Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vitamin D metabolism has an important role in the pathogenesis of osteoporosis. Vitamin D deficiency is very common in elderly people in central Europe. This leads to secondary hyperparathyroidism and to increased bone resorption, resulting in osteoporosis. Combined with the elevated risk of falling that results from vitamin D deficiency, this increases the frequency of bone fractures. Severe vitamin D deficiency also causes impaired bone mineralization (osteomalacia). Controlled intervention trials with native vitamin D (and calcium) yielded no consistent results in terms of the prevention of extravertebral fractures. It appears likely that treatment with plain vitamin D is effective only in populations with vitamin D deficiency. Treatment with active vitamin D (1-alpha-hydroxylated metabolites such as alfacalcidol) has to be considered a pharmacological intervention that exerts pleiotropic effects on the gut (calcium absorption), bone (stimulation of formation), muscle (decreasing of the risk of falling), and immune system. Target groups are patients with disturbed vitamin D metabolism (renal insufficiency, glucocorticoid therapy, inflammatory disease such as rheumatoid arthritis). Alfacalcidol can prevent glucocorticoid-induced bone loss (high-grade evidence). In comparative studies alfacalcidol was superior to plain vitamin D.
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PMID:[Relative value of plain vitamin D and of biologically active vitamin D in the prevention and treatment of osteoporosis]. 1694 81

Complementary and alternative medicines (CAM) are widely used by those with pain and/or musculoskeletal problems, and previous research has shown that high proportions of individuals with rheumatoid arthritis have used these therapies. One of the largest CAM modalities is that of naturopathy, which combines nutritional, herbal, and other complementary practices to treat such conditions. In this review, evidence is examined in relation to those factors which naturopaths believe are significant contributors to rheumatoid arthritis, and are hence the main focus of therapeutic management. These factors include food allergy, increased gut permeability, increased circulating immune complexes, excessive inflammatory processes, and increased oxidative stress. Naturopathic treatment attempts to alleviate symptoms by altering these factors through dietary modification, manipulation of dietary fats, and use of antioxidants and proteolytic enzymes. An understanding of the rationale for these treatments and evaluation of the evidence from their use in clinical settings will assist with the integration of complementary and conventional practices in the treatment of rheumatoid arthritis.
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PMID:Naturopathic management of rheumatoid arthritis. 1702 41

The nervous system in the intestine controls motility, secretion, sensory perception, and immune function. Peptidergic neurones with neurotransmitters such as substance P and nerve growth factors have been the main focus of neuroimmunomodulation research in the gut. This review summarises the present knowledge concerning the role of the sympathetic nervous system (SNS) in modulating intestinal inflammation. The role of the SNS for gut inflammation is compared with its role in rheumatoid arthritis which demonstrates notable similarities. Nerve fibres of the SNS not only enter the enteric plexuses but also innervate the mucosa and gut associated lymphoid tissue (GALT). The SNS has pro- and anti-inflammatory functions. Neurotransmitters such as norepinephrine, adenosine, and others can evoke remarkably different opposing effects depending on concentration (presence of sympathetic nerve fibres and extent of neurotransmitter release), receptor affinity at different receptor subtypes, expression of adrenoceptors, availability of cotransmitters, and timing of SNS activity in relation to the inflammatory course. This review attempts to integrate the different perspectives of the pro- and anti-inflammatory effects of the SNS on inflammatory disease of the gut.
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PMID:The role of the sympathetic nervous system in intestinal inflammation. 1704 10

The aim of this study was to review the process of microbial colonization and the environmental and host factors that influence colonization and microbial succession. The impact of some diseases on intestinal microbiota composition is also described. Microbial colonization of the gut by maternal vaginal and fecal bacteria begins during and after birth. During the first 2 years of life, specific microbes become established in a process designated microbial succession. Microbial succession in the gastrointestinal tract is influenced by numerous external and internal host-related factors, and by the second year of life, the intestinal microbiota composition is considered identical to that of adults. Nevertheless, intestinal microbiota in both infants and adults remain incompletely characterized and their diversity poorly defined. The main explanation is that many intestinal bacteria that live in an anaerobic environment are difficult or impossible to culture outside the intestine. However, recent advances in molecular biology techniques have initiated the description of new bacteria species. The composition of gut microbiota can be modulated by host, environmental, and bacterial factors, and strong evidence has emerged of substantial modifications during illness or exposure to threatening experiences. It has been postulated that improvements in hygienic measures have led to an increase in allergic diseases ("hygiene hypothesis"). Alterations in gut microbiota and their functions have been widely associated with many chronic and degenerative diseases, including inflammatory bowel disease, colon cancer, and rheumatoid arthritis.
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PMID:Colonization and impact of disease and other factors on intestinal microbiota. 1742 Sep 34

