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PubMed1997

Simultaneous analysis of several non-steroidal anti-inflammatory drugs in human urine by high-performance liquid chromatography with normal solid-phase extraction.

A practical and reproducible high-performance liquid chromatographic method using normal solid-phase extraction has been developed for the simultaneous analysis of twelve non-steroidal anti-inflammatory drugs (NSAIDs) in human urine. A urine specimen mixed with acetate buffer pH 5.0 was purified by solid-phase extraction on a Sep-Pak Silica cartridge. The analyte was chromatographed by a reversed-phase Inertsil ODS-2 column using a phosphate buffer-acetonitrile at pH 5.0 as the mobile phase, and the effluent from the column was monitored at 230 or 320 nm. Absolute recoveries were greater than 73% for all of the twelve NSAIDs. The present method enabled simple manipulation and isocratic HPLC with UV analysis as well as high sensitivity of 0.005 microg/ml for naproxen, and 0.05 microg/ml for sulindac, piroxicam, loxoprofen, ketoprofen, felbinac, fenbufen, flurbiprofen, diclofenac, ibuprofen and mefenamic acid as the quantitation limit in human urine using indomethacin as an internal standard.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

The non-aqueous titrimetric assay of the selected anti-inflammatory agents using tetra-n-butylammonium hydroxide as titrant.

A potentiometric titration method in non-aqueous media is proposed for the determination of some commonly used anti-inflammatory agents. The direct potentiometric titration of three anti-inflammatory agents, namely mefenamic acid, fenbufen and ibuprofen; and the indirect potentiometric titration of diclofenac sodium was carried out in acetonitrile solvent using tetra-n-butylammonium hydroxide as titrant, at 25 degrees C and under a nitrogen atmosphere. The method was found to be highly accurate and precise, having a relative standard deviation of <1.0% for all anti-inflammatory agents studied. Also, it was shown that the method could be successfully applied to the assay of commercial pharmaceuticals containing the above-mentioned anti-inflammatory agents. The validity of the method was tested by the recovery studies of standard addition to pharmaceuticals and the results were found to be satisfactory. The proposed method is simple, rapid and sufficiently precise for quality control purposes.

Analysis of Variance↗
PubMed2002

Optimized conditions for MDCK permeability and turbidimetric solubility studies using compounds representative of BCS classes I-IV.

The solubility enhancing effects of various excipients, including their compatibility with in vitro permeability (P(app)) systems, was investigated using drugs representative of Biopharmaceutics Classification System (BCS) classes I-IV. Turbidimetric solubility determination using nephelometry and transport experiments using MDCK Strain I cell monolayers were employed. The highest usable concentration of each excipient [dimethyl sulfoxide (DMSO), ethanol, hydroxypropyl-beta-cyclodextrin (HPCD), and sodium taurocholate] was determined by monitoring apical (AP) to basolateral (BL) [14C]mannitol apparent permeability (P(app)) and the transepithelial electrical resistance (TEER) in transport experiments done at pH 6.0 and 7.4. The excipients were used in conjunction with compounds demonstrating relatively low aqueous solubility (amphotericin B, danazol, mefenamic acid, and phenytoin) in order to obtain a drug concentration >50 microM in the donor compartment. The addition of at least one of the selected excipients enhanced the solubility of the inherently poorly soluble compounds to >50 microM as determined via turbidimetric evaluation at pH 6.0 and 7.4. Ethanol and DMSO were found to be generally disruptive to the MDCK monolayer and were not nearly as useful as HPCD and sodium taurocholate. Sodium taurocholate (5 mM) was compatible with MDCK monolayers under all conditions investigated. Additionally, a novel in vitro system aimed at more accurately simulating in vivo conditions, i.e., a pH gradient (6.0 AP/7.4 BL), sodium taurocholate (5 mM, AP), and bovine serum albumin (0.25%, BL), was shown to generate more reliable P(app) values for compounds that are poorly soluble and/or highly protein bound.

Animals↗
PubMed1989

Dysfunctional uterine bleeding.

