Acetazolamide respiratory acidosis
Normal Subjects-- During the first 3 minCirculaiion Research, Vol. XXIV, June 1969.
217. Samson RR, McClelland DBL Vitamin B12 in human colostrum and milk: quantitation of the vitamin and its binder and the uptake of bound vitamin B, 2 by intestinal bacteria. Acta Paedio, tr Scand. 1980; 69: 93-99 Cancela L, LeBoulch N, Miravet L Relationship between the vitamin D content of maternal milk and the vitamin D status of nursing women and breast-fed infants. J EndocrinoL 1986; 110: 43-50 Rothberg AD, Pettifor JM, Cohen DF, et a!. Maternalinfant vitamin D relationships during breast-feeding. J Pediatr. 1982; 101: 500-503 Greer FR, Hollis BW, Napoli JL High concentrations of vitamin D2 in human milk associated with pharmacologic doses of vitamin D, . J Pediatr. 1984; 105: 61-64 Retief EF, Heyns ADuP, Oosthuizen M, et al. Aspects of folate metabolism in lactating women studied after ingestion of `4C-methylfolate. JMed ScL 1979; 277: 281-288 Dyggve HV, Dam H, Sondergaard E. Influence on the prothrombin time of breast-fed newborn babies of one single dose of vitamin K or synkavit given to the mother within 2 hours after birth. Acta Obstet Gynecol ScasuL 1956; 35: 440 Kries RV, Shearer M, McCarthy PT, et al. Vitamin K1 content of maternal milk: influence of the stage of lactation, lipid composition, and vitamin K1 supplements given to the mother. Pediatr Res. 1987; 22: 513-517 Soderman P, HartVig P. Fagerlund C. Acetazolamide excretion into human breast milk. Br J Clin PharmacoL 1984; 17: 599-600 Hofmeyr GJ, Sonnendecker EWW. Secretion of the gastrokinetic agent cisapride in human milk. EurJ Clin PharmacoL 1986; 30: 735-736 Somogyi A, Gugler R. Cimetidine excretion into breast milk. Br J Clin PharmacoL 1979; 7: 627-629 Hofmeyr GJ, van Icklekinge B. Dompridone and lactation. Lancet. 1983; 1: 647 Olsson B, Bolme P, Dahistrom B, et al. Excretion of noscapine in human breast milk. Eur J Clin PharmacoL 1986; 30: 213-215 Hardell L-I, Lindstrom B, Lonnerhoim G, et al. Pyridos.
Females, aged 1848 years ; using a higher 2% ; acetazolamide concentration. In this case, acetazolamide was applied on one side of the tongue while a solution of 0.4 mM quinine, matched to acetazolamide pH 9.2 ; and taste intensity, was simultaneously applied to the other side, after which subjects rated the sensation elicited by carbonated water. Acetazolamide effect on citric acid irritation. To control for non-specific effects of acetazolamide on proton-evoked irritation, the identical experiment was conducted using citric acid 40 l; applied by filter papers onto both sides of the tongue; Figure 1C ; , rather than carbonated water, in a separate session. Capsaicin cross-desensitization. We also tested if capsaicin cross-desensitized the sensations elicited by both carbonated water and citric acid. Capsaicin was sequentially applied to one side of the tongue with cotton swabs, five times successively at 1 min intervals; dH2O was simultaneously applied in an identical manner on the other side Figure 1A ; . After the last application the subject waited 10 min, followed either by immersion of the tongue into carbonated water Figure 1B ; or application of citric acid by filter paper Figure 1C ; . To ensure that the capsaicin indeed had a desensitizing effect, 18 subjects were pretreated with capsaicin on one side of the tongue and then tested 10 min later with capsaicin applied to both sides of the tongue via filter papers as with citric acid. pH control. To assess the possibility that the alkalinity of the acetazolamide solution affected the sensation elicited by carbonated water, a control experiment was performed on a separate group of 20 subjects 11 males, 9 females, aged 1948 years ; by applying dH2O titrated with NaOH to a pH 9.2, which matched that of the acetazolamide solution, on one side of the tongue and dH2O at neutral pH on the other side. Subjects then dipped their tongue into the carbonated water and performed the 2-AFC and rating tests as above. Tactile control. To control for possible local anesthetic effects of acetazolamide or capsaicin, the tactile sensitivity of the tongue was measured as follows. A weak von Frey monofilament Stoelting, bending force 0.045 or 0.229 mN ; was applied in random order 30 times to the tongue 10 stimuli to the side treated with acetazolamide or capsaicin, 10 to the non-treated side and 10 blanks ; . Subjects were asked to close their eyes and were prompted by a tone indicating impending stimulation, after which they indicated if they perceived whether a stimulus had been applied or not, and if they were sure or not sure of their judgement. From the response matrix an index of sensitivity R-index ; O'Mahony, 1992 ; was calculated for individual subjects on each side of the tongue separately to determine if detection was poorer on the treated side. Responses were also pooled in a single matrix to compute an R-index across the entire.