Psoriatic arthritis is an inflammatory joint disease that is heterogeneous in presentation and clinical course. Evidence that this disease is distinct from rheumatoid arthritis and other spondyloarthropathies is based on data derived from characteristic clinical features, histopathologic analyses, immunogenetic associations and musculoskeletal imaging. Emphasis has centered previously on a dominant role for the T lymphocyte in the inflammatory process; however, studies provide support for a major contribution from monocyte-macrophages in the initiation and perpetuation of joint and skin inflammation. The occurrence of arthritis in the absence of psoriasis in a minority of patients with psoriatic arthritis, coupled with divergent genetic risk factors, indicates that psoriatic arthritis is distinct from psoriatic skin inflammation. A new terminology, psoriatic disease, has emerged that encompasses the various manifestations of tissue and organ involvement observed in many psoriasis patients, including inflammation in the joint, eye and gut. Moreover, adverse cardiovascular and metabolic outcomes in patients with psoriasis or psoriatic arthritis might be directly linked to the cutaneous and musculoskeletal manifestations of these diseases via subsets of circulating monocytes and tissue macrophages activated by inflammatory cytokine networks that arise in the skin and possibly the joint.
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PMID:Psoriatic disease--from skin to bone. 1803 29

Amyloidosis remains one of the three major types of multisystemic amyloidosis, with immunoglobulinic (AL) and hereditary varieties. Recently, however, its incidence has been decreasing in Western countries. Inflammatory disorders are currently the major causes of amyloid-associated (AA) amyloidosis; first of all it is rheumatoid arthritis, then ankylosing spondylarthropathy and auto-inflammatory syndromes. Some tumours may lead to amyloidosis, including Castleman's disease. Complete surgery can result in regression of amyloid. It is not exactly known why some patients develop a progressive amyloidosis, whereas others do not. A permanent acute phase response, ideally evaluated with serial measurement of serum protein SAA, the precursor of the AA protein deposited in tissues, seems to be a prerequisite to the development of inflammatory (AA) amyloidosis. Genetic factors have however been recently emphasized. Nephropathy is the main clinical manifestation of amyloidosis. Serial search for proteinuria and serum creatinine measurement remain quite useful for detecting the first sign of renal impairment during chronic inflammatory disorders. A thorough diagnosis of AA amyloidosis deserves to gather whole clinical and pathological data, including immunohistochemistry. Some pitfalls exist and another type of amyloidosis should not be misdiagnosed as the AA variety. Ultimate renal failure and gut involvement with denutrition account for the persistent poor prognosis of AA amyloidosis. Current treatment aim at decreasing the inflammatory response; drugs targeting other steps of amyloid deposition are currently developed.
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PMID:[Amyloidosis AA]. 1851 52

Acute rehabilitation refers to the multidisciplinary rehabilitative treatment of patients in continuing need of integrated acute and rehabilitative longterm care. As a result of the advances in acute rheumatology and improved emergency services, an increasing number of patients survive episodes of severe disease and complications of immunosuppressive therapy. These patients require not only treatment of their acute medical problems but also specialized multidisciplinary acute rehabilitation starting as early as possible during their hospital stay. We describe 4 typical cases from the major fields of rheumatology. (1) Acute rehabilitation of a 63-year-old woman with rheumatoid arthritis after replacement of both preexisting knee endoprostheses in one session and removal of the left hip endoprosthesis due to infection and sepsis. (2) Rehabilitation of a 29-year-old man with a 7-year history of ankylosing spondylitis who lived in an adjustable easy chair for 2 years due to severe pain prior to admission. (3) A 61-year-old woman with active refractory Wegener's granulomatosis who developed respiratory insufficiency due to aspergillus and pseudomonas pneumonia. (4) The acute rehabilitation of a 21-year-old woman with systemic lupus erythematosus and a history of 14 laparotomies due to severe acute pancreatitis and multiple gut perforations. Acute rehabilitation was complicated by a large defect of the abdominal wall and significant critical illness polyneuropathy. Our report points out differences between acute, postacute, and longterm rehabilitation, describes the mobilization of patients in acute rheumatology units, and defines specific problems encountered in acute hospital-based rehabilitation of rheumatological patients.
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PMID:Severe disease activity and complications of immunosuppressive therapy: a challenge for acute hospital-based rehabilitation in rheumatology. 1953 61

