years. Most of the available abstracts have been read and approximately 800 full papers have been studied. RESULTS: RAGE, a member of the immunoglobulin superfamily of cell surface molecules and receptor for advanced glycation end products, known since 1992, functions as a master switch, induces sustained activation of nuclear factor kappaB (NFkappaB), suppresses a series of endogenous autoregulatory functions, and converts long-lasting proinflammatory signals into sustained cellular dysfunction and disease. Its activation is associated with high levels of dysfunctioning proteins in body fluids and tissues, and is strongly associated with a series of diseases from allergy and Alzheimers to rheumatoid arthritis and urogenital disorders. Heat treatment, irradiation, and ionization of foods increase the content of dysfunctioning molecules. CONCLUSIONS: More than half of the studies are performed in diabetes and chronic renal diseases; there are few studies in other diseases. Most of our knowledge is based on animal studies and in vitro studies. These effects are worth further exploration both experimentally and clinically. An avoidance of foods rich in deranged proteins and peptides, and the consumption of antioxidants, especially polyphenols, seem to counteract such a development.
17695142 Exploring effects of different nonsteroidal antiinflammatory drugs on lipid peroxidation. 2007 May Non-steroidal anti-inflammatory drugs (NSAIDs) are common in alleviating pain, pyrexia and inflammation, in patients with rheumatoid arthritis and osteoarthritis. As these drugs are associated with high incidence of gastrointestinal ulceration, bleeding and kidney damage which may be linked with lipid peroxidation. our study was aimed to examine lipid peroxidation induction capacity of NSAIDs (diclofenac sodium, ibuprofen, flurbiprofen, paracetamol, nimesulide, celecoxib and indomethacin) by determining 4-hydroxy-2-nonenal (4-HNE) concentration as an index of lipid peroxidation and to see the suppressive potential of ascorbic acid on NSAID induced lipid peroxidation. The results suggest that diclofenac sodium, ibuprofen, flurbiprofen, paracetamol, nimesulide and celecoxib exerted mild antioxidant activity. Indomethacin exerted statistically significant increase in 4-HNE content, indicating statistically significant peroxidation activity. Ascorbic acid could significantly reduce indomethacin-induced lipid peroxidation.
17684398 Nutrigenetics. 2007 Nutrients interact with the human genome to modulate molecular pathways that may become disrupted, resulting in an increased risk of developing various chronic diseases. Genetic polymorphisms affect the metabolism of dietary factors, which in turn affects the expression of genes involved in a number of important metabolic processes. Genetic polymorphisms affecting nutrient metabolism may explain some of the inconsistencies among epidemiological studies relating diet to chronic diseases such as cancer, diabetes, rheumatoid arthritis, osteoporosis and cardiovascular disease. Understanding how genetic variations influence nutrient digestion, absorption, transport, biotransformation, uptake and elimination will provide a more accurate measure of exposure to the bioactive food ingredients ingested. Furthermore, genetic polymorphisms in the targets of nutrient action such as receptors, enzymes or transporters could alter molecular pathways that influence the physiological response to dietary interventions. Among the candidate genes with functional variants that affect nutrient metabolism are those that code for xenobiotic-metabolizing enzymes (also called drug-metabolizing enzymes). These enzymes are involved in the phase I and II biotransformation reactions that produce metabolites with either increased or decreased biological activity compared to the parent compound. A number of dietary factors are known to alter the expression of these genes that, in turn, metabolize a vast array of foreign chemicals including dietary factors such as antioxidants, vitamins, phytochemicals, caffeine, sterols, fatty acids and alcohol. Knowledge of the genetic basis for the variability in response to these dietary factors should result in a more accurate measure of exposure of target tissues of interest to these compounds and their metabolites. Examples of how 'slow' and 'fast' metabolizers respond differently to the same dietary exposures will be discussed. Identifying relevant diet-gene interactions will benefit individuals seeking personalized dietary advice as well as improve public health recommendations by providing sound scientific evidence linking diet and health.
