ObjectiveTo explore the pathogenesis of cervical spondylosis combined with cervicogenic vertigo, and to investigate the clinical results of anterior discectomy and fusion in treating the disease. MethodsA retrospective study was performed on 83 patients with cervical spondylosis myelopathy (n=60, 72%) or radiculopathy (n=23, 37.3%) accompanied by sympathetic symptoms such as dizziness between March 2008 and November 2012. The disease involved single segment in 29 cases, double segment in 50 cases, and triple in 4 cases. All the segments involved were treated with anterior discectomy and fusion. Vertigo alleviation was observed before surgery, 3 days after surgery, and during the final follow-up. Neurological status was evaluated by Japanese Orthopedic Association (JOA) score system and sympathetic symptoms were evaluated with vertigo symptom and function scoring system. ResultsThe average follow-up was 21 months (ranging from 12 to 30 months). Significant difference was observed between sympathetic symptom scores and JOA scores before surgery and 3 days after surgery or at the final follow-up (P<0.05), but no significant difference was found between the scores 3 days after surgery and during the final follow-up (P>0.05). ConclusionThe surgical effect for cervicogenic vertigo is often accompanied by the relief of spinal cord and nerve roots symptoms. Surgery is effective for cervical spondylosis combined with cervicogenic vertigo.
ObjectiveTo systematically review the clinical features of chronic fatigue syndrome (CFS) cases with pathogens infection. MethodsWe electronically searched databases including VIP, WanFang Data, CNKI, CBM, PubMed, MEDLINE, EMbase, The Cochrane Library, Web of Science, Elsevier and Google Scholar from 1994 to 2014 for CFS-related studies. Two reviewers independently screened literature and extracted data. Then we systematically reviewed and analyzed the information on demographic characteristics, clinical manifestations, types of infected pathogens, and results of some biochemical examinations. ResultsA total of 84 studies (case reports and case series) involving 2 565 CFS cases from 18 countries were included. The major infected pathogens of included CFS cases were mycoplasma, EB virus, intestinal virus, Bernat rickettsia, human-herpes virus, and Gram-negative intestinal bacteria. Fifty-seven studies reported that there might be associations between the pathogenic infection and CFS pathogenesis. Although there were different types of CFS-related pathogens, almost all the studies inferred that pathogens infection linked with immune dysfunction, which might cause CFS symptoms. ConclusionThere may be associations between the pathogenic infection and CFS pathogenesis.
ObjectiveTo summarize basic research progress and current status of clinical diagnosis and therapy for gastroesophageal reflux disease. MethodRelated literatures were collected to review the pathogenesis, clinical manifestations, diagnosis and therapy of gastroesophageal reflux disease. ResultsGastroesophageal reflux disease was caused by many factors, such as hiatus hernia, hypotensive lower esophageal sphincter pressure, acid pocket, prolonged esophageal clearance, and delayed gastric emptying. Extra-esophageal symptoms was a common clinical presentation to gastroesophageal reflux disease. The diagnosis methods for gastroesophageal reflux disease included the symptom observation, gastroscopy examination, 24 h pH monitoring of esophageal, proton pump inhibitor test, questionnaire of gastroesophageal reflux disease and so on. The laparoscopic fundoplication could essentially treat the pathophysiologic abnormalities of gastroesophageal reflux disease, which had an obvious curative effect and wide application prospect. ConclusionPathogenesis, diagnosis, and therapy of gastroesophageal reflux disease are associated with multiple factors, which is still controversial and remains to be further studied.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
Acute carbon monoxide poisoning is a common and frequently occurring disease in winter and spring in China, with high disability and mortality. Delayed encephalopathy is a serious sequela after the pseudo-convalescence. Its mechanism is complex, including environmental and genetic factors, hypoxia and energy metabolism disorder, cytotoxicity and oxygen free radical damage, immune disorder and inflammatory activation, neurotransmitter disorder, brain parenchymal changes, vascular and hemorheological abnormalities, calcium overload, and cell apoptosis. At present, methods for predicting delayed encephalopathy in acute carbon monoxide poisoning include detailed inquiry of medical history, laboratory examination of relevant indicators, electrophysiological examination, brain imaging examination, and evaluation scale prediction. This review summarizes the research status of the pathogenesis and early prediction methods of delayed encephalopathy in acute carbon monoxide poisoning, with a view to providing reference for future research directions.
