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Biomedical subjects

D C Ihde

Publications and source records attributed to D C Ihde.

At least 163 records · Page 9Linked to original sources
PubMed1976

Splenectomy in the chronic phase of chronic granulocytic leukemia. Effects in 32 patients.

Splenectomy in the chronic phase of chronic granulocytic leukemia was done in 32 patients, in 24 as part of a trial of elective splenectomy in early disease and in 8 because of thrombocytopenia preventing adequate therapy of the chronic phase. Patients with splenectomy had a median survival after diagnosis of 60 months. However, survival of patients operated on within 1 year of diagnosis was no different (median, 44 months) from that recorded in 120 consecutive Philadelphia chromosome-positive patients treated during the same time period (median, 42 months). After blastic transformation of disease, splenectomy patients survived slightly longer, responded more frequently to platelet transfusions, and avoided the morbidity of massive splenomegaly seen in 30% of patients treated with spleens retained. Response to blastic phase chemotherapy, however, was not improved. Prophylactic splenectomy in the chronic phase of disease did not influence survival but may ameliorate some complications of the terminal stages of illness.

Adult↗
PubMed1976

Effect of splenectomy on tolerance to combination chemotherapy in patients with lymphoma.

Enhanced tolerance to combination chemotherapy has been cited as an ancillary benefit of staging laparotomy and splenectomy in Hodgkin's disease. Seventeen patients with Hodgkin's disease and 15 with non-Hodgkin's lymphoma were subjected to nontherapeutic splenectomy as part of the staging procedure prior to their initial treatment with MOPP (nitrogen mustard, vincristine, procarbazine, and prednisone) or CVP (cyclophosphamide, vincristine, and prednisone) chemotherapy, respectively. Matched control patients of comparable age, pathologically proven stage, and presence or absence of bone marrow lymphoma and previous radiotherapy were selected. Although leukocyte (in non-Hodgkin's patients) and platelet counts (in both groups) were significantly higher in the patients with splenectomy during most of the first six cycles of therapy, there was no difference in the number of cycles during which a leukocyte count below 1000 (or below 2000 in Hodgkin's disease) or platelet count below 50,000 was recorded in the splenectomized and control patients. The total dose of all drugs actually delivered, time required to complete six cycles of treatment, and the portion of patients entering complete remission were not significantly different in the two groups. We have found no evidence that splenectomy per se, in lymphoma patients without findings of hypersplenism, improves the ability to administer planned amounts of drugs during initial combination chemotherapy.

Cyclophosphamide↗
PubMed1975

Osteonecrosis of the femoral head in patients with lymphoma treated with intermittent combination chemotherapy (including corticosteroids).

Four adult patients with malignant lymphoma were treated with combination chemotherapy including an alkylating agent, vincristine, procarbazine (in all but one case), and intermittent high-dose prednisone. Twenty to 42 months after initiation of therapy, osteonecrosis of the femoral head developed. This was bilateral in two patients and unilateral in two, and presumably represented a complication of steroid administration, even though three of the patients received only 4 to 6 weeks of therapy. Necrosis of bone may be a low-frequency long-term complication of combination chemotherapy in lymphoma.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Non-small cell lung cancer. Part II: Treatment.

