Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-three patients with clinical Stage IA-IIIB Hodgkin disease underwent extended-field radiotherapy, including the intact spleen. In 17 of those patients, there was little evidence of renal dysfunction resulting from partial irradiation of the left kidney, which is inherent in such treatment. While isotopic images revealed an anatomic defect in the upper pole of the left kidney in one-third of the patients, dynamic studies showed that this anatomic alteration was not accompanied by any demonstrable dysfunction. Consistently normal serum BUN and creatinine levels in all patients tended to affirm that conclusion.
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PMID:Assessment of renal function following irradiation of the intact spleen for Hodgkin disease. 10 62

Anemia is a common complication of lymphoproliferative syndromes. The exact pathogenic mechanism of this anemia is unclear. Many patients require progressive and persistent blood transfusions. We treated 10 patients (8 with multiple myeloma, 1 with non Hodgkin Lymphoma, 1 with chronic lymphocytic leukemia) by administering low doses of recombinant human erythropoietin (60 U/kg 3 times a week s.c.). All patients presented anemia with hemoglobin levels less than 10 gr/dl; renal function was not impaired (serum creatinine levels less than 1.2 mg/dl or creatinine clearance greater than 60 ml/min). A response was defined as an increase of hemoglobin level of at least 2 gr/dl or stop of red-cell transfusion within the first 3 months of treatment. Nine patients (90%) responded to treatment with a significant increase in the hemoglobin concentration. Two patients presented a cerebral stroke not correlated with erythropoietin administration.
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PMID:[Efficacy of erythropoietin in anemia of patients with immuno-lymphoproliferative disease]. 152 59

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

The clinical studies about the electrolyte abnormality (EA) in patients with malignant lymphoma (ML) are rarely reported. We analyzed the EA and renal insufficiency in 123 patients with ML between June. 1976 and Jan. 1989; 8 patients with Hodgkin's disease, and 115 patients with non-Hodgkin's lymphoma (NHL). Before treatment, the incidence of the EA was 24.2% and hypercalcemia, hypocalcemia, and hyperkalemia were predominant. After treatment it became to 74.7% and the number of hyponatremia and hypokalemia increased. The incidence of proteinuria and renal insufficiency (serum creatinine above 1.5 mg/dl), were 7.3% and 2.4% before treatment, and became to 26.8% and 26.8% after treatment, respectively. There was a significant difference between two groups with and without the EA before treatment as for serum lactate dehydrogenase (LDH) levels (p less than 0.01), clinical stages (p less than 0.05) and the incidence of bone marrow involvement (p less than 0.01). In 34 autopsied cases, 3 cases showed massive renal involvement and about a half of cases showed various renal changes. The EA before treatment was caused by extrarenal factors, because the incidence of proteinuria and renal insufficiency were almost same to healthy controls. And renal factors play an important role on the E.A after treatment. Above results suggest that the EA before treatment indicates the progress of malignant lymphoma and the EA after treatment means not only the progress of the disease but also therapy-related renal damages.
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PMID:[Electrolyte abnormality and renal insufficiency in malignant lymphoma; clinical and pathological analysis in 123 cases]. 177 51

Urinary neopterin levels were studied in 96 patients with malignant lymphomas. Twenty-eight had Hodgkin's disease and 68 non-Hodgkin's lymphoma. Neopterin excretion was significantly related to the clinical stage of the disease. Mean neopterin excretion in patients with active disease (634 +/- 527 mumol neopterin/mol creatinine) was significantly higher (p = 0.000) than in patients in complete remission (198 +/- 105 mumol neopterin/mol creatinine). Mean neopterin levels of patients in stage III-IV were higher than for patients in stage I-II. These findings were the same in patients with Hodgkin's disease and those with non-Hodgkin's lymphoma (659 +/- 593-425 +/- 316 mumol neopterin/mol creatinine), regardless of the histological subtype. A significant correlation was found between neopterin excretion, ESR (r = 0.31; p = 0.003) and hemoglobin (r = -0.40; p = 0.000). Longitudinal analysis showed a trend towards a correlation between response to therapy and neopterin excretion. These findings suggest that neopterin may be a useful prognostic marker in non-Hodgkin's lymphoma.
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PMID:Urinary neopterin in malignant lymphoma. 179 30