Abstract The gastrointestinal tract and the microbes colonizing it form a complex ecosystem that has various effects on the well-being of the host. In addition to acute infections, the composition of the gastrointestinal microbiota has been suspected to influence the etiopathogenesis of many chronic diseases, such as rheumatoid arthritis and inflammatory bowel diseases. It has been suggested that the bacterial colonization of the gastrointestinal tract is genetically determined. Using gas-liquid chromatography of bacterial cellular fatty acids we show in this study that modulation of the microbiota by a course of antibiotics is followed by regeneration of the murine intestinal flora depending on the genotype of the host. The mice used in our study were acclimatized to identical living conditions before treatment with ciprofloxacin and clindamycin for 1 week via drinking water. Within a few days of finishing the antibiotic course, the cellular fatty acid profiles of fecal samples resembled those of the pre-course community, showing a considerable indigenous recovery potential. Colonization of the gastrointestinal tract appeared to be genetically regulated since differences in communities between the mouse strains were observed. Our results are in harmony with earlier observations, indicating that the gut community is not established by chance and that it is influenced by host-derived factors.
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PMID:Bacterial composition of murine fecal microflora is indigenous and genetically guided. 1971 58

Interleukin-17A (IL-17A) and IL-17F are 2 of several cytokines produced by T helper 17 cells (Th17), which are able to indirectly induce the recruitment of neutrophils. Recently, human Th17 cells have been phenotypically characterized and shown to express discrete chemokine receptors, including CCR2 and CCR6. Herein, we show that highly purified neutrophils cultured with interferon-gamma plus lipopolysaccharide produce the CCL2 and CCL20 chemokines, the known ligands of CCR2 and CCR6, respectively. Accordingly, supernatants from activated neutrophils induced chemotaxis of Th17 cells, which was greatly suppressed by anti-CCL20 and anti-CCL2 antibodies. We also discovered that activated Th17 cells could directly chemoattract neutrophils via the release of biologically active CXCL8. Consistent with this reciprocal recruitment, neutrophils and Th17 cells were found in gut tissue from Crohn disease and synovial fluid from rheumatoid arthritis patients. Finally, we report that, although human Th17 cells can directly interact with freshly isolated or preactivated neutrophils via granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-alpha, and interferon-gamma release, these latter cells cannot be activated by IL-17A and IL-17F, because of their lack of IL-17RC expression. Collectively, our results reveal a novel chemokine-dependent reciprocal cross-talk between neutrophils and Th17 cells, which may represent a useful target for the treatment of chronic inflammatory diseases.
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PMID:Evidence for a cross-talk between human neutrophils and Th17 cells. 1989 92

A staggering 4000 million people cannot digest lactose, the sugar in milk, properly. All mammals, apart from white Northern Europeans and few tribes in Africa and Asia, lose most of their lactase, the enzyme that cleaves lactose into galactose and glucose, after weaning. Lactose intolerance causes gut and a range of systemic symptoms, though the threshold to lactose varies considerably between ethnic groups and individuals within a group. The molecular basis of inherited hypolactasia has yet to be identified, though two polymorphisms in the introns of a helicase upstream from the lactase gene correlate closely with hypolactasia, and thus lactose intolerance. The symptoms of lactose intolerance are caused by gases and toxins produced by anaerobic bacteria in the large intestine. Bacterial toxins may play a key role in several other diseases, such as diabetes, rheumatoid arthritis, multiple sclerosis and some cancers. The problem of lactose intolerance has been exacerbated because of the addition of products containing lactose to various foods and drinks without being on the label. Lactose intolerance fits exactly the illness that Charles Darwin suffered from for over 40 years, and yet was never diagnosed. Darwin missed something else--the key to our own evolution--the Rubicon some 300 million years ago that produced lactose and lactase in sufficient amounts to be susceptible to natural selection.
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PMID:The molecular basis of lactose intolerance. 1996 Aug 66


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