A. Di Landro
University of Milan
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Metabolism-clinical and Experimental | 1977
F. Cavagnini; A. Di Landro; Cecilia Invitti; U. Raggi; P. Alessandrini; M. Pinto; G. Girotti; P. Vigo
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.
Contact Dermatitis | 1989
R. Valsecchi; A. Di Landro; Paolo D. Pigatto; T. Cainelli
I. Wilkinson J D, Hambly E M, Wilkinson D S. Comparison of patch test results in two adjacent areas of England (II). Medicaments. Acta Dermato-venereologica 1980: 60: 245-249. 2. North American Contact Dermatitis Group. Epidemiology of contact dermatitis in North America, 1972. Arch Dermatol 1973: 108: 537-554. 3. Rietschel R L, Adams R M, Maibach HI, Storrs F J, Rosenthal L E. The case for patch test readings beyond day 2. J Am Acad Dermatol 1988: 18: 42-45. 4. MacFarlane A W, Curley R K, Graham R M, Lewis-Jones S, King C M. Delayed patch test Contact Dermatitis 1989: 21: 345
Contact Dermatitis | 2005
A. Di Landro; R. Valsecchi; Lorenzo Marchesi
Recently, temporary paint-on tattoos have become increasingly popular as a safe alternative to permanent tattoos not only in Asia and Northern Africa but also in our countries. The most common dye for such temporary tattoos is henna, a vegetable dye obtained from the dried leaves of a shrub (Lawsonia inermis), used for thousands of years to colour the hair and the skin for the ritualistic staining. Allergic reactions to this compound have frequently been reported in adults, rarely in childhood. The most likely causative agent for the eczematous reactions is p-phenylendiamine (PPD) present in the commercial black henna, added to obtain a dark, blackish colour. We describe the case of a little baby who had an allergic contact dermatitis due to temporary paint-on tattoos with a persistent hypopigmentation after the resolution of the eczematous lesions.
Contact Dermatitis | 2002
A. Di Landro; V. Greco; R. Valsecchi
A 3-month-old black girl presented with an eczematous dermatitis extending not only over the outer and upper buttocks but also over the hips, dating from 1 month before, always in this same area (Fig. 1). The mother denied any family history of atopy. At a 15-day follow-up, the dermatitis had been resistant to treatment (topical hydrocortisone and oral antihistamine) and only resolved when use of the diaper was eliminated and cotton pants substituted. One month later, the mother reported that the dermatitis had recurred after further use of the diaper. Because of the patient’s young age, we performed patch tests with a restricted European standard series, including thiuram mix, mercapto mix and mercaptobenzothiazole, augmented with a rubber series, a corticosteroid series and cyclohexyl thiophthalimide 1%, reagents supplied by Chemotechnique on IQ Chambers.
British Journal of Dermatology | 2000
A. Di Landro; Lorenzo Marchesi; A. Reseghetti; T. Cainelli
Sir, Molluscum contagiosum (MC) is a poxvirus skin infection that often complicates the course of patients with acquired or iatrogenic immunosuppression. Both the clinical and histological features of disease in these cases may be atypical. We report the unique clinical and histological features of a case of fulminant MC infection with concomitant leukaemia cutis in a patient with relapse of chronic myeloid leukaemia (CML) after allogeneic bone marrow transplantation (BMT). A 49-year-old Chinese woman underwent BMT (conditioning: busulphan, cyclophosphamide, total body irradiation) from an HLA identical sister for Ph positive CML in accelerated phase. She engrafted uneventfully with no chronic graft-vs.-host disease (GVHD). Serial bone marrow reassessments, up to 18 months post-BMT, were negative for residual disease by polymerase chain reaction and cytogenetics. At 36 months, she was found to have haematological relapse of CML, with cytogenetic subclonal evolution. She was treated with hydroxyurea and donor lymphocyte infusions (DLI) (6 ́1 10 kg cells infused in three doses) to enhance the graft-vs.