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PubMed1982

Reversal by acetylsalicylic acid of the captopril-induced inhibition of angiotensin converting enzyme in the hindquarters of guinea-pig.

The conversion of angiotensin I to angiotensin II was studied in the isolated perfused hindquarters of guinea-pig. The relative enzyme activity was determined by vasoconstrictor response to the peptides and by the contraction of rat ascending colon superfused with the venous effluent. 45% of conversion of angiotensin I to angiotensin II was determined in this preparation as measured by vasoconstrictor responses. However, only 22% of conversion was detected in the venous return as measured in the rat colon. Captopril significantly inhibited angiotensin converting enzyme activity in this preparation. Acetylsalicylic acid, however, partially prevented the inhibitory effect of Captopril on converting enzyme activity in this vascular bed. The possible interactions of angiotensin converting enzyme activity and endogenous prostaglandins are discussed.

Angiotensin I↗
PubMed1992

Inhibition of isotretinoin teratogenicity by acetylsalicylic acid pretreatment in mice.

Although isotretinoin (ITR) has been suggested to cause malformations via cytopathic effects on embryonic cells, the molecular mechanisms of ITR cytotoxicity in teratogenesis are not clear. Since ITR undergoes metabolism by prostaglandin synthase to a potentially cytotoxic peroxyl free radical, the possible role of prostaglandin synthase metabolism as a modulator of ITR teratogenicity was evaluated. Craniofacial and limb abnormalities were noted in fetuses on day 18.5 of gestation following administration of ITR to pregnant CD-1 mice in a three dose regimen of 100 mg/kg at 4 hr intervals on day 10.5 of gestation (plug day = day 0.5 of gestation). Mice were also treated with acetylsalicylic acid (ASA), an irreversible inhibitor of the cyclooxygenase component of prostaglandin synthase, at doses of 20 and 60 mg/kg body weight 2 hr prior to each ITR dose. ASA pretreatment of mice receiving ITR treatment showed a dose-dependent decrease in the overall incidence of malformations, number of defects per fetus, and the incidence of specific craniofacial and limb defects. Equivalent doses of ASA given to control mice did not cause malformations or alter the incidence of resorptions. These results demonstrate that ASA is able to ameliorate the teratogenic effects of ITR observed in fetal mice near term and indicate that prostaglandin metabolism could play a mechanistic role in ITR teratogenicity.

Animals↗
PubMed2001

Acetylsalicylic acid and other salicylates in relation to Stevens-Johnson syndrome and toxic epidermal necrolysis.

AIMS: Various nonsteroidal anti-inflammatory drugs are known to increase the risk of Stevens-Johnson syndrome and toxic epidermal necrolysis. The relationship between salicylate treatment and these conditions is not known. METHODS: A case-control study was conducted in four countries in Europe from 1989 to 1995. RESULTS: Among 373 cases and 1720 controls, the multivariate relative risk estimate for any salicylate use in the previous week was 1.3 (95% confidence interval, 0.8-2.2); no statistically significant elevations were observed for single ingredient preparations or for salicylate-containing combination products. CONCLUSIONS: Acetylsalicylic acid and other salicylates are not associated with a measurable increase in the risk of these rare but severe reactions.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1984

Platelet aggregation in arterioles of the hamster cheek pouch and in heart transplants: its tissue-dependent influencibility by acetylsalicylic acid and nafazatrom.

Different, tissue-dependent antiaggregatory properties of endothelial cells are suggested by in vitro findings, which show different spectra and amounts of arachidonic acid products to be synthesized by vessels of different type and origin. Platelet aggregation was assessed in vivo in native arterioles of the hamster cheek pouch and in arterioles of heart transplants by intravascular excitation of fluorescein isothiocyanate-dextran (FITC-d). The time to aggregate appearance (TAA) was determined, i.e. the interval from onset of FITC-d excitation until the first aggregate was seen to adhere to the vessel wall. Two groups were pretreated with 100 micrograms/kg nafazatrom and 100 mg/kg acetylsalicylic acid (ASA), both potent antithrombotic drugs. Nafazatrom has been shown to stimulate prostacyclin release from endothelial cells, whereas ASA blocks cyclooxygenase both in platelets and vessel walls. TAA was the same for native arterioles of both types. Nafazatrom was equally effective in both vessels, and about three orders of magnitude more potent than ASA in prolonging TAA. ASA was twice as effective in arterioles of the heart as it was in those of the skin type, indicating that tissue-dependent mechanisms achieve the antiaggregatory potency of the vessel walls. It is concluded that further in vivo studies on platelet aggregation and thrombus formation should be performed on cardiac vessels directly and not on vessels of different origin. The presented model may be a useful tool for investigating the mentioned tissue-dependent mechanisms of thrombus formation in vivo.

