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PubMedDate not supplied

Rosacea: where are we now?

Advances continue to be made in the classification and treatment of rosacea, a chronic dermatologic syndrome. A new empiric classification system identifies 4 rosacea subtypes (erythematotelangiectatic, papulopustular, phymatous, and ocular) that may aid in more precise diagnosis. Several new therapies have recently been approved for treatment of rosacea. Azelaic acid 15% gel is a new first-tier topical agent proven effective in reducing inflammatory lesions and erythema. New formulations of metronidazole and sulfacetamide 10%/sulfur 5% that offer cosmetic or tolerability advantages are now available. Intense pulsed light therapy has demonstrated effectiveness in reducing flushing, erythema, and telangiectases, with greater tolerability than existing laser systems. Other treatments under investigation include low-dose doxycycline hyclate (which may provide greater safety than existing oral antibiotics), benzoyl peroxide/clindamycin gel, and tacrolimus ointment (for steroid-induced rosacea). With this expanded armamentarium of medical and light-based therapies, clinicians can now implement a multifaceted approach to treatment, crafting new treatment combinations to address the unique and evolving features of rosacea in each individual patient.

Administration, Cutaneous↗
PubMed2005

Present and future rosacea therapy.

Despite its prevalence, rosacea has not received the same attention of researchers as other dermatologic disorders. Nevertheless, new pharmacologic and nonpharmacologic therapies for the condition continue to be developed. The future of rosacea treatment will probably involve a combination of drugs and devices. Certain core therapies (i.e., topical metronidazole, topical azelaic acid, oral tetracyclines, and topical sulfur/sodium sulfacetamide) are validated by the greatest amount of high-order clinical evidence and will undoubtedly remain first-line therapeutic choices. However, more research is necessary to validate the efficacy and safety of newer pharmacologic agents and light-based therapy. Because rosacea is a chronic condition, pharmacologic maintenance therapy is necessary to maintain remission.

Anti-Infective Agents↗
PubMed2005

Evidence-based dermatology.

Evidence-based dermatology (EBD) is the application of the principles of evidence-based medicine to the diagnosis and treatment of skin disorders. EBD does not discount the individual dermatologist's clinical judgment. In fact, EBD is based on the interaction of external evidence, the physician's clinical experience, and the patient's experience. Randomized controlled trials constitute one of the highest levels of evidence and are the gold standard for validating a therapeutic intervention. For the treatment of rosacea, oral tetracycline, topical metronidazole, topical azelaic acid, and topical sulfur/sodium sulfacetamide have been validated by more than one randomized controlled trial.

Anti-Infective Agents↗
PubMed2005

The pharmacologic therapy of rosacea: a paradigm shift in progress.

A number of topical and systemic pharmacologic therapies, some of which remain investigational, have been used to treat rosacea. The pathophysiology of rosacea appears to be inflammatory, and most of the interventions modulate the inflammatory process in some way. Topical agents include various formulations of sodium sulfacetamide and sulfur, metronidazole, azelaic acid, and benzoyl peroxide/clindamycin. Oral agents include antibiotics in conventional and subantimicrobial doses. A paradigm shift in progress in the management of rosacea encompasses the use of these and other agents either alone or, increasingly, in different combinations, based on the subtype of rosacea.

Adrenal Cortex Hormones↗
PubMedDate not supplied

Simultaneous determination of 16 sulfonamides in honey by liquid chromatography/tandem mass spectrometry.

A method is described for the determination of 16 sulfonamides in honey. Samples are dissolved in phosphoric acid solution (pH2), cleaned up with 2 solid-phase extraction (SPE) cartridges, an aromatic sulfonic cation-exchange cartridge and an Oasis HLB SPE cartridge, and analyzed both qualitatively and quantitatively by liquid chromatography/tandem mass spectrometry (LC/MS/MS) under the selected conditions. Without exception, calibration curves were linear (r = > 0.995), when sulfamethizole was between 1.0 and 25.0 microg/kg; sulfacetamide, sulfapyridine, sulfadiazine, sulfachloropyridazine, sulfamethoxazole, sulfamerazine, sulfisoxazole, sulfamonomethoxine, and sulfadoxine were between 2.0 and 50.0 microg/kg; sulfamethoxypyridazine, sulfadimethoxine, and sulfathiazole were between 4.0 and 100.0 microg/kg; sulfamethazine and sulfameter were between 8.0 and 200.0 microg/kg; and sulfaphenazole was between 12.0 and 300.0 microg/kg. Average recoveries at 4 fortification levels in the range of 1.0-300 microg/kg in honey were 70.9-102.5%, and relative standard deviations were 2.02-11.52%. The limits of quantitation for the 16 sulfonamides were between 1.0 and 12.0 microg/kg, with the LC/MS/MS method.