Squamous, large cell, and adenocarcinoma, collectively termed non-small cell lung cancer (NSCLC), are diagnosed in approximately 75% of patients with lung cancer in the United States. The treatment of these three tumor cell types is approached in virtually identical fashion because, in contrast to small cell carcinoma of the lung, NSCLC more frequently presents with localized disease at the time of diagnosis and is thus more often amenable to surgical resection but less frequently responds to chemotherapy and irradiation. Cigarette smoking is etiologically related to the development of NSCLC in the great majority of cases. Genetic mutations in dominant oncogenes such as K-ras, loss of genetic material on chromosomes 3p, 11p, and 17p, and deletions or mutations in tumor suppressor genes such as rb and p53 have been documented in NSCLC tumors and tumor cell lines. NSCLC is diagnosed because of symptoms related to the primary tumor or regional or distant metastases, as an incidental finding on chest radiograph, or rarely because of a paraneoplastic syndrome such as hypercalcemia or hypertrophic pulmonary osteoarthropathy. Screening smokers with periodic chest radiographs and sputum cytologic examination has not been shown to reduce mortality. The diagnosis of NSCLC is usually established by fiberoptic bronchoscopy or percutaneous fine-needle aspiration, by biopsy of a regional or distant metastatic site, or at the time of thoracotomy. Pathologically, NSCLC arises in a setting of bronchial mucosal metaplasia and dysplasia that progressively increase over time. Squamous carcinoma more often presents as a central endobronchial lesion, while large cell and adenocarcinoma have a tendency to arise in the lung periphery and invade the pleura. Once the diagnosis is made, the extent of tumor dissemination is determined. Since most NSCLC patients who survive 5 years or longer have undergone surgical resection of their cancers, the focus of the staging process is to determine whether the patient is a candidate for thoracotomy with curative intent. The dominant prognostic factors in NSCLC are extent of tumor dissemination, ambulatory or performance status, and degree of weight loss. Stages I and II NSCLC, which are confined within the pleural reflection, are managed by surgical resection whenever possible, with approximate 5-year survival of 45% and 25%, respectively. Patients with stage IIIa cancers, in which the primary tumor has extended through the pleura or metastasized to ipsilateral or subcarinal lymph nodes, can occasionally be surgically resected but are often managed with definitive thoracic irradiation and have 5-year survival of approximately 15%.(ABSTRACT TRUNCATED AT 400 WORDS)

Carcinoma, Non-Small-Cell Lung↗
PubMedDate not supplied

Non-small cell lung cancer. Part I: Biology, diagnosis, and staging.

Squamous, large cell, and adenocarcinoma, collectively termed non-small cell lung cancer (NSCLC), are diagnosed in approximately 75% of patients with lung cancer in the United States. The treatment of these three tumor cell types is approached in virtually identical fashion because, in contrast to small cell carcinoma of the lung, NSCLC more frequently presents with localized disease at the time of diagnosis and is thus more often amenable to surgical resection but less frequently responds to chemotherapy and irradiation. Cigarette smoking is etiologically related to the development of NSCLC in the great majority of cases. Genetic mutations in dominant oncogenes such as K-ras, loss of genetic material on chromosomes 3p, 11p, and 17p, and deletions or mutations in tumor suppressor genes such as rb and p53 have been documented in NSCLC tumors and tumor cell lines. NSCLC is diagnosed because of symptoms related to the primary tumor or regional or distant metastases, as an incidental finding on chest radiograph, or rarely because of a paraneoplastic syndrome such as hypercalcemia or hypertrophic pulmonary osteoarthropathy. Screening smokers with periodic chest radiographs and sputum cytologic examination has not been shown to reduce mortality. The diagnosis of NSCLC is usually established by fiberoptic bronchoscopy or percutaneous fine-needle aspiration, by biopsy of a regional or distant metastatic site, or at the time of thoracotomy. Pathologically, NSCLC arises in a setting of bronchial mucosal metaplasia and dysplasia that progressively increase over time. Squamous carcinoma more often presents as a central endobronchial lesion, while large cell and adenocarcinoma have a tendency to arise in the lung periphery and invade the pleura. Once the diagnosis is made, the extent of tumor dissemination is determined. Since most NSCLC patients who survive 5 years or longer have undergone surgical resection of their cancers, the focus of the staging process is to determine whether the patient is a candidate for thoracotomy with curative intent. The dominant prognostic factors in NSCLC are extent of tumor dissemination, ambulatory or performance status, and degree of weight loss. Stages I and II NSCLC, which are confined within the pleural reflection, are managed by surgical resection whenever possible, with approximate 5-year survival of 45% and 25%, respectively. Patients with stage IIIa cancers, in which the primary tumor has extended through the pleura or metastasized to ipsilateral or subcarinal lymph nodes, can occasionally be surgically resected but are often managed with definitive thoracic irradiation and have 5-year survival of approximately 15%.(ABSTRACT TRUNCATED AT 400 WORDS)

Biopsy, Needle↗
PubMedDate not supplied

Laboratory parameters as an alternative to performance status in prognostic stratification of patients with small cell lung cancer.

