Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Depression represents a major public health problem. It is estimated that 13-20% of the population has some depressive symptoms at any given time and about 5% of the population is assumed to suffer from major depression. Known pathological processes include ischemia, neoplasia, necrosis, apoptosis, infection, and inflammation. Of those, inflammation is the most compatible with the waxing and waning course of depression, and could explain the biology of this disorder that has a fluctuating course with severe episodes that can be followed by partial or complete remission. Over the years a body of evidence has been accumulated suggesting that major depression is associated with dysfunction of inflammatory mediators. Major depression commonly co-occurs with ischemic heart disease and decreased bone mineral density. Depressive symptoms are known to have a negative impact on cardiovascular prognosis, increasing the mortality rate of coronary artery disease. Several lines of evidence indicate that brain cytokines, principally interleukin-1beta (IL-1beta) and IL-1 receptor antagonist may have a role in the biology of major depression, and that they might additionally be involved in the pathophysiology and somatic consequences of depression as well as in the effects of antidepressant treatment. A particularly unique and novel aspect of the studies and views discussed here is their potential to lead to interventions which may reduce the morbidity and mortality risks for osteoporosis, cardiovascular disease, and behavioral symptoms in patients with major depression. We also discuss the emerging concept of peripheral and central cytokine compartments: their integration and differential regulation is a key element for the optimal functioning of the immune and nervous systems.
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PMID:The role of inflammatory mediators in the biology of major depression: central nervous system cytokines modulate the biological substrate of depressive symptoms, regulate stress-responsive systems, and contribute to neurotoxicity and neuroprotection. 1048 47

Diagnosis and management of giant cell (temporal) arteritis (GCA) should be performed by physicians who can accurately monitor the ophthalmologic, neurologic, and systemic sequelae of the disease as well as the numerous side effects of systemic corticosteroids, which are typically necessary for treatment. When the diagnosis of giant cell arteritis is seriously entertained, early treatment with adequate doses of oral or intravenous corticosteroids should not be delayed until laboratory confirmation has been obtained. Unilateral or bilateral temporal artery biopsy should be performed on all patients with suspected GCA. A positive biopsy result mandates that higher doses of corticosteroids be used during the first 2 months, which comprise the critical period for risk of new ocular ischemia. A definitive, biopsy-proven diagnosis requires at least 6 months, and typically 12 months, of corticosteroid therapy. Common pitfalls include increasing the dose and prolonging the use of corticosteroids in response to increases in the erythrocyte sedimentation rate (ESR) unrelated to GCA or visual blurring that may be related to benign tear film abnormalities, corticosteroid-induced lens changes, and other ophthalmic conditions. The muscle stiffness of polymyalgia rheumatica (PMR) must be distinguished from the osteoarthritis and other painful conditions common in the elderly. After corticosteroid therapy has begun, continuing ophthalmologic evaluation is necessary to evaluate the effectiveness of treatment and whether ocular complications, such as glaucoma or cataract, develop. Careful attention must be given to early detection and prevention of systemic side effects of corticosteroid treatment. Patients may be given gastrointestinal protective agents, such as histamine (H(2))-blocking agents; vitamin D and calcium; oral hypoglycemic agents; and, if necessary, insulin and antihypertensive drugs. If bone density measurements warrant, hormones/supplementation to prevent or reverse osteoporosis may be prescribed. After the initial diagnosis and first 4 weeks of treatment, elevation of the ESR or C-reactive protein alone should generally not be used as signs of disease activity nor as a reason to increase the daily dose of steroids. If symptoms or signs of disease activity occur, the dose should be raised regardless of test results. Even with vigorous physician-patient education, however, a patient is occasionally unable to provide adequate historical information about response to therapy, and the physician is forced to rely on laboratory values as a measure of disease activity. After initial high-dose corticosteroid therapy, patients without a classic history and with negative biopsy results will generally receive a rapid taper to low doses of corticosteroids. The role of repeated temporal artery biopsy in the clinical management of GCA is unclear. Despite persistence of PMR and, in some cases, histologic evidence of inflammation in temporal arteries, patients do not frequently have recurrence of symptomatic GCA after 6 months or more of corticosteroid therapy. Under these circumstances, late vision loss is rare.
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PMID:Giant Cell Arteritis. 1109 95

The emergence of heart transplantation as the ultimate treatment for end-stage heart failure has been accompanied by new diagnostic challenges. Computed tomography (CT) has emerged as an important diagnostic tool in the evaluation of heart transplant recipients because many infectious, ischemic-hemorrhagic, and neoplastic complications are amenable to early detection with this modality. In the early postoperative period, CT is mostly indicated in the evaluation of infectious complications or cerebral symptoms. Later, CT is mostly performed for staging of infectious or neoplastic disease. Infectious complications include mediastinitis, soft-tissue inflammation, abscess formation, cerebral infarction, and aspergillosis. Complications related to ischemia or hemorrhage include allograft rejection and coronary allograft vasculopathy, the latter being the leading long-term cause of death in heart transplant recipients. CT is also indicated in malignant disease (eg, lymphoma, visceral carcinoma, skin tumors), which is the second most important long-term cause of death. Moreover, CT is helpful in identifying disease caused by immunosuppressive therapy (eg, leukoencephalopathy, osteoporosis, thoracic lipomatosis). CT has proved superior to both ultrasound and magnetic resonance imaging in the evaluation of heart transplant recipients. It has become the diagnostic modality of choice for many transplant-related complications and may help improve postoperative treatment of affected patients.
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PMID:CT of heart transplant recipients: spectrum of disease. 1111 18

