A study on the use of magnesium hydroxide during breastfeeding found no adverse reactions in breastfed infants. Intravenous magnesium increases milk magnesium concentrations only slightly. Oral absorption of magnesium by the infant is poor, so maternal magnesium hydroxide is not expected to affect the breastfed infant's serum magnesium. Magnesium hydroxide supplementation during pregnancy might delay the onset of lactation, but it can be taken during breastfeeding and no special precautions are required.

After aspirin ingestion, salicylic acid is excreted into breastmilk, with higher doses resulting in disproportionately higher milk levels. Long-term, high-dose maternal aspirin ingestion probably caused metabolic acidosis in one breastfed infant. Reye's syndrome is associated with aspirin administration to infants with viral infections, but the risk of Reye's syndrome from salicylate in breastmilk is unknown. An alternate drug is preferred over continuous high-dose, aspirin therapy. After daily low-dose aspiring (75 to 325 mg daily), no aspirin is excreted into breastmilk and salicylate levels are low. Daily low-dose aspirin therapy may be considered as an antiplatelet drug for use in breastfeeding women.[1][2][3].

Accelerated stability testing was performed on aspirin-magaldrate double layer tablets as well as aspirin-maalox marketed double layer tablets (Ascriptin) in order to evaluate the effect of the presence of the alkaline moieties of the antacid (magaldrate and maalox) on the chemical stability of aspirin. The results were compared simultaneously with that obtained from the marketed Aspro plain tablets. The results revealed that the presence of the alkaline moieties in the tested tablets has increased the rate of aspirin decomposition and reduced its shelf-life. This effect was more pronounced for aspirin tablets containing magaldrate antacid. Determination of shelf-lives at 25 degrees C for the prepared and the marketed tablets was carried out using Arrhenius plots and the results showed that they were 35, 34.5 and 13.5 months for Aspro, Ascriptin and aspirin-magaldrate double layer tablets, respectively. The effect of storage for 50 days and at different temperatures, on the crushing strength and the disintegration time of the prepared and the marked tablets showed a slight decrease in the disintegration time and the crushing strength of the tablets as the storage temperature increased. Aspro tablets did not produce the same results. The in vitro release data of the prepared aspirin-magaldrate double layer tablets and the marketed Ascriptin tablets stored for 50 days and at different storage temperatures as well as Aspro tablets stored at 70 degrees C were best fitted to the first-order kinetics model. The release data of Aspro tablets stored at 50 and 60 degrees C for 50 days were best fitted to Higuchi's model.

Double layer 325 mg oral aspirin tablets buffered with magaldrate antacid, 100, 150, 175 and 200 mg (F1, F2, F3 and F4, respectively) were prepared by direct compression. The new formulae were of remarkable hardness and friability. The tablets complied with the requirements of the acid neutralizing capacity, uniformity of dosage units, disintegration and dissolution tests (USP XXIII) for buffered aspirin tablets. The in vitro release pattern of F1 and F1 followed first order kinetics (r = 0.999), while F3 and F4 were released according to a zero order model (r = 0.993). Formulations F2, F3 and F4 as well as the marketed preparations, pure Aspro tablets (Acetylsalicylic acid 320 mg per tablet), or Ascriptin tablets (aspirin 325 mg plus 150 mg Maalox per tablet) were administered to fasted rats by gavage at doses that provided 400 mg aspirin kg-1 and the extent of the induced gastric damage was quantified 6 h later. Ascriptin, F3 and F4 preparations produced significantly less gastric damage (p < 0.05, n = 6) when compared with pure Aspro tablets. There was a clear dose-dependent decrease in the gastric damage following treatment with F2, F3 and F4 preparations, but there was no significant difference between the effects of F3 and F4 which were equipotent with Ascriptin.

Reported herein are two endoscopic studies performed to compare the gastrointestinal mucosal effects of encapsulated enteric-coated aspirin granules with several other well-known aspirin products. The first study compared the effects of Ascriptin A/D, Bayer, Bufferin, and 325 mg enteric-coated aspirin granules (325 mg Ecotrin capsules); the second study compared Anacin Arthritis Pain Formula, Arthritis Strength Bufferin, Ascriptin A/D, Bayer, and 500 mg enteric-coated aspirin granules (500 mg Ecotrin capsule). In both of these studies the Ecotrin capsule induced less stomach damage than did any of the other aspirin products tested. The Ecotrin capsule was also shown to cause less damage to the proximal duodenum than did Bayer.