Animals↗
PubMed1994

Amaurosis fugax: prognosis and the role of acetylsalicylic acid.

Amaurosis fugax has been grouped together with other forms of transient ischemic attacks (TIAs) in the neurologic literature in analyses of prognosis. Although episodes of transient visual loss (TVL) are presumed to be due to ischemia, the prognosis with respect to subsequent stroke and myocardial infarct (MI) appears to differ from cerebral TIAs. We reviewed the clinical course of 73 patients above the age of 45 years who presented to our clinics with a distinct history of TVL. With an average follow-up period of 38 months, the incidence rates of cerebrovascular accident, cerebral TIA and MI following presentation with TVL were 1%, 4% and 7% respectively. Although there was a trend toward fewer episodes of amaurosis with use of acetylsalicylic acid (ASA), the difference was not statistically significant. In addition, ASA did not appear to offer a benefit with respect to future ischemic events. Patients with monocular TVL appeared more likely to experience a TIA, whereas those with binocular TVL appeared more likely to experience an MI.

Aged↗
PubMed1995

[Treatment of chronic virus hepatitis with acetylsalicylic acid].

The treatment of chronic hepatitis B and C with recombinant interferon (IFN) has only poor durable response rates. In the past only the lack of any prior effective therapy regimen could justify the use of this expensive agent. Dose escalating or prolonged treatment courses did not enhance the rate of sustained remissions. Pre- or cotreatment with antiviral (e.g. acyclovir, ribavirin, isoprenosin) or immunomodulating (e.g. prednisone, gamma IFN) drugs have not influenced the resistance to exogenous (IFN) of many patients. The mechanisms underlying resistance to this drug remain unknown. Some hypotheses focus on IFN antibodies, down regulation of IFN receptors or defects in the postreceptor response of cells to IFN. In 1991 Hannigan and Williams (Science 1991; 251: 204-207) described a synergistic signal transduction effect in human fibroblasts after exposure to IFN. Arachidonic acid (AA) activation from membrane phospholipid pools is common to many receptors and can be followed by metabolization of AA by cyclooxygenase to prostanoids, thromboxanes and eicosanoids and by lipoxygenase to leukotrienes; inhibition of these AA oxidation pathways by addition of inhibitors of these enzymes (e.g. indomethacin) resulted in marked amplification of the IFN signal, possibly by using the epoxygenase enzyme family as an alternative pathway. Our data are taken from the pretreatment part of a current study for evaluation of pre- and combination treatment with acetylsalicylic acid (ASA) as cyclooxygenase inhibitor and IFN in chronic hepatitis C. 27 patients with histologically proven chronic active hepatitis C were divided into two groups. Group A (16 patients) were treated with a daily dose of 100 mg ASA orally, and the 11 patients in group B served as untreated controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2001

Acetylsalicylic acid and microembolic events detected by transcranial Doppler in symptomatic arterial stenoses.