Serum testosterone levels decline gradually and progressively with aging in men. Many manifestations associated with aging in men, including muscle atrophy and weakness, osteoporosis, reduced sexual functioning, and increased fat mass, are similar to changes associated with testosterone deficiency in young men. These similarities suggest that testosterone supplementation may prevent or reverse the effects of aging. A MEDLINE search was performed to identify studies of testosterone supplementation therapy in older men. A structured, qualitative review was performed of placebo-controlled trials that included men aged 60 and older and evaluated one or more physical, cognitive, affective, functional, or quality-of-life outcomes. Studies focusing on patients with severe systemic diseases and hormone deficiencies related to specific diseases were excluded. In healthy older men with low-normal to mildly decreased testosterone levels, testosterone supplementation increased lean body mass and decreased fat mass. Upper and lower body strength, functional performance, sexual functioning, and mood were improved or unchanged with testosterone replacement. Variable effects on cognitive function were reported, with improvements in some cognitive domains (e.g., spatial, working, and verbal memory). Testosterone supplementation improved exercise-induced coronary ischemia in men with coronary heart disease, whereas angina pectoris was improved or unchanged. In a few studies, men with low testosterone levels were more likely to experience improvements in lumbar bone mineral density, self-perceived functional status, libido, erectile function, and exercise-induced coronary ischemia with testosterone replacement than men with less marked testosterone deficiency. No major unfavorable effects on lipids were reported, but hematocrit and prostate specific antigen levels often increased. Based on these results, testosterone supplementation cannot be recommended at this time for older men with normal or low-normal testosterone levels and no clinical manifestations of hypogonadism. However, testosterone replacement may be warranted in older men with markedly decreased testosterone levels, regardless of symptoms, and in men with mildly decreased testosterone levels and symptoms or signs suggesting hypogonadism. The long-term safety and efficacy of testosterone supplementation remain uncertain. Establishment of evidence-based indications will depend on further demonstrations of favorable clinical outcomes and symptomatic, functional, and quality-of-life benefits in carefully performed, long-term, randomized, placebo-controlled clinical trials.
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PMID:Testosterone supplementation therapy for older men: potential benefits and risks. 1253 54

Endogenous nucleoside and nucleotide mediate a lot of functions via cell surface P receptors (receptors for purines and pyrimidines) in many organs. Nucleoside and nucleotide have protective roles in the events such as cancer, apoptosis, ischemia, wound healing, osteoporosis, drug toxicity, inflammation and pain. Moreover, the development of selective agonists and antagonists for P1, P2 receptors and P receptor subtypes may provide novel drugs in therapeutic strategies.
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PMID:[New targets for drug therapeutics: receptors for purines and pyrimidines]. 1288 42

Osteoporosis is the most common contributing factor of spinal fractures, which characteristically are not generally known to produce spinal cord compression symptoms. Recently, an increasing number of medical reports have implicated osteoporotic fractures as a cause of serious neurological deficit and painful disabling spinal deformities. This has been corroborated by the present authors as well. These complications are only amenable to surgical management, requiring instrumentation. Instrumenting an osteoporotic spine, although a challenging task, can be accomplished if certain guidelines for surgical techniques are respected. Neurological deficits respond equally well to an anterior or posterior decompression, provided this is coupled with multisegmental fixation of the construct. With the steady increase in the elderly population, it is anticipated that the spine surgeon will face serious complications of osteoporotic spines more frequently. With regard to surgery, however, excellent correction of deformities can be achieved, by combining anterior and posterior approaches. Paget's disease of bone (PD) is a non-hormonal osteometabolic disorder and the spine is the second most commonly affected site. About one-third of patients with spinal involvement exhibit symptoms of clinical stenosis. In only 12-24% of patients with PD of the spine is back pain attributed solely to PD, while in the majority of patients, back pain is either arthritic in nature or a combination of a pagetic process and coexisting arthritis. In this context, one must be certain before attributing low back pain to PD exclusively, and antipagetic medical treatment alone may be ineffective. Neural element dysfunction may be attributed to compressive myelopathy by pagetic bone overgrowth, pagetic intraspinal soft tissue overgrowth, ossification of epidural fat, platybasia, spontaneous bleeding, sarcomatous degeneration and vertebral fracture or subluxation. Neural dysfunction can also result from spinal ischemia when blood is diverted by the so-called "arterial steal syndrome". Because the effectiveness of pharmacologic treatment for pagetic spinal stenosis has been clearly demonstrated, surgical decompression should only be instituted after failure of antipagetic medical treatment. Surgery is indicated as a primary treatment when neural compression is secondary to pathologic fractures, dislocations, spontaneous epidural hematoma, syringomyelia, platybasia, or sarcomatous transformation. Five classes of drugs are available for the treatment of PD. Bisphosphonates are the most popular antipagetic drug and several forms have been investigated.
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PMID:Principles of management of osteometabolic disorders affecting the aging spine. 1450 19

