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PubMed1989

5-Aminosalicylic acid derivatives. Clinical and pharmaceutical evaluation.

Several new 5-aminosalicylic acid (5-ASA) derivatives have been introduced for the treatment of chronic inflammatory bowel disease (CIBD). In azo-bond preparations, 5-ASA is linked to an inert carrier (Balsalazide) or to another 5-ASA molecule (Dipentum). The pharmacokinetic profile is similar to salazosulphapyridine (SASP) and the preparations are as effective as SASP in treatment of ulcerative colitis (UC) and with fewer side effects. In controlled release preparations (Asacol, Pentasa, Salofalk), 5-ASA is coated with compounds resistant to low pH, but which deliver 5-ASA to the intestines at various rates at higher pH values. The drugs are as effective as SASP in maintenance of remission and in the treatment of mild to moderate flare ups in UC. A larger systemic absorption is found for the three preparations compared to SASP. The controlled release preparations seem promising in the treatment of Crohn's disease, but further studies are needed. The controlled release preparations should be the drugs of choice in patients with UC allergic to or intolerant of SASP and to males who wish to have children.

Aminosalicylic Acids↗
PubMed1995

Chromonyl-aminosalicylic acid derivatives as possible antimycobacterial agents.

N-(2H,3H,4H-4-oxo-6-R1-2-R2O-benzopyran-3-ylidenmethyl) derivatives and imino derivatives of 3-, 4-, 5-aminosalicylic acids were prepared. It was found that some of the synthesized derivatives of 4-aminosalicylic acid are as effective against typical and atypical strains of mycobacteria as isoniazid (INH). Interesting activity of some derivatives against yeast was also found.

Aminosalicylic Acids↗
PubMed1986

5-Aminosalicylic acid in patients with an ileo-rectal anastomosis. A comparison of the fate of sulfasalazine and Pentasa.

The pharmacokinetics of 5-aminosalicylic acid (5-ASA) from sulphasalazine (SASP) and the slow-release 5-ASA preparation Pentasa was investigated in a cross-over study in 9 otherwise healthy patients with an ileo-rectal anastomosis. The 24-hour recoveries of the drugs were 90.5% and 84.7%, respectively. The median release of 5-ASA from SASP was 50% and from Pentasa 75%. Equal amounts of 5-ASA (18.0% vs 17.9%) were found in the faeces, and a significantly larger amount (4.4% vs 28.9%) of the metabolite N-acetyl-5-aminosalicylic acid (ac-5-ASA) was found in faeces following Pentasa. A larger amount of 5-ASA was absorbed and subsequently excreted in the urine, mainly as the metabolite (2.5% vs 20.5%) from Pentasa. This confirms previous results in ileostomized patients treated with Pentasa. The present findings also demonstrate that bacterial azo-reduction of SASP in patients with ileorectal anastomosis may be an adequate way to deliver 5-ASA in this type of patient. Both treatments may be used in these patients during a flare up of ulcerative colitis, but randomized studies are needed.

Aminosalicylic Acids↗
PubMed1987

Azodisalicylate (azodisal sodium) causes intestinal secretion. Comparative study of the effect of azodisalicylate, sulfasalazine, 5-aminosalicylic acid and sulfapyridine on the water and electrolyte transfer and the morphology of the rat ileum and colon in vivo.

Azodisalicylate (ADS) is one of the possible successors of sulfasalazine in the treatment of ulcerative colitis. The following results were obtained when comparing the influence of ADS on net water and electrolyte transfer in tied-off loops of the rat ileum and colon in vivo with sulfsalazine, 5-aminosalicylic acid, and sulfapyridine. (1) Sulfasalazine, 5-aminosalicylic acid and sulfapyridine had no effect on water and electrolyte transfer of the healthy intestinal mucosa in concentrations up to 400 mg%. (2) ADS showed a concentration-dependent inhibition effect on net water, sodium and chloride absorption and stimulated secretion at concentrations higher than 100 mg%. (3) No morphological alterations of the mucosa could be observed by light and transmission electron microscopy. The observed effect of ADS might have some clinical significance in patients with a decreased absorptive capacity of the colon in ulcerative colitis, in contrast to healthy volunteers, where the high absorptive capacity of the colon might compensate the decreased absorption or stimulated secretion in the small intestine.

Aminosalicylic Acids↗
PubMed1988

Effect of disodium azodisalicylate on electrolyte transport in rabbit ileum and colon in vitro. Comparison with sulfasalazine and 5-aminosalicylic acid.