The diagnosis of DUB is made by the exclusion of organic disease as a cause of the abnormal menses; the condition accounts for about 80% of cases of menorrhagia. Of these, over 80% will have no abnormality of the hypothalamo-pituitary-ovarian axis, and it is likely that the disorder is the result of local endometrial factors. There appears to be not only a preponderance of vasodilatory prostaglandins in the endometrium of women with menorrhagia, but also an excessive increase in fibrinolytic activity within the uterine cavity. Once a diagnosis has been reached with the aid of history, examination, haematological and endocrine investigations, and dilatation and curettage when appropriate, medical treatment is the usual first line approach. Non-steroidal anti-inflammatory drugs such as mefenamic acid, or antifibrinolytic agents such as tranexamic or epsilon aminocaproic acids, will reduce blood loss by between 25 and 50%. Though the former drugs are relatively free from side-effects in healthy women, intracranial thrombosis has been reported with the latter (Agnelli et al, 1982). Medications which suppress ovarian function, such as danazol or gonadotrophin releasing hormone analogues, are highly effective in lessening, or inhibiting, menstrual loss, but at the expense of side-effects and convenience respectively. The combined contraceptive pill may reduce blood loss by 50% but is not appropriate for older women. Cyclical gestagens such as norethisterone have been widely employed, particularly for the treatment of anovulatory cycles, but their place in the management of ovulatory DUB is less clear. If medical treatment fails hysterectomy should be considered, though less invasive surgical methods of endometrial ablation are being developed. Finally, it should be remembered that in the absence of associated signs or symptoms of iron-deficiency anaemia, heavy menstrual bleeding is a subjective complaint and up to 50% of women describing menorrhagia will have a measured monthly blood loss within normal limits.

Female↗
PubMed1998

Enhancement of chemotherapeutic drug toxicity to human tumour cells in vitro by a subset of non-steroidal anti-inflammatory drugs (NSAIDs).

The effect on cytotoxicity of combining a range of clinically important non-steroidal anti-inflammatory drugs (NSAIDs) with a variety of chemotherapeutic drugs was examined in the human lung cancer cell lines DLKP, A549, COR L23P and COR L23R and in a human leukaemia line HL60/ADR. A specific group of NSAIDs (indomethacin, sulindac, tolmetin, acemetacin, zomepirac and mefenamic acid) all at non-toxic levels, significantly increased the cytotoxicity of the anthracyclines (doxorubicin, daunorubicin and epirubicin), as well as teniposide, VP-16 and vincristine, but not the other vinca alkaloids vinblastine and vinorelbine. A substantial number of other anticancer drugs, including methotrexate, 5-fluorouracil, cytarabine, hydroxyurea, chlorambucil, cyclophosphamide, cisplatin, carboplatin, mitoxantrone, actinomycin D, bleomycin, paclitaxel and camptothecin, were also tested, but displayed no synergy in combination with the NSAIDs. The synergistic effect was concentration dependent. The effect appears to be independent of the cyclo-oxygenase inhibitory ability of the NSAIDs, as (i) the synergistic combination could not be reversed by the addition of prostaglandins D2 or E2; (ii) sulindac sulphone, a metabolite of sulindac that does not inhibit the cyclooxygenase enzyme, was positive in the combination assay: and (iii) many NSAIDs known to be cyclo-oxygenase inhibitors, e.g. meclofenamic acid, diclofenac, naproxen, fenoprofen, phenylbutazone, flufenamic acid, flurbiprofen, ibuprofen and ketoprofen, were inactive in the combination assay. The enhancement of cytotoxicity was observed in a range of drug sensitive tumour cell lines, but did not occur in P-170-overexpressing multidrug resistant cell lines. However, in the HL60/ADR and COR L23R cell lines, in which multidrug resistance is due to overexpression of the multidrug resistance-associated protein MRP, a significant increase in cytotoxicity was observed in the presence of the active NSAIDs. Subsequent Western blot analysis of the drug sensitive parental cell lines, DLKP and A549, revealed that they also expressed MRP and reverse-transcription-polymerase chain reaction studies demonstrated that mRNA for MRP was present in both cell lines. It was found that the positive NSAIDs were among the more potent inhibitors of [3H]-LTC4 transport into inside-out plasma membrane vesicles prepared from MRP-expressing cells, of doxorubicin efflux from preloaded cells and of glutathione-S-transferase activity. The NSAIDs did not enhance cellular sensitivity to radiation. The combination of specific NSAIDs with anticancer drugs reported here may have potential clinical applications, especially in the circumvention of MRP-mediated multidrug resistance.

Adenocarcinoma↗
PubMed2002

Molecular modelling of the differential interaction between several non-steroidal anti-inflammatory drugs and human prostaglandin endoperoxide H synthase-2 (h-PGHS-2).

