Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003862 (arthralgia)
 7,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

110 patients with benign gastric ulcer and concomitant joint diseases (rheumatoid arthritis, osteoarthrosis) were treated in a comparative short-term clinical trial to assess the relative efficacy of calcitonin (daily 100 MRC of salmon calcitonin intramuscularly), cimetidine (daily 1000 mg orally) and colloidal bismuth subcitrate (De-Nol-four times a day in doses of 5 ml diluted with 15 ml of water). Groups of patients were comparable according to age, sex, duration of ulcer disease, smoking habits, gastric acid secretion and mean ulcer size. The ulcer healing was controlled endoscopically after 2 and 4 weeks of the treatment. There was no significant difference in the ulcer healing rate between three groups neither after 2 weeks (calcitonin-36.7% of healed ulcers, cimetidine-37.5% and De-Nol-35.0% nor after 4 weeks respectively (76.7%, 72.5% and 77.5%). In the calcitonin group a gradual joint pain relief was observed in 84% of patients who complained arthralgia. The moderate side effects (headache, nausea, flush) were observed only in the patients treated with calcitonin (8 subjects). We suggest that calcitonin may be considered as a valid anti-ulcer drug in the peptic ulcer patients with concomitant rheumatological diseases especially with osteoporosis.
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PMID:Calcitonin versus cimetidine or De-Nol in gastric ulcer treatment. An endoscopically controlled trial. 307 78

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

Postmenopausal osteoporosis is not a well-defined disease, but summarizes women with different severity of changes in bone metabolism and different clinical complaints. The only common feature in women with 'postmenopausal osteoporosis' is the deficiency of estrogen. Postmenopausal women can be subdivided into four groups, according to their risk for fractures: 1. women without evident increase of fracture risk (bone mineral content between 0 and 2 SD of age-related normal range, no known risk factors from history); 2. women with possible increase of fracture risk (bone mineral content between 0 and -2 SD of age-related normal range, with or without known risk factors from history); 3. women with clear increase of fracture risk (bone mineral content below age-related normal range, with or without known risk factors from history); 4. women with already occurred fracture (manifest osteoporosis). Therapeutic intervention in postmenopausal women should be adapted to the risk for fracture. In all four groups a secondary prevention or basic therapy should be performed, focusing on calcium intake, vitamin D supply and sufficient physical activity. Calcium intake should be 1500 mg/day in women without estrogen substitution and 1000 mg in women with estrogen substitution. In patients living mainly inside or with malnutrition, a daily substitution of 500 E. Vitamin D3 is recommended. In group 2, regular control of bone mass is recommended to start additional estrogen replacement therapy, if accelerated loss of bone mass occurs. In group 3, estrogen replacement therapy is recommended urgently and is the therapy of first choice to prevent development of fractures. In group 4 (manifest osteoporosis), therapy should aim on improvement of the patient's symptoms and on increase of bone stability to avoid further fractures. The symptomatic therapy includes pain medications and an intensive physical therapy adapted to the patient's needs. Physical therapy should be performed for long time to reduce complaints and to improve musculoskeletal function in order to prevent falls. Different agents influencing bone metabolism by inhibition of bone resorption (estrogens, calcitonin, bisphosphonates) or stimulation of bone formation (fluoride) are used in manifest osteoporosis to increase bone stability. But the present efficacy to avoid further fractures has not been shown sufficiently for all available agents, so that a final evaluation and recommendation can't be done. Therapy decisions in manifest osteoporosis are often influenced by the possible side effects of the drugs (bleeding, gastrointestinal problems, joint pain), other, not bone-related effects of the drugs (improvement of climacteric complaints, pain relief) and other concomitant diseases and medications.
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PMID:[Therapeutic concepts in the treatment of postmenopausal osteoporosis]. 783 32

Irrespective of the underlying mechanisms, joint pain usually originates in activation of nociceptors, or free nerve endings. Nociceptive signals release a large number of neuromediators, such as substance P and the calcitonin gene-related peptide. Complex neuronal activation occurs, which involves not only local sensitization of joint nociceptors but also modifications in central pain pathways. Additional complexity results from the ability of numerous environmental, psychological, and constitutional factors to influence joint pain.
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PMID:Pathophysiology of joint pain. 889 62

Paget's disease of bone is important in geriatric populations because it is the second most common bone disorder after osteoporosis. In older people, it may be responsible for chronic back pain and joint pain, skeletal deformities, hearing loss, and cranial nerve compression. Paget's disease can reduce both function and mobility in the older people. In addition to newer tests for assessing the activity of Paget's disease, effective therapy is available in the form of salmon calcitonin for nasal administration and new third generation bisphosphonates. Frequently, treatment can reverse the course of the disease. For these reasons, it is feasible for the physician to adopt an aggressive approach to diagnosis and treatment. The objective should be to relieve pain, improve mobility, and forestall debilitating complications. This review will focus on the manifestations and clinical management of Paget's disease. Two cases are presented that illustrate common management problems in older patients.
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PMID:Paget's disease of bone (osteitis deformans). 970 97

