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V M Lauta

Publications and source records attributed to V M Lauta.

8 recordsLinked to original sources
PubMed1990

Maintenance treatment with recombinant interferon alfa-2b in patients with multiple myeloma responding to conventional induction chemotherapy.

The use of interferon for the induction treatment of multiple myeloma has been shown to be effective in about 20 percent of patients. We studied its effects on long-term survival when it was used for maintenance treatment. Between April 1985 and May 1988, 101 patients with symptomatic multiple myeloma who had had a substantial objective response or a lesser objective response with disappearance of symptoms ("disease stabilization") after 12 courses of induction chemotherapy were randomly assigned to receive recombinant interferon alfa-2b as maintenance therapy (n = 50) or to receive no treatment (n = 51). As of December 1989, 66 of the 101 patients have relapsed (25 given interferon and 41 not treated). The median duration of response (from the time of randomization) was 26 months in the patients given interferon and 14 months in the untreated patients (P = 0.0002). A total of 37 patients have died (14 given interferon and 23 not treated). The median duration of survival (from randomization) was 52 months in the interferon group and 39 months in the control group (P = 0.0526). Among the patients who had had a substantial objective response to induction chemotherapy, the difference in survival time was statistically significant (P = 0.03526). Interferon had to be stopped because of toxic effects in 3 of 12 patients initially treated with 10 MU (megaunits) per square meter of body-surface area. After the dose was reduced to 3 MU per square meter, the only toxic effect was a mild influenza-like syndrome lasting two to three weeks. We conclude that maintenance treatment with interferon prolongs response and survival in patients with multiple myeloma who have responded to conventional induction chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1990

[ACE: physiopathology and role in the diagnosis and prognosis of systemic granulomatosis, neoplasms and lung toxicity caused by antineoplastic agents].

Several studies have been performed in the last ten-years on the biochemical and physiopathologic properties of angiotensin-converting enzyme (ACE). Human lung and kidney are a rich source of ACE and the enzyme is bound to the plasma-membrane of vascular endothelial cells; however, the small intestine and the choroid plexus are also particularly rich in ACE, where it is concentrated on the surface of cuboidal epithelial cells facing the cerebrospinal fluid. The ACE is a glycoprotein with a molecular weight of 150,000 daltons and it cleaves C-terminal dipeptides of several oligo-peptides, including angiotensin I and bradykinin. It catalyzes conversion of angiotensin I to angiotensin II and induces inactivation of bradykinin. Synthetic acylated tripeptides such as radiolabelled hippuryl-histidyl-leucine and hippuryl-glycyl-glycine have been found to be the most suitable substrates for determining the activity of ACE with radiochemical assays. The mean-normal values for ACE activity is 25 U/ml; there are no significant differences in ACE activity between different sexes and races, but there is significant decrease in adults. The measurement of ACE activity in sarcoidosis suggests the following results: 1) There is a relationship between the increased SACE and LACE activity and active disease and between normal ACE activity and inactive disease. 2) Normal or decreased ACE activity is useful for therapeutic evaluation of sarcoidosis. 3) Increased SACE activity can be a sensitive parameter for predicting clinical relapse of the disease. An increased SACE activity is found in a wide variety of non-sarcoid granulomatous diseases and non-granulomatous systemic diseases. A decreased SACE and LACE activity is found in non-granulomatous pulmonary diseases such as "Adult Respiratory Distress Syndrome", lung cancer and lung toxicity caused by antineoplastic drugs. Moreover, a low preoperative SACE is associated with poor prognosis in lung cancer and its levels may be useful for predicting clinical relapse of this disorder after operation. Finally, a low SACE activity is found in malignant lymphomas, leukemia and multiple myeloma. A relationship is also found between decreased enzyme activity and a poor prognosis and clinical relapse of these diseases.

Adolescent↗
PubMed1987

Early-onset diagnosis of lung toxicity caused by cyclophosphamide, melphalan and procarbazine therapy.

Lung function studies were performed in 33 patients with lymphomyeloproliferative diseases (25 cases of multiple myeloma and 8 cases of Hodgkin's disease) who received cyclophosphamide, procarbazine, and melphalan therapy. Lung function was investigated by spirometric tests, indicative tests of small airways disease, and diffusing capacity of the lung for carbon monoxide (DUCO). Indicative tests of small airways disease and other lung function tests such as forced expiratory volume in 1 second (FEV1), vital capacity (VC), total lung capacity (TLC) etc. were markedly improved in 18 patients (55%), whereas 24 patients (73%) showed a decreased diffusing capacity of the lung for carbon monoxide. Furthermore, most of the patients (77%-83%) showed contemporaneous involvement of spirometric tests and DUCO. The DUCO was also found more constantly impaired than other function tests because it had decreased with and without other spirometric tests. Impaired lung function tests were found to be related to a cumulative dose of antineoplastic drugs. The absence of increased lung toxicity was found to be related to several drugs administered in combination. In view of the absence of previous bronchopathies, lung involvement signs in multiple myeloma (25, 26) or lymphoma, and concomitant bronchopneumonias, the impaired functional tests could be ascibed to drug-induced lung toxicity. In the absence of clinical symptoms, roentgenographic and pathologic features, impaired lung function tests may play a role as early-onset signs of drug-induced lung toxicity.

Adult↗