The prostaglandin endoperoxide H synthase-1 (PGHS-1) and prostaglandin endoperoxide H synthase-2 (PGHS-2) are the targets of non-steroidal anti-inflammatory drugs (NSAIDs). The high degree of selectivity for inhibition of PGHS-2 shown by certain compounds appears to stem from two mechanisms (time-dependent, time-independent inhibition) by which they interact with each isoform. Molecular models of the complexes between indomethacin, fenamates, 2-phenylpropionic acids and the selective cyclooxygenase-2 (COX-2) inhibitors, with the cyclooxygenase active site of human PGHS-2 have been built by combining homology modelling, conformational searching and automated docking techniques. The stability of the resulting complexes has been assessed by molecular dynamics simulations combined with extended linear response calculations. The results allow us to identify regions of biological significance consistent with both X-ray crystallographic and kinetic results. The selective PGHS-2 inhibitors exploit the extra space of a side-pocket in the active site of PGHS-2 that is not found in PGHS-1. The results obtained point out a marked relationship between the experimental affinity and the electrostatic interaction energy alone for a series of NSAIDs. Analysis of the structural and the energetic data provides evidence supporting that network of hydrogen bonds between Tyr355, Glu524, Arg120 and Arg513 might be involved in mediating the binding of the time-dependent inhibitors of PGHS-2.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2000

In vivo selectivity of nonsteroidal antiinflammatory drugs and gastrointestinal ulcers in rats.

The aim of the present work was to study in vivo COX-2-COX-1 selectivity of 16 nonsteroidal anti-inflammatory drugs (NSAIDs) in equipotent ulcerogenic doses in two in vivo experimental models. Indomethacin, ibuprofen, nimesulide, aceclofenac, aspirin, sodium diclofenac, meloxicam, naproxene, paracetamol, piroxicam, tenoxicam, nabumetone, ketoprofen, mefenamic acid, etodolac, and ketorolac were administered to female Wistar rats (N = 10 each group). In experiment I, solid food plus subcutaneous NSAIDs were given. In experiment II, NSAIDs were given by oral gavage and in bolus. Macroscopic gastric antral ulcer area (30%) and intestinal erosiva area (295 mm2) in experiment I and necrotic gastric fundus area (65%) and erosive intestinal area (182 mm2), "in vivo" the NSAIDs COX-1 was showed. Neutrofilia assessed in gastric intestinal mucosa where also ibuprofen and paracetamol not given neotrophilic infiltration. In conclusion, COX-2-COX-1 selectivity was demonstrated in vivo with the drugs aceclofenac, nabumetone, meloxicam, nimesulide, and paracetamol.

Administration, Oral↗
PubMed1993

Solid-state nuclear magnetic resonance (NMR) spectra of pharmaceutical dosage forms.

Solid-state 13C NMR spectra of tablets or capsules of prednisolone, enalapril maleate, lovastatin, simvastatin, ibuprofen, flurbiprofen, mefenamic acid, indomethacin, diflunisal, sulindac, and piroxicam were obtained in the CP/MAS mode at 50 MHz. These studies show that (1) solid-state NMR spectroscopy can detect the active ingredients in low-dose tablets and capsules; (2) the use of interrupted decoupling often results in suppression of resonances due to excipients, thereby allowing better detection of resonances from the drug; and (3) the technique permits discrimination between two prednisolone polymorphs present in tablets obtained from various manufacturers even though the tablets contain only approximately 5% (w/w) of the drug.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1997

Impairment of endothelium-dependent but not of endothelium-independent dilatation in guinea-pig aorta rings incubated in the presence of elevated glucose.

1. Purine compounds such as ATP and adenosine, respectively endothelium-dependent and- independent vasodilators, are largely involved in the control of vascular tone and vascular reactivity to contracting stimuli. We investigated the relaxing activity of ATP and adenosine in guinea-pig aorta rings exposed for 6 h to elevated glucose concentration (50 mM), in order to mimic hyperglycaemic conditions. Guinea-pigs were reserpine-treated (2 mg kg-1, i.p., 48 and 24 h before death). 2. Rings of aortae incubated in 50 mM glucose, contracted submaximally by 1 microM noradrenaline, lost endothelium-dependent relaxation in response to acetylcholine (10 nM to 10 microM). Aortae incubated with 50 mM mannose, as a hyperosmotic control, relaxed to acetylcholine normally. Rings of aortae incubated in 50 mM glucose, contracted submaximally by 3 mM 4-aminopyridine, lost endothelium-dependent relaxation in response to ATP (30 microM) whereas endothelium-independent relaxation in response to adenosine (0.3 mM) was well preserved. 4. The relaxation induced by A23187 or sodium nitroprusside (10 nM to 0.1 microM) did not differ between rings exposed to control (5.5 mM) or elevated glucose (50 mM) and contracted submaximally by 3 mM 4-aminopyridine. 5. When incubated with aortic tissue in the presence of elevated glucose, the cyclo-oxygenase inhibitors, indomethacin (10 microM) and mefenamic acid (30 microM), or the scavenger of superoxide anions, superoxide dismutase (150 u ml-1), prevented the impairment of ATP-mediated relaxation. 6. The present results indicate that endothelium-dependent, receptor-induced relaxation in response to acetylcholine and ATP is impaired in guinea-pig aorta rings exposed to elevated glucose. The endothelial dysfunction caused by glucose might be located at a step between receptor activation and intracellular calcium increase, and might be related to an increased metabolism of arachidonic acid coupled to an increased production, or to a reduced inactivation of superoxide anions.