Buffers↗
PubMed1986

[Significance of sarcolemma damage in the pathogenesis of myocardial ischemia induced by pituitrin-isadrin and its correction using the antioxidant dibunol].

The elevation of cardiomyocyte membrane permeability has been demonstrated during pituitrin-isadrin-induced myocardial ischemia. Preventive 7-day oral administration of an antioxidant dibunol (30 and 120 mg/kg) preserved sarcolemmal integrity, decreased myocardial membrane permeability to sulfacetamide sodium, and reduced peroxide and mechanical erythrocyte hemolysis. Inhibition of lipid peroxidation with an antioxidant dibunol improved myocardial injury and decreased the death rate of animals with catecholamine-induced myocardial ischemia. These data suggest the involvement of lipid peroxidation in the development of ischemic myocardial injury.

Animals↗
PubMed1989

[Antiseptic sensitivity of clinical strains of Pseudomonas aeruginosa].

MICs, the frequency of clinical and statistic resistance and the antiseptic activity index were studied in complex on out-of-hospital and hospital ecovars of P. aeruginosa. The forms resistant to a number of antiseptics, i.e. chloramine B, chlorhexidine, decamethoxine and dioxidine whose frequency eventually increased were shown to be widely distributed. The antiseptic sensitivity spectrum was more narrow and more heterogeneous than that of other bacteria, the heterogeneity level being dependent on the antiseptic type and bacterial ecovar. The activity of pervomur, phenol, resorcin and boric acid was higher against the clinical strains of P. aeruginosa while iodopyrin, sulfacetamide sodium and dioxidine were less active. The P. aeruginosa strains had natural resistance to cetylpyridinium chloride, rokkal, ethonium, sodium laurate and laurylsulfate and rivanol. It was recommended to assay antiseptic sensitivity of agents causing purulent inflammatory infections and to control circulation of antiseptic resistant variants of bacteria in hospitals.

Anti-Infective Agents, Local↗
PubMed1980

[Folliculitis decalvans].

The author describes the main clinical and pathological aspects of Folliculitis decalvans, rare dermatosis, probably related with Staphylococcus sensibilization of the follicle. Although in some cases Staphylococcus are present in the lesions, the treatment is disappointing. Tetracycline oral and topically, sodium sulfacetamide and fusidic acid are mentioned by Rook. Alopecia is always definitive.

Alopecia↗
PubMed1994

In vitro susceptibility of equine Salmonella strains to trimethoprim and sulfonamide alone or in combination.

The in vitro activity of trimethoprim (TMP) and 9 sulfonamides and their combinations in 6 concentration ratios was tested against 62 Salmonella strains isolated from horses over a 3-year period in the Netherlands, using the agar-dilution method. Most of the isolates were S typhimurium strains (n = 52); the others were S heidelberg (n = 3), S hadar (n = 2), S thompson (n = 2), S enteritidis (n = 1), S infantis (n = 1), and S derby (n = 1). The minimal TMP concentration at which 50% of the Salmonella strains were inhibited (MIC50) was 0.12 micrograms/ml. Sulfachlorpyridazine (SCP; MIC50, 16 micrograms/ml), sulfamethoxazole (SMX; MIC50, 32 micrograms/ml), and sulfadiazine (SDZ; MIC50; 32 micrograms/ml) were the most potent of the sulfonamides tested. The antimicrobial effect of the sulfonamides, in combination with TMP (additive, synergistic, or antagonistic), was expressed by the fractional inhibitory concentration (FIC) index. Concentrations of SDZ and SCP with TMP had marked synergism at all tested TMP-to-sulfonamide concentration ratios (1:1 to 1:160; FIC index, 0.10 to 0.50); SMX had synergy with TMP at all ratios, except 1:1 (FIC index, 0.10 to 0.27). Sulfamethazine, sulfamerazine, sulfadoxine (SDX), sulfatroxazole, sulfadimethoxine, and sulfacetamide had MIC50 greater than their breakpoint MIC value and are, therefore, less potent drugs. However, synergy with TMP was found for these less potent sulfonamides at certain concentration ratios, depending on the sulfonamide used. Sixteen Salmonella strains were resistant to TMP, all sulfonamides, and TMP-sulfonamide combinations; 14 of these strains were S typhimurium phage type 200, 1 was S typhimurium phage type 61, and 1 was S typhimurium phage type 10.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Confirmatory method for sulfonamide residues in animal tissues by gas chromatography and pulsed positive ion-negative ion-chemical ionization mass spectrometry.