-leukaemia (GVL) effect. There was good control of the peripheral cell counts and no evidence of GVHD. A repeat marrow biopsy at 40 months showed suppression of the abnormal clone to 3% of analysed metaphases. Unfortunately, at 46 months the disease progressed again with increased neutrophil counts (52 10 L), and leukaemia cutis documented by skin biopsy (Figs 1a, 1b). This was treated with combination chemotherapy (cytosine arabinoside 150 mg 5, thioguanine 160 mg 5) resulting in normalization of cell count and resolution of all skin lesions. A second course of DLI (4 ́2 10 kg cells) was administered at 49 months post-BMT. Three weeks after DLI, however, the patient presented with a dense eruption of erythematous papular lesions over the entire face, upper limbs and upper trunk. Photography of the lesions was refused. A biopsy of one lesion showed lobules of abnormal epidermal cells with cytoplasm packed with eosinophilic viral inclusion bodies (Fig. 2a). Electron microscopy showed numerous intracytoplasmic poxvirus particles (240 95 nm in size) within the abnormal epidermal cells, consistent with MC (Fig. 2b). In addition, an infiltrate of promyelocytes and immature myeloid blast cells was seen, consistent with recurrent leukaemia cutis. She died 1 week later of an intracranial haemorrhage, probably related to intracerebral disease. The use of DLI is the treatment of choice for relapse of CML after BMT. The main side-effects are profound marrow and immune suppression, with or without acute and chronic GVHD. Reactivation of dormant DNA viruses like cytomegalovirus, varicella zoster and hepatitis B viruses are potential complications of immunosuppression caused by DLI. This is the first report of severe MC complicating DLI. In immunosuppressed hosts, due to the fulminant replication of the poxvirus, the clinical and pathological features of MC can be highly variable, and aggressive treatment is often needed. Viral particles have even been found in the histologically normal skin epidermis adjacent to MC lesions in patients infected with HIV. There have been two previous reports of skin changes in MC mimicking haematological malignancy involving the skin. In our case, the clinical setting and pathological features are highly supportive of a genuine double pathology. It is recognized that post-BMT patients have an increased incidence of leukaemic involvement of extramedullary sites, including the skin. The incidence may be even higher in patients salvaged with DLI, due to a weaker GVL effect outside the marrow. The precise colocalization of MC replication and leukaemic infiltration in the skin lesions may have been due to a high concentration of chemotactic
Contact Dermatitis | 1993
R. Valsecchi; Bruno Pansera; A. Di Landro; T. Cainelli
Case no. 1 A 36-year-old man presented in May 1992 with an erythematous, edematous, vesicular dermatitis with severe itching of the abdomen, inguinal region and legs. His practitioner had prescribed a cream containing ketoconazole for tinea cruris. 2 weeks later, the patient developed intensely itchy erythema, edema and vesicles in the inguinal region, with subsequent spread to the abdomen and legs. The dermatitis completely cleared with boric acid solution dressings and topical and systemic corticosteroid therapy within 2 weeks. There was no personal or family history of atopy, contact dermatitis or previous drug reaction. A month later, he was patch tested with the GIRDCA standard series and Nizoral cream (as is). At 3 days, there was a + + + reaction to the cream. Subsequent patch tests with the pure imidazole component of the cream (1% and 2% eth.) and with other ingredients were carried out. All reactions were negative, except for a + + + reaction to ketoconazole.
The Journal of Clinical Endocrinology and Metabolism | 1977
F. Cavagnini; Cecilia Invitti; A. Di Landro; L. Tenconi; C. Maraschini; G. Girotti
European Journal of Endocrinology | 1980
F. Cavagnini; Cecilia Invitti; M. Pinto; C. Maraschini; A. Di Landro; A. Dubini; A. Marelli
The Journal of Clinical Endocrinology and Metabolism | 1976
F. Cavagnini; U. Raggi; Piero Micossi; A. Di Landro; Cecilia Invitti
Contact Dermatitis | 2007
R. Valsecchi; P. Leghissa; A. Di Landro; F. Bartolozzi; M. Riva; C. Bancone