Search PubMed⌕ Search

Biomedical subjects

H M Lemon

Publications and source records attributed to H M Lemon.

At least 55 records · Page 3Linked to original sources
PubMed1977

The glucagonoma syndrome and its management.

The glucagonoma syndrome occurs in some but not all patients with a benign or malignant islet cell tumor and hyperglucagonemia. Manifestations may include anemia, diabetes mellitus, pruritic skin rash, glossitis, stomatitis, weight loss, diarrhea, flexible fingernails, venous thromboses, low plasma amino acid levels, and coarse folds of the jejunum and ileum. Most patients are postmenopausal women, but men and women ages 40 to 65 have been affected. The course is variable depending upon the nature of the underlying tumor. Twenty-two cases of probable glucagonoma syndrome have been reported; twelve documented with glucagon levels. The hyperglucagonemia results from elevation of the proglucagon and true glucagon immunoreactive fractions of pancreatic glucagon. Management of the rash can be accomplished rarely with topical or systemic antibiotics or corticosteroids. If the tumor is resectable, surgery reverses the syndrome. Patients with metastatic disease have responded to streptozotocin and DTIC.

Adenoma, Islet Cell↗
PubMed1977

The therapeutic dilemma of carcinomas of unknown origin.

The charts of 23 patients with metastatic carcinoma were reviewed retrospectively in hospitalized patients who had no apparent primary lesion. Eleven patients eventually had autopsies. The primary became apparent in 8 patients either pre- or post mortem. Treatment by operative intervention, and/or radiation therapy, and/or chemotherapy are discussed. The discussion reviews mechanisms of metastasis, problems in pathological interpretation, and considerations for evaluation of such patients.

Adult↗
PubMed1977

Clinical and experimental aspects of the anti-mammary carinogenic activity of estriol.

Intermittent implantation of 600--1,300 microgram estriol subcutaneously beginning 48 h before oral administration of 7,12-dimethylbenz(a)anthracene or procarbazine prevents development of 80--90% of carcinomas of the breast occurring during the natural life span of the intact female Sprague-Dawley rat. Some estriol precursors were less inhibitory of breast cancer development among 23 other estrogens and androgens, progestins and glucocorticoids tested. More frequent or lower estriol doses than 100--200 microgram/kg/24 h every 2 months were less inhibitory of breast carcinogenesis. No other types of neoplasms were reduced in incidence by estriol implants, which also reduced uterine weights by 20--25%. Intermittent substitution of estriol for estrone or estradiol in the nuclear receptor complexes of target cells probably accounts for these observations, which resemble the effect of castration in reducing breast cancer incidence. Human studies indicate excellent tolerance for oral estriol doses of 10--200 microgram/kg/24 h, which may correct subnormal estriol/estrone + estradiol urinary quotients associated with elevated risk of breast carcinogenesis in epidemiologic investigations.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1976

Distribution of plasma glucagon immunoreactivity in a patient with suspected glucagonoma.

Gel filtration of plasma from a patient with a clinical syndrome of glucagonoma and a total plasma glucagon level of 2600 pg/ml, revealed the four glucagon immunoreactive fractions found in normal subjects. The total hyperglucagonemia observed was due to high levels of true glucagon and proglucagon moieties. The so-called "big plasma glucagon" (BPG) measured 190 pg/ml (normal average 113 +/- 79 pg/ml, Mean +/- SD, N = 10); the large glucagon immunoreactivity, LGI (9000 mol wt), measured 625 pg/ml (normal average 11 +/- 16 pg/ml); the true glucagon accounted for 1435 pg/ml (normal average 31 +/- 29 pg/ml); and the small glucagon immunoreactive fraction (approximately 2000 mol wt) measured 35 pg/ml (normal average 26 +/- 18 pg/ml). The high levels of LGI, considered a candidate for proglucagon, may reflect the increased secretory activity of the tumor.

Adenoma, Islet Cell↗
PubMed1976

Quadrichemotherapy for advanced ovarian carcinoma.

In an effort to improve the length and rate of objective responses in patients with advanced ovarian carcinoma, a combination of four drugs was administered. Vincristine (10 mug/kg intravenously weekly), actinomycin D (500 mug intravenously weekly), oral methotrexate (1.25 mg daily), and oral cyclophosphamide (50 mg daily) were given to 25 evaluable patients with FIGO Stage III and IV ovarian carcinoma. After 12 weeks the vincristine and methotrexate were discontinued; cyclophosphamide and methotrexate were continued until disease progression was evident. Objective responses occurred in 56% of the patients. Toxicity was minimal. Patients not previously treated with radiotherapy or chemotherapy had a higher complete response rate (30%) than patients previously treated (13.3%). Mean length of complete response was 10.6+ months. The 1-year survival rate of these patients was 69.5% and the 5-year rate 22.7%. While the results are encouraging, single agent chemotherapy with an alkylating agent produces similar responses.

Carcinoma↗
PubMed1975

Estriol prevention of mammary carcinoma induced by 7,12-dimethylbenzanthracene and procarbazine.

The concentration of estrogenic, androgenic, progestational, and adrenocortical steroid hormones in body fluids of mature intact Sprague-Dawley female rats was increased by s.c. implantation of 5 to 7 mg NaCl pellets containing 1 to 20% steroid 48 hr before administration p.o. of either 7,12-dimethylbenz(a) anthracene or procarbazine. The incidence of rats developing one or more mammary carcinomas in each treated group was compared to that ovserved in simultaneously treated groups receiving only the carcinogen, steroid, or no treatment whatsoever, with weekly observation of all rats until palpably growing tumors were biopsied and proven carcinomatous or until death occurred from other causes determined by autopsy. A total of 105 untreated or steroid-implanted rats followed to death (234 to 256 days median observation) developed no breast carcinomas. Rats fed either of the carcinogens developed initial evidence of breast carcinoma, after 136 to 156 days median observation, in 51 to 57% of 318 total treated rats. Nonbreast carcinomas and sarcomas developed in 5 to 10% of the carcinogen-treated rats.

Animals↗