The indwelling transcutaneous vascular access device is easily implantable with little more skill or time required than is typically used in placement of standard intravenous needles or catheters. With routine maintenance of the device site, the infection rate in our studies are negligible. Biocompatibilty, assessed by the lack of destruction of blood components and by the paucity of signs of initimal or systemic disease, was good. Over the period of 10 to 21 days, all but one unit maintained adequate flow rates. The device is stable. There was no blood leakage from the area around the limbs in the chronic flow studies or the hemodialysis studies. The one episode of malpositioning occurred after a sudden strong tug on the tubing. A second dacron retaining cuff will be placed on the distal limb. This will be sutured into place and should increase unit stability. There was little evidence of pain or irritation from the device. No thrombotic tendencies were noted at the access site or systemically. The dogs were on Ascriptin and also the model (canine) is not prone to thromboembolic events. Further improvements on the device will include using smoother, more compatible materials: carbon-coated steel, brushed titanium, or covering the steel with PTFE or ceramic rather than the silastic-dacron cuff. Other future changes include the improvement of the device-tubing connection to one in which no blood will be lost when the device is attached to the dialyzer.(ABSTRACT TRUNCATED AT 400 WORDS)

Larger-than-conventional doses of nonsteroidal antiinflammatory drugs (NSAIDs) are known to lower plasma glucose levels. This phenomenon has raised the questions whether or not NSAIDs in conventional dosage can be used for the treatment of hyperglycemia in patients who have non-insulin-dependent diabetes mellitus and whether or not NSAIDs added to preexistent hypoglycemic drug therapy taken orally may lead to unanticipated hypoglycemia. In this study we evaluated aspirin, sodium salicylate and ibuprofen given in conventional dosage to hyperglycemic patients with adult-onset (type II) diabetes. Half the patients were usually treated for hyperglycemia by means of diet only and half with diet plus hypoglycemic drugs given orally. Significant changes in plasma glucose levels were not seen after the administration of a combination drug containing aspirin and magnesium-aluminum hydroxide (Ascriptin, 650 mg three times a day; glucose change = 236+/-30 to 236+/-31 mg per dl) or sodium salicylate (600 mg three times a day; glucose change=284+/-76 to 273+/-84 mg per dl). A statistically significant but small change was seen with the administration of ibuprofen (600 mg three times a day; glucose change=196+/-60 to 179+/-47 mg per dl) but not when giving ibuprofen (300 mg three times a day; glucose change=267+/-78 to 282+/-60 mg per dl). The results of this study indicate that conventional doses of NSAIDs should not be used for treating hyperglycemia and that, since the additive hypoglycemic effect of NSAIDs in conventional doses was minimal or negligible, they can be used safely for other purposes in diabetic patients taking hypoglycemic drugs orally.

In a single dose clinical investigation two buffered acetylsalicylic acid formulations (Ascriptin and Ascriptin A/D) were shown to be significantly less irritating to the human gastric mucosa than acetylsalicylic acid, and no more irritating than a pharmacologically inert placebo. The measurements were taken using a minimally invasive method for recording transmural gastric potential difference changes versus time.

Despite venous stasis and a hypercoagulable state during pregnancy, the reported incidences of deep venous thrombosis and pulmonary embolism are remarkably low, about 1 in 2,000 and 1 in 10,000 cases, respectively. Mortality from antepartum thromboembolism has been reported in about 15 percent of untreated patients and less than 1 percent of treated patients. Adequate anticoagulant therapy significantly reduces maternal mortality and decreases postpartum morbidity. The proper anticoagulant agent for use during pregnancy has been widely debated. Coumarin compounds pass through the placenta and into the fetus. Hemorrhagic complications in the fetus are uncommon if prothrombin times are carefully controlled and if the drug is discontinued before delivery. However, coumarin during the first trimester has the teratogenic hazard of producing chondrodysplasia punctata. Heparin, in contrast, does not cross the placental barrier and is considered more effective treatment for deep venous thrombosis; however, long-term intravenous administration during pregnancy has been considered both impractical and possibly hazardous due to the risk of osteoporosis after 6 months of therapy. In our study, a combined regimen of intravenous and subcutaneous heparin was used successfully in four women with deep venous thrombosis. One patient who had recurrent embolization while on adequate intravenous heparin underwent vena caval clipping and had an uneventful Cesarian section at term with a normal infant. Another patient also underwent Caesarian section with a normal infant, while the other two women had normal vaginal deliveries at term. Miniheparin therapy was continued for 3 months postpartum, followed by long-term aspirin and Ascriptin therapy. Carefully controlled heparin therapy in a pregnant woman with deep venous thrombosis both safe and beneficial for mother and fetus.