Azodisalicylate, used to treat ulcerative colitis, causes diarrhea in up to 12.5% of patients. We compared the in vitro effects of azodisalicylate, sulfasalazine, and 5-aminosalicylic acid on rabbit intestinal electrolyte transport. Distal ileal mucosae mounted in Ussing chambers were exposed to varying concentrations of the drugs. Mucosal addition of azodisalicylate (greater than 5 mM) caused the greatest anion-dependent increase in short-circuit current of 83 microA/cm2 (ED50 = 0.3 mM). Isotope flux measurements suggest that azodisalicylate may stimulate predominantly electrogenic HCO3 secretion and induces net NaCl secretion. In contrast, serosal addition of azodisalicylate and sulfasalazine (greater than 5 mM) decreased short-circuit current, and 5-aminosalicylic acid had no effect. Azodisalicylate had no effect on ion transport in distal colon. The effects of azodisalicylate in ileum were not inhibited with piroxicam (an inhibitor of cyclooxygenase). Mucosal cyclic adenosine monophosphate and cyclic guanosine monophosphate levels were unchanged after ileal exposure to azodisalicylate. Azodisalicylate appears to be a mechanistically unusual secretagogue, possibly explaining the increased incidence of diarrhea seen in patients taking the drug.

Aminosalicylic Acids↗
PubMed2006

Schiff base conjugates of p-aminosalicylic acid as antimycobacterial agents.

Schiff base conjugates of p-aminosalicylic acid have been synthesized and characterized by elemental analysis, IR and (1)H NMR spectroscopy and cyclic voltammetry. Compounds containing hydroxyl-rich side chains show enhanced antimycobacterial activity against Mycobacterium smegmatis and Mycobacterium bovis BCG. Higher ClogP values and superior radical scavenging activities are thought to be the contributing factors for their enhanced antimycobacterial activities.

Aminosalicylic Acid↗
PubMedDate not supplied

Use of old and new oral 5-aminosalicylic acid formulations in inflammatory bowel disease.

Although sulfasalazine, a 5-aminosalicylic acid (5-ASA) agent, is still the anti-inflammatory agent of choice for ulcerative colitis and Crohn's disease, newer formulations, which release drug to specific regions of the colon for maximal efficacy, also can be appropriate first-line agents. This article reviews recent clinical studies of therapy with older and newer 5-ASA formulations.

Administration, Oral↗
PubMed1990

Effect of food coadministration on 5-aminosalicylic acid oral suspension bioavailability.

Single doses of 1 gm 5-aminosalicylic acid (5-ASA) suspension was administered to 24 healthy volunteers during both fasting and fed conditions. For subjects in a fasting state, plasma 5-ASA and acetyl 5-ASA concentrations peaked rapidly 1 hour after dosing to 14.72 micrograms/ml and 11.4 micrograms/ml, respectively. The elimination half-life of 5-ASA was 51.9 minutes, whereas the acetyl 5-ASA half-life could not be determined. A mean of 78.3% of the dose was excreted in the urine, with 5-ASA accounting for 21.2% of the dose and acetyl 5-ASA accounting for the balance. Only 11.3% of the dose was eliminated in the feces, consisting mostly of acetyl 5-ASA. Food coadministration reduced 5-ASA and acetyl 5-ASA systemic relative bioavailability to 44% and 76%, respectively, compared with the fasting treatment. Urinary excretion of the salicylates was reduced to 46.8%, and fecal salicylate elimination increased almost 100%--to 24.2% of the total dose.

Administration, Oral↗
PubMed1987

Possible mode of action of 5-aminosalicylic acid.

Despite the extensive use of sulfasalazine (SAS) and/or 5-aminosalicylic acid (5-ASA) in patients with inflammatory bowel disease and, more recently, rheumatoid arthritis, their mode of action has not been elucidated so far. None of the numerous pharmacological and biochemical effects described, including immunosuppressive, antifolate, and modulatory actions on lymphocyte and leukocyte functions, could be defined unequivocally as mediating their beneficial activity. Recently, interest has focused on actions of SAS and 5-ASA on the various enzymes of the arachidonic acid cascade. Mucosa of patients with inflammatory bowel disease generates excessive amounts of cyclooxygenase products such as prostaglandins (PG) as well as 5-lipoxygenase products such as leukotriene (LT) B4 and sulfidopeptide-LT. Both PG and LT exert proinflammatory actions and are potentially important mediators of mucosal inflammation. SAS and 5-ASA, however, have been found to inhibit PG synthesis under certain experimental conditions only, while increasing PG formation under other conditions. While SAS was found to inhibit colonic LTB4 synthesis, 5-ASA was reported to selectively affect the cyclooxygenase pathway of arachidonate metabolism in this tissue. Our results demonstrate that, like the parent compound, the metabolite 5-ASA in a dose-dependent manner inhibits release of LTB4 and sulfidopeptide-LT from normal human colonic mucosa (IC50 3.5 and 3.7 mmol/liter, respectively). Indomethacin, which has no efficacy in the treatment of patients with inflammatory bowel disease, on the other hand, selectively inhibited PGE2 formation in normal and inflamed colonic mucosa (IC50 1.7 and 1.0 mmol/liter, respectively) without reducing synthesis of LTB4 or sulfidopeptide-LT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminosalicylic Acids↗
PubMed1997

Comparative cytotoxicity of 5-aminosalicylic acid (mesalazine) and related compounds in different cell lines.

