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Biomedical subjects

A Di Landro

Publications and source records attributed to A Di Landro.

At least 19 recordsLinked to original sources
PubMed2000

p53, cyclin-D1, PCNA, AgNOR expression in squamous cell cancer of the lip: a multicenter study.

BACKGROUND: The development of squamous cell carcinoma of the lower lip is an interesting model of photocarcinogenesis because of the structural and topographic characteristics of the lips. The purpose of this study was to evaluate the expression of immunohistochemical markers on the lips of patients with lower lip squamous cell carcinoma (LLSCC), compared with a control population. METHODS: Of the 98 subjects involved in the study, 58 were suffering from squamous cell carcinoma of the lower lip. The remaining 40 acted as a control. The case studies were taken from six university and hospital dermatology and plastic surgery departments. Questionnaires were administered to assess the risk factors for LLSCC. The cases involving squamous cell carcinoma underwent surgical excision and punch biopsy specimens were obtained from 20 control patients. Tissues were prepared in 5-microm-thick sections to carry out the following immunohistochemical study: PCNA, p53, AgNOR, cyclin-D1, bcl-2. RESULTS: The lower lip was the predominant location of squamous cell carcinoma, with the following factors playing important roles: chronic sun exposure, history of smoking, alcohol use and familial risk of cutaneous tumors. The male/female ratio in our survey was 5:1. The p53 protein was positive in approximately 50% of SCC cases and in 20% of controls. This protein is mostly associated with chronically photoexposed skin areas. AgNOR positivity increased with the loss of cellular differentiation; a progressive increase in size and a poorly defined shape were evident in poorly differentiated carcinomas. CONCLUSIONS: The results of this multicenter study showed that there is a noticeable difference in the expression of PCNA, p53, cyclin-D1, and AgNOR in tissues from patients with LLSCC and controls.

Aged↗
PubMed1997

Autoimmune C1 inhibitor deficiency and angioedema.

C1 inhibitor (C1-INH) deficiency results in bouts of mucocutaneous edema and may be inherited (hereditary angioedema) or acquired (acquired angioedema). The syndrome of acquired angioedema, characterized by the adult onset of angioedema and by the lack of evidence of inheritance of the disease, may be associated with lymphoproliferative or other malignant diseases (type I) or with the presence of autoantibodies to C1-INH (type II); this is a rare variant form of C1-INH deficiency with angioedema. We report here a case of acquired C1-INH deficiency with angioedema, hypotension and abdominal discomfort observed in a 71-year-old man in whom complement abnormalities and autoantibodies against C1-INH have been observed and who was classified as having an autoimmune C1-INH deficiency. From the therapeutic point of view after resolution of the acute attacks, high doses of tranexamic acid have been able, at first, to decrease the frequency and the severity of the symptoms, and subsequently to provide a long symptom-free time.

Aged↗
PubMed1995

Idiopathic atrophy of the nails: clinical and pathological study of 2 cases.

BACKGROUND: Whether idiopathic atrophy of the nails (IAN) should be considered a separate entity or a clinical variant of nail lichen planus is still controversial. OBJECTIVE: We report here the pathological study of 2 patients with IAN. METHODS: Our patients had similar clinical features consisting of severe nail atrophy with and without pterygium. RESULTS: The nail matrix architecture was markedly deformed with complete disappearance of the keratogenous zone that was replaced by a 3- to 10-cell-thick granular layer. CONCLUSION: The hypothesis that IAN is an acute and self-limited variety of lichen planus is still the most presumable. Even though this hypothesis can not be definitely proven, it is nevertheless not excluded by the clinical and pathological findings of our cases.

Adult↗
PubMed1992

Segmental lentiginosis with "jentigo" histologic pattern.

We report a case of segmental lentiginosis (unilateral lentiginosis), that is, asymmetric distribution of lentigines on one side of the body, in a 23-year-old woman. Lesions involved the right side of the face and the cervical region, mostly within the area of division of the trigeminal nerve. Histologic examination disclosed a lentiginous pattern as well as some nests of melanocytes at the dermal-epidermal junction (so-called jentigo pattern). Similar cases have been described in the literature under the term "zosteriform lentiginous nevus," which in our opinion makes for confusion since the same term has also been used to describe cases that fit the diagnostic criteria for speckled lentiginous nevus (nevus spilus).

