Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0235394 (wasting)
 8,040 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From 1985 to 1987 148 patients underwent mastectomy for breast cancer, of whom 91 underwent modified radical mastectomy. Of these patients (median age 60 years (range 31-86 years)), 89 have been assessed for early (< 30 days) and late (> 30 days) non-tumour morbidity and mortality. A total of 41 patients had nodal metastases. Adjunctive therapy used was tamoxifen in 70 patients and radiotherapy in 20. Overall, 47 patients (53%) developed a total of 75 complications, and there was one 30-day mortality. Of the patients, 26 developed one complication, 14 had two complications and 7 three complications. Early complications were lymphocoele/seroma (n = 22), wound infection (n = 9) and cardiopulmonary problems (five deep vein thrombosis, two pulmonary embolus (1 death), one myocardial infarct). Late complications were lymphoedema (n = 10), pectoralis major wasting (n = 6), frozen shoulder (n = 7), intercostobrachial neuralgia (n = 4), and a small number of self-limiting wound problems (n = 9). There were two late deaths (myocardial infarcts). Early complications were not related to nodal status, and late complications were related to neither nodal status nor radiotherapy. Significant morbidity is attached to radical surgery for breast cancer. Most complications are minor and self-limiting, but there are a small number of late complications which may affect quality of life.
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PMID:Non-tumour morbidity and mortality after modified radical mastectomy. 141 1

The ability of ciliary neurotrophic factor (CNTF) to induce sprouting by undamaged adult motor neurons was studied in gluteal muscles of adult ICR mice. Low doses of CNTF (0.02 mg kg-1 day-1) only induced sprouting in gluteus muscles that were beneath the site of injection, whereas high doses of CNTF (0.4-1.2 mg kg-1 day-1) acted systemically to induce motor neuron sprouting. We found little difference between the type or quality of sprouting induced by CNTF compared with muscle paralysis. Both stimuli induced sprouts of the same length, although muscle paralysis tended to induce more sprouts per end-plate. Paralysis also induced more nodal sprouting than did CNTF, but both were weaker stimuli for nodal sprouting than was partial denervation. In addition to its effects on motor neuron sprouting, high doses of CNTF induced loss of up to 36% of the body weight of treated mice. The substantial wasting caused by CNTF indicates that the factor has potent cachectic activity.
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PMID:Systemic injections of ciliary neurotrophic factor induce sprouting by adult motor neurons. 801 51

A 35-year-old homosexual man developed a composite nodal Kaposi's sarcoma and peripheral T-cell lymphoma that were associated with a peripheral blood CD4-positive lymphocyte count of only 43/mm3. The patient subsequently developed Pneumocystis carinii pneumonitis and eventually died due to disseminated Cryptococcus neoformans. Numerous premortem tests for the presence of human immunodeficiency virus (HIV) types 1 and 2 were negative by the enzyme-linked immunosorbent assay, Western blot, viral isolation, and polymerase chain reaction techniques. Postmortem evaluations for HIV-1, HIV-2, human T-cell lymphotropic virus (HTLV)-I, and HTLV-II also were negative by polymerase chain reaction, immunofluorescence assays, and viral isolation. A systemic infection by Mycoplasma fermentans, however, was documented by immunohistochemistry and polymerase chain reaction in premortem and postmortem tissues. This recently recognized human pathogen has produced systemic infections in patients with the acquired immunodeficiency syndrome (AIDS) and in previously healthy non-AIDS patients who characteristically have a fulminant flu-like illness. Additionally, M fermentans has enhanced the cytopathic effect of HIV in in vitro studies and has produced fatal wasting illnesses with terminal lymphopenia in inoculated adult silvered leaf monkeys. This report is the first description of an association between M fermentans infection and an AIDS-like illness in an HIV-negative individual. The etiology of the severe immunosuppression in this patient and the associated role of M fermentans remain to be determined by further investigations.
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PMID:Acquired immunodeficiency syndrome-like illness associated with systemic Mycoplasma fermentans infection in a human immunodeficiency virus-negative homosexual man. 849 93