BACKGROUND: In patients with symptomatic carotid artery stenosis, high-intensity transient signals detected by transcranial Doppler (TCD) have been related to particulate microemboli originating at the stenotic lesion. The occurrence of these microembolic events within the Doppler spectrum should be influenced by antithrombotic agents of proven efficacy in these patients mainly by reducing cerebral embolism. METHODS: Seventy-four of 192 consecutive patients with symptomatic arterial stenosis in the anterior circulation and clinical symptoms within the last 30 days underwent 1-hour bilateral TCD monitoring. Patients were selected, if they presented temporal bone windows enabling transcranial insonation, revealed normal Doppler CO2 test excluding hemodynamic impairment, had not received antithrombotic therapy other than acetylsalicylic acid (ASA) before sonographic examination, and gave informed consent to 1-hour monitoring which could be performed immediately on admission/presentation of the patient at the Department of Neurology. RESULTS: Microembolic events were detected in 38 patients (51%). The proportion of patients with events among 26 patients without antithrombotic medication was 73% as compared with 40% in 48 patients receiving ASA at the time of TCD monitoring (p = 0.023). Multivariate analysis including time from ischemia to TCD, presence and start of ASA prevention, degree and localization of stenosis, and presence of a single or recurrent ischemia revealed that absence of an ASA prevention (odds ratio OR 7.1, 95% confidence interval CI 1.6-31.4, p = 0.010), recurrent ischemic events (OR 7.1, 95% CI 1.6-32.7, p = 0.011), and extracranial localization of the stenosis (OR 3.8, 95% CI 1.1-13.2, p = 0.038) were independent predictors for microembolic events. CONCLUSION: In patients with symptomatic arterial stenosis, the absence of an ASA medication is associated with the occurrence of TCD-detected microembolic events, suggesting a relation between these events and ASA-sensitive microemboli from the stenotic lesion.

Aged↗
PubMed2003

Effect of metamizol on promyelocytic and terminally differentiated granulocytic cells. Comparative analysis with acetylsalicylic acid and diclofenac.

Metamizol is an analgesic and antipyretic agent that can induce agranulocytosis in certain patients. However, its effects on granulocyte viability and differentiation have been poorly evaluated. Here we analysed the effects of metamizol and its active metabolite, 4-methylaminoantipyrine (MAA), on the viability of HL60 promyelocytes and their dimethyl sulphoxide-induced differentiated granulocytes. Metamizol and MAA at 75 microM (above the peak of plasmatic concentration after 2g intake) did not alter granulocytic differentiation of HL60 cells. Only at concentrations above 100 microM, well over the pharmacological range, metamizol-induced apoptosis in about 30% of the HL60 promyelocytes, while HL60-granulocytic terminally differentiated cells were more resistant to this apoptotic action. When the effects of metamizol were compared with those of acetylsalicylic acid (ASA) and diclofenac on cell viability, at equivalent concentrations used in analgesic and antipyretic therapy (75 microM for metamizol, and ASA and 3 microM for diclofenac) their apoptotic effects were similar. Again, the HL60 promyelocytes were more sensitive to apoptosis than granulocytic differentiated cells, as measured by the percentage of sub-G(1) cells detected by flow cytometry and by determination of caspase activity as a function of poly(ADP-ribose) polymerase cleavage. Furthermore, when human blood-derived granulocytes were treated with metamizol, MAA, and ASA at 75 microM or diclofenac at 3 microM, less than 10% of apoptotic granulocytes were detected, whereas at toxicological/suprapharmacological concentrations (10mM), about 90% of granulocytes were apoptotic. These results demonstrate that metamizol, MAA, ASA, and diclofenac, at pharmacological concentrations, neither affect the granulocytic differentiation process nor induce relevant apoptosis on terminally differentiated granulocytes.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2004

Characterisation of reversed-phase liquid-chromatographic columns by chromatographic tests comparing column classification based on chromatographic parameters and column performance for the separation of acetylsalicylic acid and related compounds.

Selection of RP-LC columns with suitable selectivity for a given analysis is difficult. For example, the European Pharmacopoeia (Ph. Eur.) and other official compendia for drug analysis only give a general description of the stationary phase in the operating procedure of a liquid chromatographic method. The need for a general test method to characterise RP-LC columns has been rising since the 1970s. A project to define a chromatographic procedure characterising RP-LC columns was started earlier. A procedure to measure test parameters was introduced and a classification of the columns, based on a minimal number of parameters, was obtained. This paper focuses on correlating the column classification with the selectivity obtained for a real separation. The separation of acetylsalicylic acid (aspirin) and related compounds was performed according to the Ph. Eur. monograph on the stationary phases previously characterised chromatographically. It was examined whether the classes of columns, determined using test parameter results, contain either suitable or unsuitable supports for the aspirin separation. The system suitability test prescribed by the Ph. Eur. in order to distinguish between suitable or unsuitable columns for this separation was also evaluated.

Aspirin↗
PubMed1985

Reduction in locomotor activity of arthritic rats as parameter for chronic pain: effect of morphine, acetylsalicylic acid and citalopram.