Adult↗
PubMed1988

HLA-DR and DQ antigens in lichen planus.

A study on HLA-DR and DQ typing in 40 patients with lichen planus (26 males and 14 females) and in 92 normal blood donors of both sexes was performed. Twenty-seven patients had cutaneous lesions, 11 cutaneous and mucosal involvement and 2 patients had oral erosive lesions. Serological typing revealed a highly significant increase of HLA-DR 1 antigen in the patient group. No difference has been observed on the prevalence of DR1 antigen among the different clinical status of the disease.

Adult↗
PubMed1980

Effect of acute and repeated administration of gamma aminobutyric acid (GABA) on growth hormone and prolactin secretion in man.

A single oral dose of 5 g gamma aminobutyric acid (GABA) was given to 19 subjects and serial venous blood samples were obtained before and 3 h after drug administration. A placebo was administered to 18 subjects who served as controls. GABA caused a significant elevation of plasma growth hormone levels (P less than 0.001), but did not consistently alter plasma prolactin concentration since only 5 out of 15 subjects showed an increase of the hormone. Eight additional subjects were submitted to an insulin tolerance test before and after per os administration of 18 g GABA daily for 4 days. Protracted GABA treatment significantly blunted the response of growth hormone and enhanced that of prolactin to insulin hypoglycaemia (P less than 0.01). These results indicate that pharmacological doses of GABA affect growth hormone and prolactin secretion in man. The precise nature of GABA's effects as well as its mechanism of action remains to be clarified.

Administration, Oral↗
PubMed1979

Effect of two prostaglandin synthesis inhibitors, indomethacin and acetylsalicylic acid, on plasma ACTH and cortisol levels in man.

The aim of this study was to investigate the possible role of prostaglandins (PG) in the control of the hypohtalamic-pituitary-adrenocortical axis in normal volunteers. Acute oral administration of 100 mg indomethacin (ID) or 1.5 g acetylsalicylic acid (ASA) did not alter ACTH and cortisol plasma levels. Administration of 300 mg daily ID for 4 days delayed the onset, but increased the magnitude, of the response of ACTH to insulin hypoglycaemia, while it blunted the cortisol response. Administration of 3.2 g ASA daily depressed ACTH response to hypoglycaemia leaving the cortisol response unchanged, except for a 15 min delay in onset. These results are interpreted assuming that ID and ASA chiefly acted at the pituitary and hypothalamic level, respectively, and that ID, but not ASA, interfered with adrenocortical cortisol production. Our findings support the concept, based on animal studies, that PG enhance hypothalamic CRF release and adrenocortical steroidogenesis and may restrain ACTH secretion in the pituitary.

Administration, Oral↗
PubMed1977

Effects of acetylsalicylic acid and indomethacin on growth hormone secretion in man.

To investigate the possibility that prostaglandins (PG) take part in the control of growth hormone (GH) secretion in humans, we have studied the effects of protracted and acute administration of acetylsalicylic acid (ASA) and indomethacin (ID), two PG synthesis inhibitors, on basal and insulin-stimulated GH secretion in normal volunteers. In eight subjects, oral administration of 3-2 g daily of ASA for 4 days clearly reached GH response to insulin hypoglycemia (p less than 0.01, ANOVA). In six additional subjects, GH response to hypoglycemia was not modified by a 4-day oral treatment with 300 mg daily of ID. The pattern of plasma free fatty acids (FFA) and blood glucose during the insulin tolerance test was not significantly affected by ASA treatment. After ID the O time value of the above parameters was somewhat higher than under basal conditions, while the drop of blood glucose, but not to FFA, was slightly more pronounced. Acute oral administration of 1.5 g ASA in 12 subjects did not appreciably modify baseline plasma GH, FFA, and blood glucose levels. By contrast, a single oral dose of 100 mg ID in 12 subjects caused a moderate but significant rise (p less than 0.05) of plasma GH levels together with a clear elevation (p less than 0.01) of plasma FFA and blood glucose levels with respect to a group of controls treated with a placebo. Collectively these results are compatible with the possibility that PG play a physiologic stimulating role in the control of GH secretion, although an effect of ASA and ID unrelated to PG inhibition cannot be ruled out, In any event, in view of the number of endocrine and metabolic alterations induced by ASA and ID, these drugs seem to merit further study.

Adult↗