Bone disease is a side effect of concern regarding chronic glucocorticoid (GC) administration. Most GC-treated patients exhibit a process of bone loss, frequently leading to osteoporosis, with increased fracture risk, especially in spinal vertebrae. Some GC-treated patients will develop osteonecrosis, a disease with distinct clinical and histopathological features, most often occurring underneath the articular surface of the femoral head. Remarkably, both of these GC-induced bone diseases are associated with osteoblast and osteocyte apoptosis, which is emerging as a potential primary pathogenic mechanism. Here, we review the evidence for osteoblast and osteocyte apoptosis in GC-induced bone disease and highlight current debates: (1) With recent reports describing the antiapoptotic effect of GCs in some in vitro osteoblast models, and with the known adverse effects of GCs on osteoblast cell cycle and differentiation, could the in vivo osteoblast apoptosis be an indirect rather than a direct effect of GCs? (2) What is the pathogenic relationship between GC-induced osteoporosis and osteonecrosis? Could the latter be a mere manifestation of the former? and (3) How does apoptosis fit into the traditional concept of ischemia as a key etiology in osteonecrosis? Regardless of the answers, recent studies with cells, animals, and humans point out bone cell apoptosis as a potential target in the design of treatment for GC-induced bone disease.
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PMID:Role of apoptosis in glucocorticoid-induced osteoporosis and osteonecrosis. 1469 69

Metabolic bone disease (MBD) is abnormal bone metabolism and includes the common disorders of osteoporosis and osteomalacia, which can develop in patients receiving long-term parenteral nutrition (PN). Patients who require long-term PN have significant gastrointestinal failure and malabsorption, which is generally caused by severe inflammatory bowel disease, intestinal ischemia, or malignancy. The exact cause of MBD in long-term PN patients is unknown, but its origin is thought to be multifactorial, with factors including underlying disease, effect of medications used to treat this disease (eg, corticosteroids), and various components of the PN solution. Caring for patients on long-term PN requires routine assessment and monitoring for MBD. Appropriate adjustments of the PN solution can help reduce the risk for developing PN-associated MBD and in some instances improve bone mineral density. Recent developments in pharmacologic treatment for osteoporosis show promise for patients with MBD receiving PN.
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PMID:Metabolic bone disease and parenteral nutrition. 1524 4

Through-transmission alveolar ultrasonography (TAU) is a novel imaging modality in dental medicine. A brief introduction to through-transmission ultrasonography (TTU) is followed by a description of the first commercially available TAU device, the Cavitat CAV 4000 (Cavitat Medical Technologies, Inc., Alba, TX). Recent associations between systemic osteoporosis, oral osteoporosis, periodontal diseases, and cardiovascular diseases underline the importance of early detection and treatment of oral cancellous bone pathologies associated with low bone density (LBD), such as regional ischemic osteoporosis, chronic nonsuppurative osteomyelitis, bone marrow edema, and cavitational ischemic osteonecrosis (osteocavitation). While the impact of osteoporosis on maxillofacial bones is acknowledged, there is a lack of reliable prevalence rate, and the National Institutes of Health (NIH) recommend that more attention should be paid to skeletal health, especially in persons with conditions known to be associated with secondary osteoporosis. TAU, a safe and effective imaging modality, can be a valuable tool in research as well as for the clinical assessment of alveolar cancellous bone pathologies associated with LBD and ischemia.
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PMID:Introduction to through-transmission alveolar ultrasonography (TAU) in dental medicine. 1589 66

Bone mineral density (BMD) was evaluated in 52 patients with HbS/beta-thalassemia. Seventeen (32%) patients had osteopenia/osteoporosis and 30 (57%) had osteosclerosis. Bone resorption was diminished in patients with osteosclerosis and increased in those with osteopenia/osteoporosis. The sRANKL/osteoprotegerin ratio was elevated in the osteosclerotic group. Osteoporosis patients had mild renal impairment and their BMD correlated with osteoprotegerin, and bone resorption markers. Osteosclerosis patients had multiple infarctions in the studied bones that led to reduced osteoclast activity and increased BMD. In conclusion, HbS/beta-thalassemia patients may develop osteopenia/osteoporosis mainly due to marrow expansion or osteosclerosis because of ischemia after a vaso-occlusive crisis. The RANKL/ osteoprotegerin axis participates in these phenomena.
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PMID:Osteoporosis and osteosclerosis in sickle cell/beta-thalassemia: the role of the RANKL/osteoprotegerin axis. 1670 59


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