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At least 73 records · Page 4Linked to original sources
PubMed2003

Review of the safety, tolerability, and drug interactions of the new antifungal agents caspofungin and voriconazole.

Managing invasive fungal infections often presents a challenge for clinicians in the treatment of immunocompromised patients. Two very different systemic antifungal agents, voriconazole and caspofungin, have recently been introduced into the market place. Voriconazole is a new triazole antifungal, while caspofungin is the first echinocandin antifungal. Voriconazole acts by inhibiting the synthesis of ergosterol in the fungal cell membrane. Caspofungin inhibits beta-1,3-D-glucan synthesis in the cell wall, a target present in fungal cells, but absent from mammalian cells. Both agents are broad-spectrum, with efficacy against invasive Aspergillus and Candida infections. The safety and tolerability profile of caspofungin presented with a low incidence of adverse events in clinical trials. Pending further data, coadministration of cyclosporine has been recommended only if the benefit outweighs the risk for patients. Voriconazole has three important side-effects that the clinician must consider: liver abnormalities, skin abnormalities and visual disturbances. Liver abnormalities in particular should be monitored very carefully. The drug interaction profile of voriconazole also warrants a careful evaluation of the concomitant medication, mainly due to cytochrome P450 metabolism. This article reviews the available data concerning the safety and tolerability profiles of each drug, as well as drug interactions and contraindications.

Antifungal Agents↗
PubMed1993

The association between an abnormal nuchal skin fold, trisomy 21, and ultrasound abnormalities identified during the second trimester of pregnancy.

Fetal echocardiography and a detailed non-cardiovascular ultrasound examination were performed prospectively between 14 and 23 weeks of gestation prior to genetic amniocentesis in 2800 consecutive fetuses at increased risk for trisomy 21 due to advanced maternal age or a low maternal serum alpha-fetoprotein. An abnormal nuchal skin fold was defined as >or=6 mm. Of 2800 fetuses, 23 (0.82%) had an abnormal nuchal skin fold. Seven of 35 fetuses (20%) with trisomy 21 and one of 12 fetuses (8.3%) with trisomy 18 had an abnormal nuchal skin fold. Of the 23 fetuses with an abnormal nuchal skin fold, seven (30.4%) had trisomy 21, one (4.4%) trisomy 18, one (4.4%), 46,XY,11p+ and 14 (60.8%) had normal karyotypes. The fetuses with trisomy 18 and 46,XY,11p+ had malformations of the cardiovascular and non-cardiovascular organ systems. Five of seven (71%) fetuses with trisomy 21 and an abnormal nuchal skin fold had abnormalities of both the cardiovascular and non-cardiovascular organ systems; one of seven (14.5%) had a heart defect only; and one of seven (14.5%) an abnormality of a non-cardiovascular organ system. Of the 14 fetuses with an abnormal nuchal skin fold and normal karyotype, seven had no additional abnormalities, six an abnormality of the heart, and one a non-cardiovascular defect. Fetuses with an abnormal nuchal skin fold had a significant increased incidence of trisomy 21 when a combination of cardiovascular and non-cardiovascular abnormalities were present compared to fetuses with no additional defects or a single defect of the heart or non-cardiovascular organ system (p = 0.001). In fetuses with an abnormal nuchal skin fold, the incidence of congenital heart disease was 6155, central nervous system defects 17%, hyperechoic bowel 8.7%, and renal abnormalities 17.4%. These findings would suggest that the fetus identified with an abnormal nuchal skin fold with additional cardiovascular and non-cardiovascular abnormalities has a greater risk for chromosomal aneuploidy compared to the fetus with an isolated abnormal nuchal skin fold or with one additional abnormality of the heart or a non-cardiovascular organ system. When an abnormal nuchal skin fold is identified, careful evaluation of the fetal cardiovascular system should be made.

Journal Article↗
PubMed2003

Expression and localization of peroxisome proliferator-activated receptors and nuclear factor kappaB in normal and lesional psoriatic skin.

Abnormal epidermal proliferation and differentiation characterize the inflammatory skin disease psoriasis. Here we demonstrate that expression of PPARdelta mRNA and protein is markedly upregulated in psoriatic lesions and that lipoxygenase products accumulating in psoriatic lesions are potent activators of PPARdelta. The expression levels of NF-kappaB p50 and p65 were not significantly altered in lesional compared with nonlesional psoriatic skin. In the basal layer of normal epidermis both p50 and p65 were sequestered in the cytoplasm, whereas p50, but not p65, localized to nuclei in the suprabasal layers, and this distribution was maintained in lesional psoriatic skin. In normal human keratinocytes PPAR agonists neither impaired IL-1beta-induced translocation of p65 nor IL-1beta-induced NF-kappaB DNA binding. We show that PPARdelta physically interacts with the N-terminal Rel homology domain of p65. Irrespective of the presence of agonists none of the PPAR subtypes decreased p65-mediated transactivation in keratinocytes. In contrast p65, but not p50, was a potent repressor of PPAR-mediated transactivation. The p65-dependent repression of PPARdelta- but not PPARalpha- or PPARgamma-mediated transactivation was partially relieved by forced expression of the coactivators p300 or CBP. We suggest that deficient NF-kappaB activation in chronic psoriatic plaques permitting unabated PPARdelta-mediated transactivation contributes to the pathologic phenotype of psoriasis.