17553524 The crystal structure of the human (S100A8/S100A9)2 heterotetramer, calprotectin, illustra 2007 Jul 27 The EF-hand proteins S100A8 and S100A9 are important calcium signalling proteins that are involved in wound healing and provide clinically relevant markers of inflammatory processes, such as rheumatoid arthritis and inflammatory bowel disease. Both can form homodimers via distinct modes of association, probably of lesser stability in the case of S100A9, whereas in the presence of calcium S100A8 and S100A9 associate to calprotectin, the physiologically active heterooligomer. Here we describe the crystal structure of the (S100A8/S100A9)(2) heterotetramer at 1.8 A resolution. Its quaternary structure illustrates how specific heteroassociation is energetically driven by a more extensive burial of solvent accessible surface areas in both proteins, most pronounced for S100A9, thus leading to a dimer of heterodimers. A major contribution to tetramer association is made by the canonical calcium binding loops in the C-terminal halves of the two proteins. The mode of heterodimerisation in calprotectin more closely resembles the subunit association previously observed in the S100A8 homodimer and provides trans stabilisation for S100A9, which manifests itself in a significantly elongated C-terminal alpha-helix in the latter. As a consequence, two different putative zinc binding sites emerge at the S100A8/S100A9 subunit interface. One of these corresponds to a high affinity arrangement of three His residues and one Asp side-chain, which is unique to the heterotetramer. This structural feature explains the well known Zn(2+) binding activity of calprotectin, whose overexpression can cause strong dysregulation of zinc homeostasis with severe clinical symptoms.
17406380 Posterior spinal shortening for paraparesis following vertebral collapse due to osteoporos 2008 Jan STUDY DESIGN: Retrospective case series. OBJECTIVES: To assess the efficacy of posterior spinal shortening for paraparetic patients following vertebral collapse owing to osteoporosis, especially on instrumentation loosening. SETTING: Department of orthopaedic surgery, Jichi Medical University Hospital and Omiya Medical Center in Japan. METHODS: The clinical records and radiographs of 13 patients with paraparesis following vertebral collapse owing to osteoporosis treated with posterior spinal shortening were retrospectively reviewed to evaluate the usefulness of this method. Assessment of the clinical course was done by direct examination in all cases. Ambulatory ability was divided into four categories. RESULTS: Upon final observation, nine cases were able to walk with a cane or crutch, one case remained in gait training, two cases remained unable to stand and one case with urinary incontinence improved in urinary function. In one case, paralysis deteriorated. Vertebral compression fracture of the end vertebrae that were fixed occurred in three cases complicated with rheumatoid arthritis. CONCLUSION: The posterior spinal shortening can be a choice for treating delayed paraparesis following vertebral collapse owing to osteoporosis.
17340192 Vascular endothelial growth factor (VEGF) in autoimmune diseases. 2007 May Vascular endothelial growth factor (VEGF) is a potent stimulating factor for angiogenesis and vascular permeability. There are eight isoforms with different and sometimes overlapping functions. The mechanisms of action are under investigation with emerging insights into overlapping pathways and cross-talk between other receptors such as the neuropilins, which were not previously associated to angiogenesis. VEGF has important physiological actions on embryonic development, healing, and menstrual cycle. It also has a great role in pathological conditions that are associated to autoimmune diseases. There is considerable evidence in various autoimmune diseases such as in systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis of an interrelationship between the VEGF system and theses disorders. Serum levels of VEGF correlate with disease activity in a large number of autoimmune diseases and fall with the use of standard therapy. We raised the possible future therapeutic strategies in autoimmune diseases with the anti-VEGF or anti-VEGFR (receptor). So far, this therapy has been used in cancer and macular ocular degeneration in diabetes. This review outlines the evidence for VEGF participation in various autoimmune diseases and proposes lines for future research in this field.