An increased prevalence of intermediate- and high-grade B-cell non-Hodgkin's lymphoma (NHL) is a major manifestation of the disease spectrum associated with human immunodeficiency virus (HIV) infection. Rarely, lymphoproliferations are of T-cell, null cell, or mixed-lineage phenotypes. We describe an unusual B-cell NHL that presented as a left alar ulcer in a man with acquired immunodeficiency syndrome (AIDS) and rectal carcinoma. Biopsy of the lesion and a draining cervical lymph node showed atypical dermal lymphoid infiltration with effacement of nodal architecture and involvement of adjacent skeletal muscle by a diffuse infiltrate of large and small lymphocytes. On paraffin section immunochemistry, the large lymphoid cells expressed CD45 and CD45RO, but not CD43 or CD20. The small background cells were positive for CD3, CD43, and CD45RO. These overall results were consistent with a diagnosis of a T-cell process. Gene rearrangement studies, however, demonstrated a clonal B-cell population indicative of B-cell NHL. The clinical course was marked by rapid shrinkage of tumor with chemotherapy followed by profound wasting and death. Anomalous coexpression or lack of expression of T- and B-cell markers may be seen in AIDS-related NHL. Reliance on paraffin section immunohistology may provide misleading information, and caution is recommended in assigning a specific lineage to such lymphoproliferations without additional immunologic or genotypic analyses. Whether our case represents a distinct clinicopathologic entity or is simply a peculiar manifestation of HIV-related B-cell NHL remains uncertain.
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PMID:AIDS-associated B-cell non-Hodgkin's lymphoma masquerading as a cutaneous T-cell neoplasm: an aberrant immunophenotype requiring comprehensive analysis for lineage resolution. 905 57

Bovine immunodeficiency virus (BIV) in Holstein cows was associated with morphologic evidence of lymphoid organ deficiency. Cows were subjected to normal management practices including parturition and lactation without adverse environmental stresses. During the clinical disease process there was marked weight loss and wasting with frequent and severe concurrent infections. Lymphoid follicular hyperplasia and dysplasia in lymph nodes, and hypertrophy and hyperplasia in hemal lymph nodes were characteristics of the lymphoid tissues. Atrophy of lymphoid cell compartments with depletion of lymphocytes and a lymphocytic lymphoid folliculitis were components of the lymphoid system pathology. The nodal tissue lesions resembled those observed in feline, simian, and human lentiviral disease. A functional correlation with immune system deficiency was the development of multiple bacterial infections which failed to resolve after appropriate therapy. The BIV-associated disease syndrome in dairy cows may be useful as a model system for investigation of the pathogenesis of the lymphoid organ changes that occur in humans and animals with lentiviral infection.
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PMID:Natural bovine lentivirus type 1 infection in Holstein dairy cattle. II. Lymphoid tissue lesions. 1260 82

Glucocorticoids are highly conserved fundamental regulators of energy homeostasis. In response to stress in the form of perceived danger or acute inflammation, glucocorticoids are released from the adrenal gland, rapidly mobilizing energy from carbohydrate, fat and protein stores. In the case of inflammation, mobilized protein is critical for the rapid synthesis of acute phase reactants and an efficient immune response to infection. While adaptive in response to infection, chronic mobilization can lead to a profound depletion of energy stores. Skeletal muscle represents the major body store of protein, and can become substantially atrophied under conditions of chronic inflammation. Glucocorticoids elicit the atrophy of muscle by increasing the rate of protein degradation by the ubiquitin-proteasome system and autophagy lysosome system. Protein synthesis is also suppressed at the level of translational initiation, preventing the production of new myofibrillar protein. Glucocorticoids also antagonize the action of anabolic regulators such as insulin further exacerbating the loss of protein and muscle mass. The loss of muscle mass in the context of chronic disease is a key feature of cachexia and contributes substantially to morbidity and mortality. A growing body of evidence demonstrates that glucocorticoid signaling is a common mediator of wasting, irrespective of the underlying initiator or disease state. This review will highlight fundamental mechanisms of glucocorticoid signaling and detail the mechanisms of glucocorticoid-induced muscle atrophy. Additionally, the evidence for glucocorticoids as a driver of muscle wasting in numerous disease states will be discussed. Given the burden of wasting diseases and the nodal nature of glucocorticoid signaling, effective anti-glucocorticoid therapy would be a valuable clinical tool. Therefore, the progress and potential pitfalls in the development of glucocorticoid antagonists for muscle wasting will be discussed.
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PMID:The regulation of muscle mass by endogenous glucocorticoids. 2569 71