Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Focal or diffuse infiltration of lymphoid cells in auto-immune thyroiditis destroys the parenchyma. In the diffuse form (Hashimoto's disease), the clinical picture is characterized by fatigue and thyroid enlargement. The diagnosis is settled by cytology. All patients must be treated with thyroid hormones to avoid myxoedema. Loss of immunological tolerance and cytotoxic immune reactions is discussed.
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PMID:Human auto-immune thyroiditis. 79 Aug 89

A 60-year-old man was admitted with general fatigue and jaundice of one year's duration in February, 1981. The hemoglobin (Hb) was 11.4 g/dl and reticulocytes were 1.7%. A diagnosis of chronic cold agglutinin disease (CCAD) was made from the presence of cold agglutinin (CA) 1:2,048, increased serum IgM 267 mg/dl and indirect bilirubin 1.4 mg/dl. His Hb was approximately 11 g/dl in summer and 9 g/dl in winter for the subsequent ten years without therapy. In July, 1990, he was readmitted because of exacerbation of anemia and hepatosplenomegaly. The Hb was 4.6 g/dl, indirect bilirubin 3. 1 mg/dl, CA titer 1:232,144 and reticulocytes were 20%. Serum IgM was 1,065 mg/dl, and immunoelectrophoresis showed IgM-kappa M-protein. Peripheral blood lymphoid cells expressed surface membrane immunoglobulin (SmIg) M and kappa. The bone marrow showed an increased number of lymphoid cells which also expressed SmIg M and kappa. These findings were compatible with those of the features of primary macroglobulinemia (PMG). The M-2 protocol resulted in decrease in serum IgM and CA, but he died of heart failure in February, 1991. The relationship between CCAD and PMG in relation to the pathogenesis was discussed.
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PMID:[Chronic cold agglutinin disease terminating in primary macroglobulinemia after a 10 year history]. 146 90

Recombinant human IL-4 (rhuIL-4) is primate-specific and produces multiple biologic effects on lymphoid cells involved in protection against cancer. RhuIL-4 was evaluated in the cynomolgus monkey to support clinical studies for the immunotherapy of cancer. Administration of rhuIL-4 to monkeys by SC injection of 0, 0.5, 2.5 or 12.5 micrograms/kg BID for one-month (with two-week recovery) resulted in alterations in clinical chemistry and hematology (CCH) parameters consistent with a consumptive coagulopathy. Histomorphologic evaluation revealed increased granulopoiesis, testicular atrophy, and proliferative and inflammatory vascular lesions (VL). IVL principally affected the arterial tree with some proliferation of medial smooth muscle. During the latter part of the treatment and recovery period. CCH parameters approached or returned to pretreatment values, the former finding attributed to the production of antibody to rhuIL-4. At final necropsy, bone marrow appeared normal, and IVL decreased in incidence and severity. ELISA studies of serum indicated 50-90% of the monkeys developed antibody titers > 1000 by Day 22 (not observed in man). The frequency and severity of adverse effects due to rhuIL-4 in the clinic appear to be does-related and reversible with few objective responses to therapy observed. Common toxicities included milk to moderated fever and fatigue and an occasional change in hematopoietic, hepatic and renal function. The monkey predicted hematologic findings, but not all target organ effects.
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PMID:Preclinical evaluation of recombinant human interleukin-4. 147 Nov 85

Fludarabine phosphate is the 2-fluoro, 5'-monophosphate derivative of vidarabine (ara-A) with the advantages of resistance to deamination by adenosine deaminase (ADA) and improved solubility. The mechanism of cytotoxic action of the compound appears to involve metabolic conversion to the active triphosphate. Fludarabine phosphate has substantial activity against lymphoid malignancies, particularly chronic lymphocytic leukemia (CLL) and low-grade non-Hodgkin's lymphoma (NHL). Its single-agent activity in CLL appears at least comparable to those of other conventional combination regimens. Its activity in Hodgkin's disease, mycosis fungoides, and macroglobulinemia, although suggestive, needs to be further defined and clinical trials are warranted in hairy cell leukemia, prolymphocytic leukemia, and previously untreated myeloma. The compound does not appear active against most common solid tumors. Early clinical trials indicated significant myelosuppression and the potential for severe neurotoxicity. Toxicity on the currently used low-dose schedules includes transient and reversible myelosuppression, nausea and vomiting, diarrhea, somnolence/fatigue, and elevations of liver enzymes and/or serum creatinine. Possible pulmonary toxicity has been suggested in several patients. The currently used low-doses of fludarabine phosphate, even with repeated administration, are well tolerated and appear safe with a negligible risk for severe neurotoxicity. Based on its single-agent activity and tolerability, the Food and Drug Administration recently granted group C designation of the drug for the treatment of patients with refractory CLL outside the clinical trials setting. The use of fludarabine phosphate in combination regimens and its impact on the natural history of the lymphoid malignancies is yet to be determined. Fludarabine phosphate may well occupy a pivotal role in the management of CLL and low-grade NHL.
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PMID:Fludarabine phosphate: a synthetic purine antimetabolite with significant activity against lymphoid malignancies. 170 43