CD36 Antigens↗
PubMed1986

Permeability of abnormal rat skin.

We have measured the permeability (to water in vivo and in vitro) and examined the histology of rat skin after mild, superficial epidermal alterations: scalpel blade (Cat I) and sandpaper abrasion (Cat II), adhesive tape stripping (Cat III), and suction blister top removal (Cat IV). After each alteration the permeability was increased (Cat IV greater than Cat III greater than Cat II greater than Cat I) and the epidermis regenerated in a distinct, biphasic manner, as indicated by the permeability and histology data. The rapid first phase corresponded with a decrease in permeability and the development of a scab (the greater the increased permeability, the slower the rate of regeneration). The second phase was more gradual (with a similar rate of regeneration after each alteration) and corresponded with a return to normal permeability and gradual thickening of the stratum corneum (return to normal corresponded with degree of initial stratum corneum removal). A similar, though slower biphasic regeneration has been reported to occur in human skin following similar types of alterations. It is concluded that abnormal rat skin is suitable for quantifying absorption through abnormal epidermis.

Animals↗
PubMed1987

Limited joint mobility and other rheumatological manifestations in diabetic patients.

Limited joint mobility was diagnosed in 42.9% of Type I and 37.3% of Type II diabetic patients. Abnormally thick skin was detected in 31.4% of Type I and 33.7% of Type II diabetic patients. Skin abnormalities were observed mainly in patients with L.J.M. There was a high prevalence of hand flexor tendon abnormalities (18.6%). Decreased range of shoulders and hips and flexor tendon abnormalities were significantly more common in patients with LJM. No significant association was found between LJM and grip strength, joint complaints, family history of rheumatic diseases, hypoglycemic attacks, cardiovascular diseases and autonomic neuropathy.

Adolescent↗
PubMed2000

A TGF-beta-inducible cell adhesion molecule, betaig-h3, is downregulated in melorheostosis and involved in osteogenesis.

Melorheostosis is a rare bone disease characterized by linear hyperostosis and associated soft tissue abnormalities. The skin overlying the involved bone lesion is often tense, shiny, erythematous, and scleodermatous. In order to look for genes differentially expressed between the normal and involved skin, we cultured skin fibroblasts from the skin lesions of several afflicted patients, and identified differentially expressed genes by reverse dot-blot hybridization. We found that the genes human TGF-beta-induced gene product (betaig-h3), osteoblast-specific factor 2, osteonectin, fibronectin, and type I collagen were all downregulated in the affected skin fibroblasts, with betaig-h3 the most significantly affected. The expression of betaig-h3 was induced by TGF-beta in both affected and normal fibroblasts. In an effort to determine the mechanism of bone and skin abnormalities in melorheostosis, we made recombinant betaig-h3. Both immobilized and soluble recombinant betaig-h3 proteins with or without an RGD motif inhibited bone nodule formation of osteoblasts in vitro. Taken together, our results suggest that altered expression of several adhesion proteins may contribute to the development of hyperostosis and concomitant soft tissue abnormalities of melorheostosis, with betaig-h3 in particular playing an important role in osteogenesis.

Animals↗
PubMed1997

Systemic sclerosis associated with diabetes insipidus.

A rare case of systemic sclerosis that preceded the development of diabetes insipidus is reported. This 25-year-old man presented with Raynaud's phenomenon and ulceration of the tip of the right thumb. The diagnosis of systemic sclerosis was based on findings of proximal scleroderma, sclerodactyly, serological abnormalities, and skin abnormalities verified histologically. Partial central diabetes insipidus was later diagnosed after the sudden appearance of polyuria and polydipsia. Coexistence of systemic sclerosis with diabetes insipidus suggests that diabetes insipidus in this patient might have occurred via an autoimmune mechanism.

Adult↗
PubMed1987

[Clinical aspects of Menkes syndrome].

The difficulties of early diagnosis of Menkes' kinky hair syndrome are described guided by the clinical courses of three related patients. One of these children could be observed continuously from birth. Different from other descriptions the diagnostic value of the clinical features observed in our patients is estimated as follows: 1. severe cerebral degeneration with seizures in the first year of life; 2. subdural hygroma; 3. decreased levels of serum copper and serum coeruloplasmin; 4. hair abnormalities; 5. skin abnormalities. The diagnosis is likely, if serum copper and serum coeruloplasmin are decreased. The diagnosis is proved by increased copper uptake into cultured fibroblasts. The prenatal diagnosis is possible by chorionic villus biopsy or amniocentesis. The importance of carrier detection by cultured fibroblasts and subsequent genetic counselling is underlined.

Brain↗
PubMed1996

Polymyositis developing after prolonged injections of pentazocine.

Pentazocine is a frequently used analgesic drug. Numerous complications have been reported in association with its use, including skin fibrosis, skin ulceration, abnormal skin pigmentation and symmetrical myopathy. Fibrous myopathy is a rare but conspicuous complication of prolonged pentazocine injection. However, inflammatory myopathy has not previously been related to this substance abuse. We describe a patient who developed polymyositis after 13 months of pentazocine injections.

Abdominal Pain↗