Arthritis was induced in rats by plantar injection of a suspension of killed mycobacteria in Viscoleo. Non-treated rats served as controls. The locomotor activities of the rats were measured weekly during the following four weeks. The exploratory activity was determined in the daytime in activity cages and spontaneous locomotor activity was measured during the night in the same cages. From one week to four weeks after treatment in one hind paw the arthritic rats showed significantly lower exploratory activity than the control rats, whereas the spontaneous locomotor activity in the arthritic rats was not significantly reduced. After treatment in two hind paws both activities were significantly smaller in the arthritic group than in the control group. The low exploratory activity level of the arthritic rats was not changed by acetylsalicylic acid but was significantly increased by morphine and citalopram in doses which did not influence the exploratory activity of the control rats. The results suggest that reduction of the locomotor activity of arthritic rats might be a reliable parameter for chronic pain.

Animals↗
PubMed1992

Photochemically induced thrombosis of the rat coronary artery and functional evaluation of thrombus formation by occurrence of ventricular arrhythmias. Effects of acetylsalicylic acid and a thromboxane A2 synthetase inhibitor of thrombus formation.

During i.v. infusion of rose bengal (48 mg/kg/h), the proximal portion of the rat left coronary artery was illuminated from the outside of the myocardium by green light (540 nm) to produce a transluminal thrombus subsequent to endothelial damages. The primary endothelial damages within the illuminated vascular portion, which resulted from the photochemical reaction between the dye and green light, and the subsequent formation of transluminal platelet-rich thrombus, were easily revealed by both light and electron microscopy. The establishment of the thrombus was accompanied in all cases by the occurrence of ventricular arrhythmias due to myocardial ischaemia. The times required to initiate ventricular premature beats (VPBs) and ventricular tachycardia (VT) were 381 +/- 96 s and 444 +/- 114 s (mean +/- SEM, n = 10), respectively. Pretreatment of the rat with acetylsalicylic acid (3 and 10 mg/kg, i.v.) before the initiation of illumination had no effect on the times required to exhibit the first VPBs and VT, the incidences of both types of arrhythmias were not reduced, and the thrombus was finally formed. On the other hand, pretreatment with Y-20811, a novel thromboxane A2 synthetase inhibitor (0.3, 1 and 3 mg/kg, i.v.), delayed the onset of both VPB and VT in a dose-dependent manner. The incidences of VPBs and VT were significantly reduced at 1 and 3 mg/kg, and the thrombus formation was prevented. The formation of a transluminal thrombus in the left coronary artery by the present technique was highly reproducible and could be functionally evaluated by the occurrence of ventricular arrhythmias.

Animals↗
PubMed1983

Thromboxane A2 in skin-bleeding-time blood and in clotted venous blood before and after administration of acetylsalicylic acid.

The 'Simplate' technique for measuring skin bleeding time was adapted to quantify thromboxane A2 in the emerging blood as the stable degradation product thromboxane B2 in twelve Swedish and ten English volunteers. During the bleeding time thromboxane B2 concentrations increased, but as the rate of blood loss fell the rate of production of thromboxane A2 was constant. The English subjects had shorter bleeding times and produced more thromboxane A2 than the Swedish subjects. When the Swedish subjects were grouped according to bleeding times those with the shortest had more thromboxane A2 than those with longer bleeding times. Clotting venous blood in vitro produced much more thromboxane A2 than bleeding-time blood and there was no correlation with bleeding time. Determination of the capacity of clotting blood to form thromboxane A2 is therefore irrelevant to in-vivo haemostasis. Acetylsalicylic acid greatly diminished the appearance of thromboxane A2 in the bleeding time and prevented the increase of thromboxane A2 concentration with time.

Adenosine Diphosphate↗
PubMed1997

Ticlopidine-associated pancytopenia: implications of an acetylsalicylic acid alternative.