A phase II study was conducted by the Cancer and Leukemia Group B (CALGB) in patients with refractory and relapsed Hodgkin's disease (HD) to assess the activity of the combination of etoposide and cis-platin. Twenty-seven patients were entered; 22 were evaluated for this report. Treatment consisted of etoposide (VP-16), 80 mg/m2 IV over 1 hour and cis-platin, 20 mg/m2 IV over 1/2-1 hour; both agents were given daily for 5 days and repeated every 21 days. All patients had received at least 2 prior chemotherapy regimens, had measurable disease, and most (86%) had a performance status of 0-1. In the 22 evaluable patients, there were 4 complete responses (18%) and 4 partial responses, for an overall response rate of 36% (95% Cl: 17.2%, 59.3%). Response duration was from 2.1 to 31 months. Significant toxicity was observed with this regimen. Ten patients (45%) had leukopenia less than 1,000/microliters, and 11 patients (50%) had thrombocytopenia less than 25,000/microliters. Serum creatinine levels reached greater than 2.0 in 14% of patients. Seven patients (32%) had severe nausea and vomiting. VP-16, cis-platin appears to be an active combination in HD; however, their combined activity is only marginally better than reported single-agent activity for VP-16 in the doses and schedule used. Further studies of related combinations in HD are currently under evaluation by the CALGB.
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PMID:Phase II trial of etoposide and cis-diaminodichloro-platinum in patients with refractory and relapsed Hodgkin's disease: Cancer and Leukemia Group B (CALGB) Study 8353. 232 62

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.
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PMID:Hyponatremia and hypouricemia: differentiation from SIADH. 235 Sep 4

Neopterin excretion levels were assessed in 66 consecutive patients affected by non-Hodgkin's lymphomas (NHL). The logarithm of the mean value of the whole series was 2.71 (log [mumol neopterin/mol creatinine]), significantly higher (P less than 0.001) than the control value (2.12). Fifty-six of 66 patients had a raised excretion of neopterin in amounts statistically related to the stage of disease. The mean value (2.51) of patients in Stages I-II was lower than the mean value (2.86) of patients in Stage III-IV (P less than 0.001). The 2-year probability of survival was 64% for patients in Stages I-II and 34% for patients in Stages III-IV. However, patients with lower neopterin excretion (less than 2.65) fared better than patients with higher neopterin excretion, regardless of the stage. Longitudinal analysis showed a trend toward a correlation between response to therapy and neopterin excretion. In NHL, the raised neopterin excretion appears to be a consequence of activation of the host immune system rather than a product of the malignant cells. But this excessive activation of the monocytes-macrophages, as reflected by urinary neopterin levels, is not accompanied by a better outcome. In conclusion, although neopterin cannot be considered a typical tumor marker, nevertheless it is an useful prognostic marker in NHL.
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PMID:Prognostic relevance of urinary neopterin in non-Hodgkin's lymphomas. 291 27

46 patients suffering from various malignancies (17 non Hodgkin lymphomas, 12 Hodgkin's diseases, 11 acute leukaemias, 4 myelomas, 2 carcinomas), 6 patients with haematological disorders such as ITP, SAA, myeloproliferative disease, LAS and 3 patients without preexisting disease were treated with acyclovir for herpes virus infection diagnosed by clinical means. All but 7 patients had been given intensive treatment with various cytostatic agents and/or irradiation. Most patients were treated with 1500 mg acyclovir daily for 5 to 13 days. Dosage was adjusted according to renal function and clinical response in the remaining 10 cases. 11 patients received intravenous immunoglobulins in addition. Side effects were negligible (local irritation, minimal rise in serum creatinine levels in 5 patients). All patients responded to treatment; 6 patients complained of severe neuralgia lasting for more than one month; 5 patients relapsed.
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PMID:[Experiences with acyclovir in herpes virus infections]. 300 62

The patient was a 63-year-old female, who was admitted to the National Nagoya Hospital with complaints of left cervical and bilateral axillary lymphadenopathy on 12 May, 1987. Since May 1985, with the diagnosis of non-Hodgkin lymphoma, she had been successfully treated with combination chemotherapy (VEPA) and radiotherapy at another hospital. Left axillary lymphode biopsy revealed a diagnosis of non-Hodgkin lymphoma, diffuse large cell type. Then, she was given intravenous administration of carboplatin (400 mg/body) on 26 May, 1987. After a single course of this regimen, the lymphnode swelling subsided, and she achieved complete remission on 6 June. Thereafter, she was placed on the maintenance chemotherapy of carboplatin (400 mg/body) every 5 weeks. Through the whole course of this patient, the serum levels of blood urea nitrogen and creatinine were normal, and she did not notice nausea, vomiting and peripheral neuropathy. To our knowledge, this is the first report of complete response by the administration of carboplatin for non-Hodgkin lymphoma.
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PMID:[A case of non-Hodgkin lymphoma with complete remission achieved by carboplatin]. 304 95


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