Although dermatology now has the most extensive group of systemic medications available for the treatment of skin diseases at any time, GCSs remain the most important agents for managing inflammatory disorders. It is important that the dermatologist have a broad knowledge of guidelines for clinical use, pharmacology, and adverse effects of these drugs. Acute and chronic side reactions should be well recognized. An understanding of the HPA axis and reasons for administering GCSs in different ways is of great value. A good medical history should be taken on any patient treated with GCSs, including knowledge of conditions that would make GCSs inadvisable and other concomitant systemic medications that might produce drug interactions. During the course of therapy, physical examination should include all systems pertinent to side effects caused by these agents, including frequent evaluations of weight and blood pressure. Blood chemistries should be performed on a regular basis, including glucose, electrolytes, and serum lipids. Osteoporosis is one of the most significant adverse affects to be evaluated, with bone mineral density studies recommended on an annual basis for persons continuing on GCS therapy. If hip or other joint pain develops, MR imaging is the most specific and sensitive radiologic examination for evaluating the possibility of osteonecrosis. An ophthalmology examination should be performed every 6 to 12 months to detect early cataract or glaucoma development. Any early signs of infection should be evaluated by appropriate smears, wet preparations, and cultures. Many other studies, including gastrointestinal and pulmonary examinations, may be dictated by specific acute situations. It is important to begin early prevention of the bone loss that occurs with GCS-induced osteoporosis. The 1996 guidelines of the American College of Rheumatology, including adequate calcium and vitamin D intake, should be followed. Hormonal replacement, a bisphosphonate, calcitonin, or a thiazide diuretic may be indicated. Restriction of sodium in the diet is important, as well as adequate potassium intake. The diet should be low in saturated fat and calories and should be high in vegetable protein. Because osteoporosis is so prevalent with GCSs, keeping the patient as active as possible with mild-to-moderate exercise is important. Whenever possible, exposure to persons with infectious processes should be avoided, and proper treatment should be instituted at the initial signs of systemic or cutaneous infection. Oral doses of GCSs are best taken with food to prevent gastrointestinal irritation, and agents for gastric acidity occasionally may be indicated. Significant trauma should be prevented, as should severe exposure to the sun. Many situations may call for consultation with other medical or surgical subspecialists. The patient must be aware of the importance of regular physician evaluations and reporting of any adverse effects while on long-term GCSs. A good relationship and understanding between the patient and physician are vital in minimizing potential problems from these agents. If the dermatologist maintains the proper guidelines of care, patients on GCSs have the highest benefits and lowest risks possible.
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PMID:Update on systemic glucocorticosteroids in dermatology. 1115 87

The role of the intra-articular synovial fold as a source of facet joint pain is unclear, because the nature of nociceptive innervation in lumbar synovial folds is controversial, and there have been no such studies in cervical synovial folds. The present study aimed to demonstrate the presence of nerve fibers including nociceptive fibers in synovial folds of human cervical facet joints using immunohistochemistry. Synovial folds of cervical facet joints removed from patients undergoing cervical spine laminoplasty were analyzed immunohistochemically using antibodies to protein gene product 9.5, beta III-tubulin, substance P and calcitonin gene-related peptide. Many nerve fibers immunoreactive for protein gene product 9.5 and beta III-tubulin were demonstrated both around blood vessels and as free fibers in the stroma of the synovial fold. Also. immunostaining showed the presence of free nerve fibers immunoreactive for substance P and calcitonin gene-related peptide in the stroma. The presence of putative nociceptive fibers in cervical synovial folds supports a possible role for these structures as a source of cervical facet joint pain.
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PMID:Immunohistochemical demonstration of nerve fibers in the synovial fold of the human cervical facet joint. 1151 67

Patients with cervical facet lesions and facet joint injury sometimes experience diffuse neck pain, headache, and arm and shoulder pain. However, the pathophysiology of the intensity and expansion of facet joint pain has not yet been investigated. Retrograde transport of fluoro-gold (F-G) and immunohistochemistry of calcitonin gene-related peptide (CGRP) was used in 20 rats (control group, n=10; injured group, n=10). For the injured group, the whole facet capsule was incised. Of the total F-G labelled dorsal root ganglion (DRG) neurons innervating the C5/6 facet joint, the number and the cross-sectional area of cell profiles of F-G labelled CGRP-ir neurons were evaluated in the bilateral DRGs of both groups. The numbers of CGRP-ir F-G labelled DRG neurons as a percentage of all F-G labelled DRG neurons at C3, C4, C5, C6, C7, C8, T1, T2, and T3 respectively were 30, 22, 43, 47, 21, 19, 25, 36 and 30% in the control group, and 13, 15, 23, 17, 15, 8, 16, 28 and 35% in the injured group, with the injured group showing a significantly lower percentage of CGRP-ir F-G labelled neurons than the control group at C5 and C6 (P<0.05). However, the mean cross-sectional area of F-G labelled CGRP-ir cells from C3 to C8 DRGs increased from 625+/-22 micro m(2) to 878+/-33 micro m(2) in the injured group (P<0.001). Associated with the injured facet joints, the phenotypic switch to large neurons may complicate the mechanism of injured facet pain.
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PMID:Calcitonin gene-related peptide immunoreactive DRG neurons innervating the cervical facet joints show phenotypic switch in cervical facet injury in rats. 1270 60