Ticlopidine is an antiplatelet agent that has been proven efficacious in preventing vascular events in patients with a history of vasculopathy. Neutropenia is a significant adverse effect and pancytopenia is rarely reported. A fatal case of pancytopenia associated with unmonitored use of ticlopidine is presented. A 59-year-old woman presented with severe pneumonia and profound neutropenia (absolute neutrophil count 0%). She deteriorated with development of acute respiratory distress syndrome and a marked reduction in trilineage hematopoiesis. Despite prompt marrow response to granulocyte macrophage colony-stimulating factor (GM-CSF) and cessation of ticlopidine, appropriate antibiotics and other supportive therapy, she died 17 days after admission. Hematological monitoring is imperative to identify potential complications: if discovered late, there may be a role for GM-CSF for marrow support. Ticlopidine is indicated for patients intolerant of or nonresponsive to acetylsalicylic acid therapy. As the use of ticlopidine increases, clinicians must be aware of potential life-threatening complications associated with its use and monitor appropriately.

Aspirin↗
PubMed1997

Mechanisms involved in the early interaction between HeLa cells, platelets and endothelial cells in vitro under the influence of thrombin. Effects of acetylsalicylic acid and Na-salicylate.

The aim of the study was to obtain more information about the mechanisms involved in the initial adhesion of tumour cells to endothelial cell during metastasis. In a previous paper, we found that addition of both platelets and thrombin increased the adhesion of tumour cells to cultured endothelial cells within 15 min, compared to when either one or both of the ingredients were absent. In the present study, HeLa cells, prelabelled with radioactive 51Cr, human platelets, and thrombin, were added to the medium in dishes of endothelial cells. The dishes were then shaken for 15 min at 37 degrees C. Scanning and transmission electron micrographs showed HeLa cells adhering to the endothelium either together with platelets or without them. In other experiments, the endothelium was pretreated for 30 min with either of the following: 0.5 mM or 0.1 mM acetylsalicylic acid (ASA); 0.5 mM or 0.1 mM Na-salicylate (NaS). Pretreatment of the endothelium with 0.5 mM ASA significantly increased the percentage of adherent tumour cells, while 0.1 mM ASA and the two concentrations of NaS caused only minor changes. In addition, the ASA-treatment caused more HeLa cells to adhere without platelets while NaS-treatment caused more HeLa cells to adhere together with platelets. Release of 51Cr from HeLa cells during the experimental period was also measured; the addition of thrombin and platelets did not change the 51Cr release significantly. In separate experiments, HeLa cells and platelets were mixed without the presence of endothelial cells. Transmission electron micrographs showed that in the absence of thrombin, mixed HeLa cells and platelets did not react with each other; when thrombin was added they formed co-aggregates. In conclusion, we show that in our experimental model HeLa cells adhere to the endothelium in two ways, both with and without platelets. The production of prostacyclin in the endothelial cells has an inhibitory effect on tumour cell adhesion. Without thrombin, the HeLa cells are not capable of activating platelets.

Aspirin↗
PubMedDate not supplied

[Haemorrhagic exanthema due to dengue virus induced by acetylsalicylic acid].

Dengue fever, a viral infectious disease characteristic of tropical climates, is considered to be a re-emergent pathology responsible for several serious outbreaks in the last decade. Some factors have been involved in the spread of the virus and its vectorial mosquito carrier: human alteration of the ecosystems, improvement and speed in the transit of goods and people and climate changes. As a reflection of this, an increase in imported cases is probable, especially in tourists coming from endemic areas, considering its short period of incubation (7-10 days). The recognition of personal antecedents of journeys, the main symptoms of the disease and the potential presence of complications (haemorrhagic dengue) should be included in the examination of fever of unknown origin or feverish exanthema. The case of a patient is presented whose clinical picture of classic dengue fever was worsened by self-treatment with acetylsalicylic acid.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1996

Inhibition of thalidomide teratogenicity by acetylsalicylic acid: evidence for prostaglandin H synthase-catalyzed bioactivation of thalidomide to a teratogenic reactive intermediate.