Hydroxychloroquine retinopathy is an ocular lesions that develops following long-term or excessive use of hydroxychloroquine. The early clinical presentation of this lesion is nonspecific and is often detected when severe central vision impairment occurs in late stage. It currently mainly includes hydroxychloroquine binding to melanin, inducing degeneration of the retinal pigment epithelium, increasing the pH of lysosomes in the retinal pigment epithelium and interfering with the visual cycle. In recent years, with the development of retinal imaging technology and the in-depth study of hydroxychloroquine retinopathy, characteristic fundus structural changes such as retinal and choroidal thickness and blood vessels may occur in the early stage. This not only provides an important basis for the early diagnosis of hydroxychloroquine retinopathy, but also provides important clues for investigating its pathogenesis. Clinicians' proficiency in relevant fundus changes and pathogenesis will facilitate early diagnosis and treatment, while also minimizing irreversible central vision impairment in patients.
With the tremendous progress in fundus imaging and histopathology over the past decade, the understanding of age-related macular degeneration (AMD) has taken a qualitative leap. AMD is defined as a progressive neurodegenerative disease of photoreceptors and retinal pigment epithelium (RPE) characterized by extracellular deposits under RPE and the retina, including drusen, basal laminar and linear deposits, and subretinal drusenoid deposits, that can evolve to atrophy of the retina, RPE and choroid and neovascularization in the choroid and/or retina. It is the leading cause of blindness and visual impairment in older populations, despite recent advances in treatments. AMD is a multifactorial disease with genetic and environmental factors including advanced age, smoking, high-fat diet, and cardiovascular disorder to enhance the disease susceptibility. The physiopathologic mechanism includes inflammatory processes (complement pathway dysregulation, inflammasome activation), intrinsic (e.g., photo-oxidation) and extrinsic oxidative insult to the retina, age-related metabolic impairment (mitochondrial, autophagic and endoplasmic reticulum stress). Autophagy dysfunction and local inflammation in aged RPE specially result in the extracellular deposits, cell death and AMD. Further investigation of the pathogenesis of AMD will provide with new therapeutic targets and strategy for prevention and treatment of the disease in the early stages.
Objective To review the research progress of heterotopic ossification (HO) pathogenesis.Methods Recent articles about HO including the risk factors and pathogenesis were reviewed and comprehensively analyzed. Results The pathogenesis of HO is not completely understood, but the extracellular factors, signaling pathways, and transcription factors in the pathogenesis of HO are understood deeply, such as bone morphogenic protein, Smad signaling, and core binding factor α1/runt-related transcription factor 2, which are probably involved in HO. Furthermore, some related microRNAs are also probably involved in HO. Conclusion The pathogenesis of HO should be further investigated so as to lay a foundation for preventing and treating HO.
Objective To summarize the recent pathogenetic researches on the acute pancreatitis. Methods Relevant references about the pathogenesis of acute pancreatitis, which were published recently domestic and abroad were collected and reviewed. Results Recent experimental data indicated that the synthesis and release of pro-inflammatory cytokines and chemotactic factors were responsible for local injury and systemic dissemination of the inflammatory mediators. Experimental studies also provided evidences implying that the immune system might play a role in the development of pancreatitis, such as the activation of lymphocyte and neutrophil. Additionally, the pancreas may completely recover or become fibrotic after an attack of acute pancreatitis and the presence of pancreatic stellate cell was known as a crucial factor in the fibrogenesis. Conclusion The pathogenesis of acute pancreatitis is very complicated, the factors that determine the ultimate severity of the attack are still unknown.
Pachychoroidopathy is a type of retinal choroidal disease with similar clinical features, which is characterized by attenuation of the choriocapillaris overlying dilated choroidal veins, and associated with progressive retinal pigment epithelium dysfunction and neovascularization. At present, pachychoroidopathy includes pachychoroid pigment epitheliopathy, central serous chorioretinopathy pachychoroid neovasculopathy, polypoidal choroidal vasculopathy, focal choroidal excavationm, and peripapillary pachychoroid syndrom. These diseases not only have common imaging features, but also individual imaging features. This not only provides us with important clues about the pathogenesis of pachychoroidopathy, but also provides guidance for their treatment decisions. Although the exact pathogenesis of pachychoroidopathy is still unclear, and the treatment method is still controversial; but it is believed that with the development of imaging technology and the development of high-quality clinical and basic research, patients with pachychoroidopathy can be provided with more reasonable treatment in the future.