Acetylcholine↗
PubMed1998

Theophylline dilates rat diaphragm arterioles via the prostaglandins pathway.

1. We investigated by intravital microscopy in rats, the in vivo direct effects of theophylline on the diameters of second and third order diaphragm arterioles. 2. Theophylline (1-100 microM) dilated second and third order diaphragm arterioles significantly, and with an amplitude which was not statistically different from the one obtained with adenosine (1-100 microM). Enprofylline (1-100 microM), a theophylline analogue with poor adenosine-receptor antagonism but with similar or higher phosphodiesterases inhibition properties than theophylline, also dilated diaphragm arterioles, causing however, a significantly smaller dilatation than theophylline. 3. Neither the A1 adenosine receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX, 50 nM), nor the A2 adenosine receptor antagonist 3,7-dimethyl-1-proparglyxanthine (DMPX, 10 microM) reduced significantly theophylline-induced arteriolar dilatation. 4. Theophylline (100 nM) abolished adenosine-induced arteriolar dilatation. 5. The dilatation induced by theophylline was unchanged by the nitric oxide (NO) synthase inhibitor N(omega)-nitro-L-arginine (NNA, 300 microM). 6. Theophylline-induced arteriolar dilatation was abolished by the prostaglandin synthesis inhibitors mefenamic acid or indomethacin (20 microM). 7. These findings show that theophylline induced a significant dilatation of diaphragm arterioles via the release of prostaglandins.

Adenosine↗
PubMed2004

Salicylidene salicylhydrazide, a selective inhibitor of beta 1-containing GABAA receptors.

1. A high-throughput assay utilizing the voltage/ion probe reader (VIPR) technology identified salicylidene salicylhydrazide (SCS) as being a potent selective inhibitor of alpha2beta1gamma1 GABA(A) receptors with a maximum inhibition of 56+/-5% and an IC(50) of 32 (23, 45) nm. 2. Evaluation of this compound using patch-clamp electrophysiological techniques demonstrated that the compound behaved in a manner selective for receptors containing the beta1 subunit (e.g. maximum inhibition of 68.1+/-2.7% and IC(50) value of 5.3 (4.4, 6.5) nm on alpha2beta1gamma1 receptors). The presence of a beta1 subunit was paramount for the inhibition with changes between alpha1 and alpha2, gamma1 and gamma2, and the presence of a subunit having little effect. 3. On all subtypes, SCS produced incomplete inhibition with the greatest level of inhibition at alpha1beta1gamma1 receptors (74.3+/-1.4%). SCS displayed no use or voltage dependence, suggesting that it does not bind within the channel region. Concentration - response curves to GABA in the presence of SCS revealed a reduction in the maximum response with no change in the EC(50) or Hill coefficient. In addition, SCS inhibited pentobarbitone-induced currents. 4. Threonine 255, located within transmembrane domain (TM) 1, and isoleucine 308, located extracellularly just prior to TM3, were required for inhibition by SCS. 5. SCS did not compete with the known allosteric modulators, picrotoxin, pregnenolone sulphate, dehydroepiandrosterone 3-sulphate, bicuculline, loreclezole or mefenamic acid. Neither was the inhibition by SCS influenced by the benzodiazepine site antagonist flumazenil. 6. In conclusion, SCS is unique in selectively inhibiting GABA(A) receptors containing the beta1 subunit via an allosteric mechanism. The importance of threonine 255 and isoleucine 308 within the beta1 subunit and the lack of interaction with a range of GABA(A) receptor modulators suggests that SCS is interacting at a previously unidentified site.

Amino Acid Sequence↗
PubMed1999

Is monochromatic irradiation testing useful in the differentiation of drug-induced photosensitivity from chronic actinic dermatitis?