17237447 Increased levels of NF-ATc2 differentially regulate CD154 and IL-2 genes in T cells from p 2007 Feb 1 T cells from patients with systemic lupus erythematosus (SLE) are characterized by heightened TCR-initiated free intracytoplasmic calcium responses. We demonstrate that activated T cells from SLE patients, but not from rheumatoid arthritis patients, displayed higher levels of the calcineurin-dependent transcription factor NF-ATc2 in the nucleus compared with control T cells. DNA NF-AT-binding activity was also increased, as was the amount of NF-ATc2 bound to the promoters of CD154 (CD40L) and IL-2 genes. Nevertheless, although high NF-ATc2 levels translated into higher CD154 transcription in SLE, IL-2 transcription was decreased. The absence of important transcriptional activators (AP-1, NF-kappaBeta) and the presence of transcriptional repressors (cAMP response element modulator) on the IL-2 promoter explain this dichotomous effect.
17198310 p38 MAPK as a potential therapeutic target for inflammatory osteolysis. 2007 Jan Inflammatory osteolysis is a relatively frequent and incapacitating complication of rheumatoid arthritis and other inflammatory diseases, and is induced by accelerated osteoclast recruitment and activation in bone under the aegis of cytokines produced in the inflammatory environment. The success of antitumor necrosis factor-alpha and interleukin-1 therapy in correcting this condition highlights the central role of these cytokines in this process. Recent years have witnessed a revolution in understanding the molecular mechanism and pathogenesis of this family of diseases. It is now clear that p38 mitogen-activated protein kinase plays an essential role in the production of proinflammatory cytokines and cytokine-induced osteoclastogenesis, thus providing a potential therapeutic target for prevention of pathologic bone loss.
17155856 VEGF/VEGFR signalling as a target for inhibiting angiogenesis. 2007 Jan VEGFs and a respective family of tyrosine kinases receptors (VEGFRs) are key proteins modulating angiogenesis, the formation of new vasculature from an existing vascular network. There has been considerable evidence in vivo, including clinical observations, that abnormal angiogenesis is implicated in a number of disease conditions, which include rheumatoid arthritis, inflammation, cancer, psoriasis, degenerative eye conditions and others. Antiangiogenic therapies based on inhibition of VEGF/VEGFR signalling were reported to be powerful clinical strategies in oncology and ophthalmology. Current efforts have yielded promising clinical data for several antiangiogenic therapeutics. In this review, the authors elucidate key aspects of VEGFR signalling, as well as clinically relevant strategies for the inhibition of VEGF-induced angiogenesis, with an emphasis on small-molecule VEGFR inhibitors.
17146306 Postoperative cervical kyphosis after atlantoaxial fixation and cervical expansive laminop 2006 Dec Cervical kyphotic deformity is one of the well-known complications after atlantoaxial fixation or cervical expansive laminoplasty, but to our knowledge there is no information about postoperative cervical kyphosis after performing these operations simultaneously. The aims of this study were to evaluate the changes in the cervical alignment after simultaneous atlantoaxial fixation and cervical expansive laminoplasty, and to discuss the risk factors of this deformity. Five patients (1 man and 4 women) who underwent the simultaneous procedure were examined. Their mean age at surgery was 68.4+/-3.4 years, and the mean follow-up period was 30.8+/-9.5 months. Their underlying diseases were rheumatoid arthritis, and one of them had athetosis, too. On neutral lateral cervical radiographs, tangents were drawn to the inferior endplates of C2 to C5, respectively, and we measured the angles between C2 and C3, C3 and C4, C4 and C5, and C2 and C5 just after surgery and at the latest follow-up. The mean angles were 2.1, -1.9, 1.8, and 1.2 degrees, respectively, just after surgery; and 2.1, -3.5, -2.6, and -5.8 degrees, respectively, at the latest follow-up. Although the mean angle between C2 and 3 hardly changed postoperatively, the mean angle between C2 and C5 significantly decreased postoperatively. In summary, atlantoaxial fixation and cervical expansive laminoplasty may be an unsuitable combination because cervical kyphosis after the simultaneous procedure developed as a complication during the short-term follow-up.