We report an autopsy case of acute erythremia which terminated in generalized infiltration of immature blasts similar to proerythroblasts. A 61-year-old man was admitted because of general fatigue and fever in June, 1990. Mild anemia and severe thrombocytopenia were noted. The bone marrow was hypocellular with 25.5% blasts similar to proerythroblasts and 36.5% erythroblasts, many of which were polynuclear and megaloblastoid. The blasts were cytochemically negative for POX, but positive for PAS staining. Therefore he was diagnosed as having acute erythremia. Partial remission was achieved by BHAC-EV therapy. But three months later, his marrow was replaced by 52.7% blasts as seen in admission. Those blasts were negative for lymphoid, myelocytic, megakaryocytic markers and antiglycophorin A, but positive for OKT 9. Electron microscopy revealed that some of blasts had characteristics of immature erythroblasts. In spite of low dose Ara-C therapy, he died of sudden gastrointestinal bleeding in December, 1990. The autopsy disclosed widespread infiltration of blasts, involving liver, spleen, lung, kidney and stomach. It was interesting that dysplasia had been confined to erythroid lineage throughout his clinical course. He seemed to be a rare case of blastic form of acute erythremia which should be distinguished from erythroleukemia.
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PMID:[Blastic form of acute erythremia: report of an autopsy case]. 175 58

Pentostatin, a novel inhibitor of adenosine deaminase, has shown activity in various lymphoid malignancies of both the T and B cell lineage. This agent has unique side effects and in general myelosuppression has been mild. Interferon has both antiviral and antineoplastic properties. This agent has shown activity in hairy cell leukemia, chronic granulocytic leukemia, low grade lymphoma, and myeloma. Side effects from interferon are in general dissimilar to those that have been seen with pentostatin and in particular myelosuppression has not been a major toxicity with low doses of interferon. This current trial explored the combination of pentostatin and interferon in hematologic malignancies. Fifteen patients were enrolled in this phase I trial at a fixed dose of pentostatin of 4 mg/m2 biweekly and interferon at doses of 0.5, 1, 2, or 4 million units/m2 of interferon. At the first three dose levels of interferon nausea and vomiting were the predominant toxicity and appeared to worsen with time on study. Fatigue also was seen at the lowest level of interferon and was severe enough to cause two individuals to discontinue the study medications. At higher dose levels of interferon, myelosuppression, nausea and vomiting, and fatigue were the predominant toxicities. One patient with hairy cell leukemia had a complete response and a second patient with T cell cutaneous lymphoma had a partial response which lasted for 6 to 7 weeks. The maximum tolerated dose of interferon with pentostatin in this patient population was four million units/m2.
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PMID:A phase I trial of alpha-interferon in combination with pentostatin in hematologic malignancies. 205 72

Four patients fulfilling the case definition for eosinophilia-myalgia syndrome are described, including one whose disease began in 1986. Each displayed a variety of symptoms: one suffered principally from myalgia and recovered spontaneously on discontinuation of L-tryptophan therapy; one exhibited progressive sclerodermiform skin changes, neuropathy, and myopathy; a third had prominent neuromuscular disease and sclerodermiform skin changes; and the fourth experienced profound weight loss, an axonal polyneuropathy, and perivascular lymphoid infiltrates simulating a lymphoma. Evidence of T-cell activation was present in peripheral blood and affected tissues during the clinically active progressive phase of disease. Among other manifestations pleural effusion, cutaneous vasculitis, joint contractures, and bloody diarrhea were observed. A history of L-tryptophan ingestion should be sought in patients with myalgia, fatigue, or the above outlined symptoms.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan ingestion. Analysis of four patients and implications for differential diagnosis and pathogenesis. 217 45