Chronic actinic dermatitis (CAD) is an uncommon, eczematous photosensitive eruption affecting predominantly elderly men and to which drug-induced photosensitivity may sometimes appear clinically identical. This retrospective study compares the monochromatic irradiation results in 11 patients with CAD and 14 patients with drug-induced photosensitivity, to assess whether such testing is useful in the differentiation of these two conditions. Thus, the action spectra of the drug photosensitivity patients were plotted and compared with those of 12 nonphotosensitive control patients: 10 patients were found to be photosensitive in the UVA range; the implicated drugs included quinine, sparfloxacin, amiodarone, doxycycline, mefenamic acid, nalidixic acid, fenbrufen, diclofenac, enalapril, diltiazem and prochlorperazine maleate. One patient on doxycycline was photosensitive in both the UVA and UVB ranges. The remaining three patients were not tested until after discontinuation of their drug and their light tests were then normal. In the CAD group, five patients were photosensitive in the UVA, UVB and visible light ranges and six were photosensitive in the UVA and UVB ranges. Comparison of the mean minimal erythema dose responses then demonstrated dissociation of the drug-induced from the CAD group in the UVB region; the result was statistically significant. This suggests that UVA-sensitivity dissociated from UVB-sensitivity is a relative indicator of drug-induced photosensitivity and monochromatic irradiation testing may therefore be helpful in the differentiation of these two disorders.

Adult↗
PubMed1997

Drug-associated admissions to a district hospital in Saudi Arabia.

BACKGROUND: The modernization and expansion of the health system in the Kingdom of Saudi Arabia has led to the wide availability of drugs and with it a potential for their misuse. AIM: To study drug-associated admission to a district hospital in the Kingdom of Saudi Arabia with regard to pattern, demographic characteristics of patients and outcome. PATIENTS AND METHODS: A prospective study between 1992 and 1994 of drug-related admissions to the medical wards of a referral district hospital in Abha, southern Saudi Arabia. RESULTS: One hundred and six patients were studied, 50 with drug overdose (OD, group A) and 56 with other adverse drug reactions (group B). Those with OD were younger and predominantly female. Analgesics, especially mefenamic acid and psychotropic drugs, were the most common causes of OD. Family disputes in females and psychiatric illnesses in males were the main risk factors for overdose. In group B, the most common adverse drug reactions were upper gastrointestinal bleeding and hepatic injury caused by NSAIDs. The overall mortality was 3.8%. CONCLUSIONS: Although drug-related problems constitute a minor problem in Saudi Arabia, there is a potential for their increase in the future. Overall mortality was higher than in other countries. Doctors should be alerted and hospitals should be ready to deal with this problem in Saudi Arabia, from both a medical and social point of view.

Adolescent↗
PubMedDate not supplied

Green tea catechins evoke a phasic contraction in rat aorta via H2O2-mediated multiple-signalling pathways.

1. The contractile effects of tea polyphenols (TP) and its four principle catechins, namely (-)-epicatechin (EC), (-)-epicatechin-3-gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin-3-gallate (EGCG), on rat aorta contractility were investigated using the isometric tension recording technique. 2. At concentrations of 5-100 mg/L, TP evoked phasic contraction of rat aorta in a concentration-dependent but endothelium-independent manner. Of the four catechins tested, EGCG and EGC (3-300 micromol/L), but not EC and ECG, mimicked the contractile response to TP, suggesting that the epigallol moiety in the B ring may be associated with the contractile effect. 3. Contractions in response to EGCG and EGC were not affected by several endogenous vasoconstrictor receptor antagonists, but could be abolished by 10 micro mol/L BAPTA-AM, a membrane-permeable Ca2+ chelator, or attenuated by removal of extracellular Ca2+, suggesting the involvement of both intracellular and extracellular Ca2+ in evoking the contraction. 4. Pretreatment with non-selective Ca2+ channel antagonists mefenamic acid (10 micro mol/L), tetrandrine (30 micro mol/L) and SKF 96365 (30 micromol/L), but not nifedipine (1 micromol/L), the selective inhibitor of voltage-dependent Ca2+ channels, inhibited the contractile responses to EGC and EGCG, indicating the involvement of Ca2+ influx via non-voltage dependent Ca2+ channels. 5. Several intracellular Ca2+ channel modulators, including procaine (5 mmol/L), dantrolene (30 micromol/L) and 2-amino ethoxydiphenyl borate (50 micromol/L; an inositol 1,4,5-trisphosphate receptor inhibitor), also inhibited EGCG- and EGC-induced contractions, thus suggesting a role of intracellular Ca2+ release in these contractions. 6. Both EGCG- and EGC-induced contractions were depressed, to different degrees, by inhibitors of several receptor-coupled enzymes, including phospholipase C, protein kinase C, phospholipase A2 and tyrosine kinase. Furthermore, both EGCG- and EGC-induced contractions were completely abolished by catalase, but not by superoxide dismutase or mannitol/dimethyl sulphoxide. 7. Taken together, these data show, for the first time, that TP and its related catechins that contain an epigallol structure in the B ring, as in EGCG and EGC, exert direct contractile effects on rat aortic smooth muscle via a H2O2-mediated pathway.