Pretreatment performance status (PS)is a major prognostic factor for both treatment response and survival duration in cancer clinical trials. PS is, however, a subjective index that may be markedly influenced by acute self-limited events. The objective of this study was to develop a prognostic index, based on pretreatment laboratory results, that might serve as an alternative to PS in patients with small cell anaplastic lung cancer. Results have been analyzed in 56 newly diagnosed patients with a minimum followup of 10 months and a median followup of 21 months. Patients were divided into high and low groups for each laboratory parameter based on readings either above or below the median value. Patients with high hemoglobin or albumin levels or low serum alpha-1 globulins, gamma globulins, or LDH survived significantly longer than patients with the opposite levels. When these factors were evaluated by multivariate analysis, albumin and hemoglobin were the most influential prognostic factors for survival. After inclusion of these two laboratory parameters, PS was no longer a significant prognosticator of survival. An objective prognostic index based on pretreatment laboratory results appears feasible in patients with small cell lung cancer.

Carcinoma, Small Cell↗
PubMedDate not supplied

Phase II trial of cisplatin in small cell carcinoma of the lung.

Eighteen patients with histologically documented small cell carcinoma of the lung who had failed initial combination chemotherapy regimens were treated with single-agent cisplatin in a dose of 100 mg/m2 every 3 weeks, with mannitol and fluid diuresis. Tumor regression was limited to one partial response (response rate, 6%; 95% confidence limits. 1%-27%). Significant toxic effects were gastrointestinal (severe nausea and vomiting in 12 of 14 patients) and hematologic (severe leukopenia in one patient and severe thrombocytopenia in three). The antitumor efficacy of high-dose cisplatin in heavily pretreated patients with small cell carcinoma of the lung appears to be marginal.

Aged↗
PubMedDate not supplied

Phase I trial of pentamethylmelamine: a clinical and pharmacologic study.

Pentamethylmelamine (PMM) is a water-soluble monodemethylated derivative of hexamethylmelamine and has a similar spectrum of activity against murine tumors. Unlike hexamethylmelamine, it is suitable for parenteral administration. We conducted a phase I trial of PMM given as a weekly 1-hour iv infusion to 34 extensively pretreated patients with advanced solid tumors. Eight dose levels ranging from 80 to 1500 mg/m2 were studied. A median of three infusions (mean, 4.2; range, 1-24) were given to each patient. Severe nausea and vomiting was dose-limiting at 1500 mg/m2; it was unresponsive to antiemetics and persisted up to 48 hours. Mild to moderately depressed levels of consciousness were seen in one third of the patients at dose levels of greater than or equal to 750 mg/m2. Consistent dose-related myelosuppression was not observed. Hepatocellular toxicity manifested by elevated serum transaminases occurred sporadically, usually in patients with liver metastases, but could not be unequivocally attributed to the drug. No complete or partial tumor responses were noted. At each dose level, the pharmacokinetics of PMM disappearance from plasma were studied in one to three patients with a gas chromatograph-mass spectrometer assay which exclusively measured the unmetabolized drug. The data obtained wee consistent with a two-compartment model of drug distribution, with a mean dose-independent terminal half-life of 143 minutes (range, 43-370). Peak drug levels were directly proportional to dose. The relative lack of myelotoxicity would make PMM an attractive candidate for addition to combination regimens if antitumor activity at tolerable doses could be documented. On this schedule, the recommended dose is 100 mg/m2 for phase II trials.

Adult↗