A 60-year-old woman was admitted because of fatigue. Physical examination revealed prominent peripheral lymphadenopathy, marked tonsillar swelling and hepatosplenomegaly. The leukocyte count was 68,900/microliters with 75% lymphoid blasts and 5% basophils. The karyotype of the blood cells was 46, XX, Ph1/47, XX, Ph1, +Ph1. The diagnosis of CML in blast crisis was made. After chemotherapy using adriamycin, cyclophosphamide, vincristine, and prednisolone (CHOP), lymphadenopathy and splenomegaly reduced and lymphoid blasts disappeared from the blood and bone marrow. At that time only single Ph1 (46, XX, Ph1) clone was detected in her bone marrow. Four months later, hematological relapse accompanied by lymphadenopathy occurred and DNA analysis of the blasts showed the rearrangement of bcr gene. The simultaneous chromosomal analyses of the blood, bone marrow and lymph node revealed that almost all cells examined had the karyotype "47, XX, Ph1, + Ph1". In spite of repeated chemotherapy the patient did not improve and died. This case suggests a relationship between lymphadenopathy and double Ph1 chromosomes in CML.
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PMID:[Prominent lymphadenopathy and double Ph1 chromosomes as initial and recurrent manifestations of chronic myelogenous leukemia in blast crisis: report of a case and review of the literature]. 224 24

A 48-year-old male was admitted to our hospital on April 20, 1989 because of general fatigue and abdominal fullness. Physical examination showed hepatomegaly, massive splenomegaly, and systemic lymphadenopathy. Hematological findings revealed WBC 73,000/microliters, RBC 289 x 10(4)/microliters, Hb 8.0g/dl, and platelet 9.1 x 10(4)/microliters. WBC differential count demonstrated a mixture of 63% matured small lymphocytes and 32% prolymphocytoid cells. Bone marrow aspiration was unsuccessful with a dry tap. Surface marker analysis of peripheral blood lymphoid cells disclosed that they were positive for anti-HLA-DR, CD 5, CD 19, CD 20, CD 21, CD 25, Sm-IgM, Sm-IgD, and Sm-K. He was diagnosed as B-CLL/PL, and treated with VEPA with partial remission. CLL/PL which was advocated by Melo in 1986 is regarded as a distinct clinical entity intermediate between CLL and PLL in clinical and laboratory features. Our case is interesting with regard to good response to combination chemotherapy, though most cases of CLL/PL have a resistance to standard chemotherapy.
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PMID:[B-chronic lymphocytic leukemia/prolymphocytic leukemia (CLL/PL)--a case report]. 228 70

The genes for a number of growth factors that stimulate human hematopoietic and lymphoid cells in vitro have recently been cloned and recombinant molecules provided for clinical trials. For three of these (erythropoietin, G-CSF, and GM-CSF), phase I and II studies have been completed and promising results have been obtained. Of particular relevance to the field of bone marrow transplantation (BMT) has been the finding that G-CSF and GM-CSF could shorten the period of neutropenia in patients treated with chemotherapy, including regimens requiring BMT support. Doses of up to 240 micrograms/m2 of GM-CSF have been well tolerated and have increased the peripheral blood neutrophil count in a dose-dependent manner. At higher doses, eosinophils and monocytes were also increased. A continuous infusion over at least 2 h was found to be superior to bolus administration in terms of both efficacy and reduced side effects. These have usually been mild, but bone pain, headache, fatigue and elevated temperature have been encountered. The rise in neutrophil numbers shortly after initiating treatment with GM-CSF is probably due to neutrophil demargination. After a few days increased bone marrow cellularity has also been noted. In addition to these effects on cell numbers, enhancement of granulocyte and monocyte functions has been documented. However, a major concern with the use of G-CSF and GM-CSF in cancer patients, particularly those with hematopoietic malignancies, is the potential of these molecules to stimulate malignant cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Colony stimulating factors. 245 88


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