Nonsteroidal anti-inflammatory drugs can cause serious side-effects such as tubulo-interstitial nephritis. Mesalazine (5-ASA, 5-aminosalicylic acid) is used for the treatment of colitis ulcerosa, Crohn disease, and other diseases; it has been found to induce necrosis of both proximal convoluted tubules and renal papillaries. The comparative cytotoxicity of 3-, 4-, and 5-aminosalicylic acid, acetylsalicylic acid (AcSA), and the parent compound salicylic acid (SA) was investigated for the free acids and for their sodium salts. The interaction with endogenous glutathione (GSH) was also investigated. Four established cell lines were used: MDCK, LLC-PK1, NRK as renal cells, and HepG2 as hepatic cells. The free acid compounds were less toxic than their corresponding salts. Acidic 5-ASA was the most toxic of the three isomers in MDCK and LLC-PK1 cells, while NRK and HepG2 were more susceptible to acidic 3-ASA. Addition of NaOH modified the relative toxicity of 3-ASA and 5-ASA. The LLC-PK1 and HepG2 cells were more sensitive to the test chemicals as their salts than were the NRK and MDCK cells. SA and 5-ASA decreased the GSH content in renal cells and increased it in HepG2. GSH depletion with L-buthionine-(S,R)-sulfoximine enhanced the toxicity only for SA in NRK and for 5-ASA and AcSA in HepG2. No correlation between endogenous GSH and the susceptibility of MDCK and LLC-PK1 to the test compounds was observed. The results suggest that no typical nephrotoxic effect occurred. No explanation could be found for the tubulo-interstitial nephritis caused by 5-ASA therapy.

Aminosalicylic Acid↗
PubMed1990

Disposition of 5-aminosalicylic acid by olsalazine and three mesalazine preparations in patients with ulcerative colitis: comparison of intraluminal colonic concentrations, serum values, and urinary excretion.

To compare the disposition of 5-aminosalicylic acid (5-ASA) and its acetylated metabolite during treatment with olsalazine and mesalazine, 14 patients with inactive ulcerative colitis were randomly assigned to olsalazine (1 g twice daily) and the mesalazines, Asacol (800 + 400 + 800 mg daily), Pentasa (750 + 500 + 750 mg daily), and Salofalk (750 + 500 + 750 mg daily) in a crossover design trial so that all received each drug for seven days. Intraluminal colonic concentrations of 5-ASA were estimated after five days by the method of equilibrium in vivo dialysis of faeces. A predose serum sample and a 24 hour urine collection were obtained on day seven. The 5-ASA and acetyl-5-aminosalicylic acid (Ac-5-ASA) values were determined by high performance liquid chromatography. Olsalazine almost doubled the colonic concentrations (mean 23.7 (SEM) (1.9) mmol/l) of its therapeutically active ingredient (5-ASA) compared with equimolar doses of Pentasa (12.6 (2.2) mmol/l; p less than 0.0003) and Salofalk (15.0 (2.0) mmol/l; p less than 0.003). At the same time, olsalazine treatment was associated with lower serum concentrations and urinary excretions (p less than 0.05) of 5-ASA and Ac-5-ASA compared with the mesalazine preparations. The low systemic load of 5-ASA provided by olsalazine reduces the potential risk of nephrotoxicity during long term treatment.

Adult↗
PubMed1991

5-aminosalicylic acid in the prevention of relapses of Crohn's disease in remission: a long-term study.

The aim of the study was to evaluate the efficacy of 5-aminosalicylic acid (5-ASA) in maintaining the remission in patients with inactive Crohn's disease over a period of three years, using either the Crohn's Disease Activity Index (CDAI) and or the Laboratory Index (LI). Thirty-eight patients entered in the study; 20 received 5-ASA 1.6 g/day and 18 no specific therapy. The patients were followed for three years. Of the patients, 86% presented a relapse, 80% in the 5-ASA group and 94% in the control group. Two patients requested surgical therapy. All patients with clinical relapse had CDAI greater than 150 and LI greater than 100. 5-Aminosalicylic acid was well tolerated and was able to protect from relapse up to 60% of the patients in the first year of therapy. When treatment with 5-ASA is prolonged for periods longer than one year a progressive increase in the number of patients who present relapse can be observed, but of the 5-ASA group, 80% of relapses occurred in the three years whereas the control group showed 94% relapses at the end of the first year.

Adult↗