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Biomedical subjects

A Gervasi

Publications and source records attributed to A Gervasi.

9 recordsLinked to original sources
PubMed1987

A randomized study of methotrexate, bleomycin, hydroxyurea with versus without cisplatin in patients with previously untreated and recurrent squamous cell carcinoma of the head and neck.

The value of a combination of methotrexate, bleomycin and hydroxyurea with vs. without cisplatin was randomly examined in 62 evaluable patients with previously untreated (44 patients) and recurrent (18 patients) squamous cell carcinoma of the head and neck. Methotrexate (30 mg/m2) and bleomycin (15 mg) were given intravenously weekly, hydroxyurea (1000 mg/m2) per os 3 times per week for 4 weeks. Cisplatin (60 mg/m2) was added on Day 1 every month. A higher overall response rate was observed with the cisplatin-containing regimen (66%, included 17% complete) as compared with 27% (3% complete) with the 3-drug combination (P value 0.0025). The cisplatin-containing regimen was more active in both previously untreated patient group and in the group recurrent patients. Toxicity was more pronounced in the cisplatin regimen and necessitated frequently reduced drug dosages. No survival difference was observed between the treatment groups. Median survival in previously untreated patients was 16.2 months and 7.2 months in patients who failed conventional local treatment. It is concluded that a cisplatin-containing regimen is more effective in advanced head and neck carcinoma than the same combination without cisplatin.

Adult↗
PubMed1983

[High-dosage methylprednisolone as an antiemetic in cytostatic-induced vomiting].

The antiemetic efficacy of 375 mg methylprednisolone given as slow i.v. push injection was assessed in 27 tumor patients receiving strongly emetic cytostatic treatment. 13 of 27 patients were partially or completely protected from nausea and vomiting. Only minor side effects from methylprednisolone were observed: two patients complained of increased fatigue and four patients experienced facial rash with swelling 1 to 24 hours after the injection of methylprednisolone. High-dose methylprednisolone is an effective antiemetic treatment for patients receiving cancer chemotherapy.

Adult↗
PubMed1982

[Prevention of cytostatic-related hair loss by hypothermia of a hairy scalp using a cooling cap].

82 patients treated with adriamycin alone or in combination with other cytostatic agents underwent scalp hypothermia by application of a gel cap. The cap ws applied 10 minutes before the injection of the drugs and maintained until 30 minutes after the administration of the chemotherapy. Prevention of hair loss was achieved in 47 patients (57%). The prophylaxis was successful in 16 out of 21 males (76%) compared with 31 out of 61 female patients (p less than 0.05). No statistically significant difference was found between patients receiving higher or lower doses of adriamycin or between patients wtih or without liver dysfunction. The tolerance of the gel cap was excellent; only one patient did not tolerate the cap because of anxiety during application.

Alopecia↗
PubMed1981

[Nausea and vomiting during chemotherapy of malignant tumors].

Nausea and vomiting are frequent and unpleasant side effects of cancer chemotherapy. Current concepts of pathophysiology and clinical aspects of nausea and vomiting are reviewed. Individual and therapeutic factors are discussed which greatly modify the degree of vomiting. The commercially available antiemetics are tabulated and the individual classes of antiemetics are described. Finally, consideration is given to new approaches to the treatment of nausea and vomiting, including the search for new compounds and better use of currently available agents.

Antiemetics↗
PubMed1978

[Fat embolism syndrome without fractures].

Report on an 18-year-old patient who developed a respiratory distress syndrome after trauma without bone fractures and with only minimal soft tissue contusion. Twelve hours after the accident fever and dyspnea appeared, accompanied later by hemoptysis, microhematuria, a fall in hemoglobin and in platelet count, petechiae on the skin and in the conjunctiva, cotton-wool lesions in the retina and micronodular shadows in the lungs. Various pathogenetic mechanisms other than bone marrow fat embolism are discussed in the light of this case.

Accidents, Traffic↗
PubMedDate not supplied

[Familial hyperaldosteronism].

Primary aldosteronism is a disorder characterized by hypertension and hypokalemia due to aldosterone secretion out of renin-angiotensin control. It is generally caused by aldosterone-producing adenoma or adrenocortical hyperplasia but, in some cases, it is due to genetic alterations. Familial type I hyperaldosteronism is the result of anomalous regulation of aldosterone secretion from ACTH (which normally regulates cortisol synthesis). Aldosterone hypersecretion can be suppressed by exogenous glucocortcoids such as dexamethasone. This autosomal dominant disorder is caused by unequal cross-over between two genes with wide sequence homology: CYP11B1 and CYP11B2. The hybrid gene is the product of fusion between the ACTH-responsive regulatory portion of the 11b-hydroxylase gene (CYP11B1) and the coding region of the aldosterone synthase gene (CYP11B2). Familial type I hyperaldosteronism is a disease with incomplete penetration and variable expressivity, especially in relation to hypertension. The marked variability in hypertension severity can mirror an interaction between the hybrid gene and other hereditary factors involved in the regulation of blood pressure. Familial type II hyperaldosteronism is another autosomal dominant form of hyperaldosteronism due to aldosterone hyper-secretion not suppressible by dexamethasone. This disorder is unrelated to mutation of the hybrid gene. The genetic cause of type II hyperaldosteronism is presently unknown, but a genome-wide search has revealed that the disorder is linked with a locus on chromosome 7 in a region that corresponds to cytogenetic band 7p22.

Humans↗