Gulf War syndrome (GWS) is a perplexing multi-symptom condition comprising a constellation of signs and symptoms consistently described in the literature. These include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances, headaches, fever, arthralgia, skin rashes, and gastrointestinal and sleep disturbances. Excessive chemical sensitivity and odour intolerance is reported. Epidemiological analysis suggests association with pyridostigmine bromide (PB) use as nerve gas prophylaxis, insect repellent, certain vaccination regimes, a variety of possible chemical exposures and physical and psychological stress. Pituitary adenylate cyclase-activating polypeptide (PACAP), calcitonin gene-related peptide (CGRP) and vasoactive intestinal peptide (VIP) are potent vasoactive (vasodilatory) neuropeptides (VNs) having pleiotropic functions as immunomodulators, neuroregulators and hormones. VNs also have neurotrophic and anti-apoptotic roles. VNs act on G protein-coupled receptors (GPCRs) to activate adenylate cyclase, an important step in cyclic AMP metabolism. Autoimmune dysfunction of these VNs or their receptors is postulated to give rise to fatigue-related conditions such as chronic fatigue syndrome (CFS). Complex mechanisms involving heat shock proteins (hsps) and cytosine-guanine dinucleotide (CpG) DNA fragments may also be associated with autoimmunity to VNs or their GPCRs in contributing to fatigue-related conditions. Dysfunction of certain VNs may be the missing link in explaining the nebulous nexus between PB and GWS. This paper explores a possible link between exposures to PB and other chemical, physical and psychological stressors in producing a fatigue-related illness possibly related to autoimmune dysfunction of certain VNs. Treatment options involving restoration of VN function are considered in the context of analogues with other neurotransmitter fatigue-related conditions such as myasthenia gravis (MG). While evidence associating these conditions is thin, vasoactive neuropeptide neurotransmitters of the VIP/PACAP family have acetylcholine co-transmission functions via specific GPCRs. Autoimmune reactions to these receptors may have parallels with muscarinic (e.g., Sjogren's syndrome) and nicotinic (e.g., MG) acetylcholine neurotransmission. Hence theoretically, treatment options such as thymectomy, corticosteroids, plasma exchange, anti-idiotype antibodies and receptor genomic expression reactivation/suppression may be considered. Paradoxically pyridostigmine may prove to have a role in therapy although VN treatment/replacement may be associated with tachyphylaxis.
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PMID:Do vasoactive neuropeptide autoimmune disorders explain pyridostigmine's association with Gulf War syndrome? 1600 38

Neuropeptide-expressing small diameter sensory neurones are thought to be vital in generating inflammatory hyperalgesic responses. Within the dorsal root ganglion (DRG), both the levels of the neuropeptide calcitonin gene-related peptide (CGRP) and the numbers of CGRP-immunoreactive (CGRP-IR) DRG neurones have been shown to increase in a number of acute adjuvant-induced inflammatory pain models. The aim of this study was to look specifically at changes in numbers of CGRP-IR DRG neurones in a chronic model of inflammatory joint pain following complete Freund's adjuvant (CFA) injection into the rat knee. In this model, there were significant increases in the number of ipsilateral CGRP-IR small DRG neurones at days 1, 16 and 35 following intra-articular CFA, compared to saline-injected sham animals. This correlated with the behavioural readouts of hypersensitivity and knee joint inflammation at the same time points. There was also a significant increase in the number of ipsilateral CGRP-IR medium DRG neurones and contralateral CGRP-IR small DRG neurones at day 1. Following dosing of CFA-injected rats with rofecoxib (Vioxx) or paracetamol, there was a significant decrease in the number of ipsilateral CGRP-IR small and medium DRG neurones in rofecoxib- but not paracetamol-treated rats. These data also correlated with behavioural readouts where hypersensitivity and knee joint inflammation were significantly reduced by rofecoxib but not paracetamol treatment. In conclusion, these data show that changes in ipsilateral CGRP expression within small DRG neurones are consistent with behavioural readouts in both time course, rofecoxib and paracetamol studies in this model of chronic inflammatory pain.
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PMID:Changes in dorsal root ganglion CGRP expression in a chronic inflammatory model of the rat knee joint: differential modulation by rofecoxib and paracetamol. 1669 Mar 36


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