Animals↗
PubMed2001

Prevalence and clinical characteristics of headache in medical students in oman.

OBJECTIVES: To perform a descriptive epidemiological study of headache in medical students at Sultan Qaboos University, analyzing prevalence, symptom profile, and pattern of health care utilization. BACKGROUND: Headache is one of the most common complaints in medical practice. To our knowledge, headache has not been the subject of investigation in medical students in the Arabian Gulf. METHODS: Lifetime and last-year prevalence of headache was based on a detailed structured headache assessment questionnaire. Besides demographic data, headache characteristics and pattern of health care utilization were evaluated. In addition, questions were included referring to the use of traditional remedies. Interviewers included three previously trained final-year medical students. The evaluation was done per cohort, and the students were guided through the assessment questionnaire by the interviewers. Migraine and tension-type headache were diagnosed according to the criteria of the International Headache Society. RESULTS: Four hundred three students (95.3%) completed the questionnaire: 151 men (37.5%) and 252 women (62.5%). The lifetime and last-year prevalence of headache was 98.3% and 96.8%, respectively. A positive family history of headache was found in 57.6% of students. The prevalence rate of migraine and tension-type headache was found to be the same (12.2%), with a difference in distribution across sexes: 6.6% of the men and 15.5% of the women had migraine, while 13.9% of the men and 11.1% of the women suffered from tension-type headache. Only 23.3% of students sought medical assistance during headache episodes, and 80.3% took medication: 24.6% took prescribed medication, 72.9% took nonprescription medication, and only 2.5% took traditional remedies. Acetaminophen (83.1%) followed by mefenamic acid (24.6%) were the most commonly used drugs. CONCLUSIONS: The results of this prospective epidemiological study show that headache is highly prevalent among medical students at this university. The high prevalence rate of migraine sufferers in this student population might be due to the high female-to-male ratio (1.7:1). It is likely that analgesic use/overuse also coexists with headache in medical students at Sultan Qaboos University, since a large majority of them rely on nonprescription medications.

Adult↗
PubMed1991

Administration of prostaglandin inhibitors to the mother; the potential risk to the fetus and neonate with duct-dependent circulation.

Two infants were delivered by urgent Caesarean section at 34 weeks because of fetal distress. One rapidly developed severe cardiac failure and the other marked cyanosis. Their mothers had been prescribed indomethacin and mefenamic acid (Ponstan) to treat premature onset of labour and chronic polyhydramnios, respectively. Both infants had duct-dependent circulations, their cross-sectional echocardiography showing only a small (1-2 mm diameter) patent ductus arteriosus. The early onset and severity of their symptoms suggested that the maternal intake of prostaglandin inhibitors may have deleteriously led to early closure of their ducts, essential in duct-dependent circulations. Although such occurrences are rare, fetal cross-sectional echocardiography should be performed prior to administration of prostaglandin inhibitors during pregnancy.

Cesarean Section↗
PubMed1975

Structural requirements for time-dependent inhibition of prostaglandin biosynthesis by anti-inflammatory drugs.

Several anti-inflammatory drugs have been examined for their ability to cause a time-dependent destruction of the fatty acid oxygenase that produces prostaglandins. All of the time-dependent inhibitors contained carboxylic acid moieties, and in addition all but one of the drugs contained a halogen atom. Structural analogs (of the time-dependent inhibitors) lacking halogen atoms were unable to cause a time-dependent destruction of the enzyme. The time-dependent property of an inhibitor was totally eliminated after methylation of the carboxylate group. Methylation did not, however, alter the ability of the inhibitors to competitively inhibit the oxygenase. Thus, the reversible binding of the agents at the active site was not appreciably dependent upon the free carboxyl group, whereas the subsequent irreversible process was.

Anti-Inflammatory Agents↗