Thalidomide is a teratogenic sedative-hypnotic drug that is structurally similar to phenytoin, which is thought to be bioactivated by prostaglandin H synthase (PHS) and other peroxidases to a teratogenic reactive intermediate. The relevance of this mechanism to thalidomide teratogenicity was evaluated in pregnant New Zealand White rabbits treated with thalidomide at 11:00 A.M. on gestational days 8 to 11, with day 0 indicating the time when sperm were observed in the vaginal fluid. Thalidomide (7.5 mg/kg i.v.) produced mainly fetal limb anomalies analogous to those observed in humans. Thalidomide (25-200 mg/kg i.p.), produced a dose-related increase in a spectrum of fetal anomalies, and in postpartum lethality, but did not produce a reliable incidence of limb anomalies. In subsequent studies, pregnant does received the irreversible PHS inhibitor acetylsalicylic acid (ASA), 75 mg/kg i.p., or its vehicle, followed 2 hr later by thalidomide, 7.5 mg/kg i.v., or its vehicle. ASA pretreatment was remarkably embryoprotective, resulting in respective 61.2 and 61.4% decreases in thalidomide-initiated fetal limb anomalies (P = .002) and postpartum fetal lethality (P < .02), and a small but significant reduction in thalidomide-initiated fetal weight loss. ASA alone did not produce significant embryopathy. These results show that ASA can protect the embryo from thalidomide teratogenicity, suggesting that thalidomide may be bioactivated by PHS to a teratogenic reactive intermediate.

Animals↗
PubMed2001

Efficacy of leukotriene receptor antagonist in chronic urticaria. A double-blind, placebo-controlled comparison of treatment with montelukast and cetirizine in patients with chronic urticaria with intolerance to food additive and/or acetylsalicylic acid.

BACKGROUND: The cause and pathogenesis of chronic urticaria are still poorly understood. IgE-independent reactions, are common in adult patients with chronic urticaria, who have daily spontaneous occurrence of weals. H(1)-receptor antagonists (antihistamines) are the major class of therapeutic agents used in the management of urticaria and angioedema. Nevertheless, chronic urticaria is often difficult to treat and may not be controlled by antihistamines alone. It has been postulated that mediators other than histamine, such as kinins, prostaglandin and leukotrienes, may be responsible for some of the symptoms in urticaria which are not controlled by antihistamines. In this study, which was randomized double-blind, placebo-controlled, we compare the clinical efficacy and safety of montelukast (MT) 10 mg given once a day and cetirizine (CET) 10 mg given once a day with placebo (PLA), in the treatment of patients with chronic urticaria who have positive challenge to acetylsalicylic acid (ASA) and/or food additives. PATIENTS AND METHODS: A group of 51 patients, ranging in age from 15 to 71 years, with chronic urticaria and positive challenge to food additives and/or ASA, participated in this study for a period of 4 weeks, starting from a 3-day run-in. The assessment of the efficacy was based on scores of daily urticaria symptoms. RESULTS: MT significantly increased the percentage of symptom-free days for hive and itch. Analysis of frequency distribution of urticaria scores for each symptom gave similar results (MT vs. CET and MT vs. PLA, P < 0.001). The interference with sleep due to their skin condition was also lower in the group treated with MT (P < 0.001). In addition, the median number of days without the rescue medication was significantly higher in the MT group (24 days) than both the CET and the PLA groups (18 days, P < 0.001, and 20 days, P < 0.001, respectively). Finally, a low incidence of adverse events was observed in this study. CONCLUSION: The results of this comparative study demonstrate that montelukast orally administered once a day is very effective for the treatment of cutaneous symptoms in patients with chronic urticaria due to food additives and/or ASA.

Acetates↗
PubMed1989

[Ranitidine protects the human stomach and duodenal mucosa against low-dose acetylsalicylic acid].

In a randomized double-blind study the gastroduodenal tolerability of 300 mg ASS daily has been evaluated in the presence of 150 mg ranitidine bid or placebo in 20 healthy volunteers using upper GI-endoscopy. The treatment period lasted 14 days. Endoscopic controls were performed at entry, and repeated at day 7 and day 14. At entry, the mean endoscopic score averaged 0.8 +/- 0.1 in the ASS/placebo-group and 1.0 +/- 0.0 in the ASS/ranitidine group. 300 mg ASS daily induced in the placebo experiments marked gastroduodenal alterations both at day 7 and day 14 (4.7 +/- 1.2 and 6.5 +/- 2.1, respectively). Concomitant administration of 150 mg ranitidine bid afforded almost full protection against 300 mg ASS daily both on day 7 and day 14 (1.9 +/- 0.6 and 2.1 +/- 0.8, respectively) (p less than 0.05). Our data suggest that coadministration of ranitidine 150 mg bid reduces almost completely gastroduodenal lesions evoked by acetylsalicylic acid 300 mg daily.

Adult↗