A confirmatory method has been developed for determination of 13 sulfonamides in edible tissues. The assay involves extraction from a solution resulting from a screening procedure by liquid chromatography and subsequent derivatization. Sulfachloropyridazine (SCP), sulfadiazine (SDA), sulfadimethoxine (SDM), sulfamethazine (SMZ), sulfamerazine (SME), sulfamethoxazole (SMX), sulfamethoxypyridazine (SMP), sulfapyridine (SPR), sulfaquinoxaline (SQX), and sulfathiazole (STA) were detected as the N1-methyl-N4-trifluoroacetyl derivatives, sulfaguanidine (SGU) as the same derivative after cyclization by hexafluoroacetylacetone, and sulfacetamide (SAC) as the methyl derivative. These sulfonamides were detected by gas chromatography and pulsed positive ion-negative ion-chemical ionization mass spectrometry with methane as the reactant gas, whereas sulfanilamide (SAA) was determined as the methyl derivative by electron-impact ionization.

Acylation↗
PubMed1997

Timolol decreases aqueous humor flow but not Na+ movement from plasma to aqueous.

PURPOSE: To determine whether the well-known effect of timolol in reducing ocular pressure and aqueous humor (AH) flow is a function of reduced Na+ movement from plasma to aqueous. Previously, the authors have shown this to be the case for carbonic anhydrase inhibitors. METHODS: The rate of appearance of 22Na in rabbit posterior aqueous was measured 1 to 3 minutes after the intravenous injection (time T) of the isotope. One hour before this, the animals received one of the following: two drops of 0.5% timolol, two drops of 3.5% pilocarpine, or 25 mg/kg intravenous methazolamide. At 1 minute (T + 1), a posterior chamber sample was taken; 2 minutes later (T + 3) a second sample was removed from the fellow eye. The rate constant of sodium accession is simply the difference between the two counts/2 minutes. Aqueous flow was measured by dilution of sulfacetamide marker as described previously. RESULTS: The rate constant (k(in)) for sodium entering the posterior chamber was 0.036 +/- 0.004 minute-1 (n = 17). Corresponding to previous findings, methazolamide (25 mg/kg intravenous) reduced this to 0.023 +/- 0.003 minute-1 (n = 14). Conversely, timolol (two drops of 0.5% solution) had no effect on kin, which measured 0.037 +/- 0.004 minute-1 (n = 12). Similarly, as expected, pilocarpine had no effect on k(in) (0.035 +/- 0.003 minute-1). Control flow was 3.9 microliters/minute +/- 0.4; after timolol, 2.5 microliters/minute +/-0.1; after methazolamide, 2.4 microliters/minute +/-0.2; after pilocarpine, 3.6 microliters/minute +/- 0.2. These are converted to rate constants by dividing by volume of posterior aqueous (60 microliters). The control rate constant for fluid entry was 0.065 minute-1, 1.8-fold higher than for sodium. CONCLUSIONS: A central dogma of the formation of AH (and cerebrospinal fluid) is that fluid moves isotonically from plasma to AH or cerebrospinal fluid and, therefore, that rate constant k(in) for fluid and for sodium are approximately the same. In the authors' hands, the fluid constant was modestly higher than for sodium. This holds for normal function and also for the reduced k(in) for fluid and sodium after carbonic anhydrase inhibition. The k(in) for neither flow nor sodium was affected by pilocarpine. Surprisingly, however timolol, which reduces flow, had no effect on Na+ entry.

Adrenergic beta-Antagonists↗
PubMed1997

[Corneal ulcer caused by Nocardia asteroides after penetrating keratoplasty].

We report the case of a 43-years-old patient, to whom a corneal transplantation was made because he presented a Salzmann nodular degeneration in his left eye. The patient was observed every week and his development during the following months was good. Nine weeks later he was attended at the emergency room of the hospital, with an intensive secretion and partial loss of vision in the operated eye. It was detected a peripheral ulcer of a diffused borders with a loss of epithelium and anterior stroma in the superior temporal part of the cornea. Five days later, the microbiological cultures confirmed the presence of Nocardia asteroides. In spite of the initial good evolution of the ulcer treated topically with a 20% sulfacetamide and trimetoprim-sulfadiacine p.o., the graft ended unsuccessfully.

Adult↗