TARGETING RECEPTOR KINASES BY A NOVEL INDOLINONE DERIVATIVE IN MULTIPLE MYELOMA: ABROGATION OF STROMA-DERIVED INTERLEUKIN-6 SECRETION AND INDUCTION OF APOPTOSIS IN CYTOGENETICALLY DEFINED SUBGROUPS Guido Bisping1 * , Martin Kropff1 * , Doris Wenning1, Britta Dreyer1, Sergey Bessonov1, Frank Hilberg2, Gerald J. Roth3, Gerd Munzert3, Martin Stefanic3, Matthias Stelljes1, Christian Scheffold1, Carsten Mller-Tidow1, Peter Liebisch4, Nicola Lang5, Jelle Tchinda6, Hubert L. Serve1, Rolf M. Mesters1, Wolfgang E. Berdel1 and Joachim Kienast1 From the Department of Medicine Hematology and Oncology, University of Muenster, Muenster, Germany1 , Boehringer Ingelheim Austria GmbH, Vienna, Austria2 and Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany3 4Department of Internal Medicine III, University Hospital Ulm, Ulm, Germany, 5University Hospital Grohadern, Department of Medicine III, Ludwig-Maximilians-University, Munich, Germany, Institute of Human Genetics, University of Muenster, Muenster, Germany 6 Short title: BIBF 1000 in multiple myeloma Scientific section heading: Neoplasia Key words: myeloma, VEGF, bFGF, IL-6, receptor tyrosine kinases * G.B. and M.K. contributed equally to this work Address correspondence to: J. Kienast, MD Department of Medicine Hematology and Oncology University of Muenster, Albert-Schweitzer-Str. 33, D- 48129 Muenster, Germany Phone + 49 - 251 - 83 - 5 28 Fax + 49 - 251 - 83 - 5 28 Email: kienast uni-muenster * Several of the authors F.H. Frank Hilberg G.M. Gerd Munzert G.J.R. Gerald J. Roth ; , M.S. Martin Stefanic are employed by Boehringer Ingelheim Austria GmbH 1
8. Acetazolamide 9. Ethoxzolamide 10. Chlorothiazide 11. Cyclpenthiazide 12. Hydroflumethiazide 13. Ethacrinic acid XXI. Drugs used for Calcium therapy: 1. Calcium Glucoiuite 2. Calcium Levulinate 3. Calcium Lactate 4. Calcium Lactobionate XXII. Haematinics: 1. Ferrous Gluconate 2. Ferrous Fumerate 3. Ferrous Sulphate 4. Iron- Dextran Complex Drugs-4 5. Liver Extract 5. Ferric Ammonium Citrate 6. Iron-Sorbitol Complex r XXIII. Oral Contraceptives: I. Oestradiol 2. Lynestrenol 3. Mestranol 4. Nore-ethisterone 5. Norgestrel 6. Ethynodiol 'XXIv. Opthaimological Preparations: 1. Sulphacetamide 2. Boric Acid 3. Atropine 4. Pilocarpine 5. Phenylophrine 6. Homatropine 7. Physostigmine Salicylate XXV. Oxytocies: 1. Ergot Alkaloids 2. Oxytonic XXVI. Plasma Expanders and Transfusion Solution 1. Dextran 2. Polyvihyl Pyrrolidone 3. Dextrose Anhydrous 4. Sodium Chloride 5. Sod. Lacate 6. Pot. Chloride '" ". 1. Items 3, 6, 8 and 10 omitted by'S. O. 6]0 E ; , dated 17th August, 1982.
1. Macri, F. J.: Acetazolamide and the venous pressure of the cat eye, Pharmacologist 1: 56, 1959. Macri, F. J.: Acetazolamide and venous pressure of the eye, Arch. Ophthalmol. 63: 953, 1960. Eagle, H.- Amino acid metabolism in mammalian cell cultures, Science 130: 432, 1959. Kottler, M., Brubaker, R., and Macri, F.: The decay kinetics of substances which leave the anterior chamber by bulk flow, INVEST. OPHTHALMOL. 9: 758, 1970 and adalimumab.
And acetazolamide 500 mg IV twice a day ; administered to lower an eventual high intracranial pressure facing unexplained bilateral optic disc edema ; , his visual acuity deteriorated drastically within several days to 20 70 and hand motion OS. In addition, he developed difficulty in pursuit movements, fever, severe headache, neck rigidity, left afferent pupillary defect, rotatory nystagmus, left facial paraesthesia, and body hemiparesis. Lumbar puncture showed paradoxical lymphocytic hyperproteinic aseptic meningitis; cerebrospinal fluid opening pressure was normal. Mediastinal CT disclosed bilateral mediastinal lymphadenopathy with clear lung fields. Biopsy of the lymphatic node confirmed the diagnosis of sarcoidosis. Visual acuity continued to decline to positive nonoriented light perception OD, and no light perception OS. Oral prednisone at 90 mg day and azathioprine at 100 mg day were prescribed. One month later, BCVA was unchanged. VEPs showed an absence of P100 OS and reduced 3.8 mV, [normal, 8.7 mV] ; and delayed 140 msec ; P100 OD. A second gadolinium-enhanced, cerebral, T1-weighted axial MRI revealed a bilateral retrolaminar optic atrophy and 2 hyperintense signals on the left optic nerve and acidophilus.
Oxoid Ltd. ; to which 5 jtg of vancomycin, 3 p.g of 2 Fg amphotericin B, and 10 or 15 p.g of acetazolamide per ml were added were evaluated as selec
Acetazolamide lowers intraocular pressure and has mild anticonvulsant activity and acitretin.
Acetazolamide diamoxYILDIZ, M.: Effect of diphenylhydantion sodium on atrial flutter and fibrillation provoked by focal application of aconitine or delphinine. Am. Heart J. 60: 937, 1960.
Low-Dose Acetazolamide 50 mg kg ; . Of the 75 rats from 3 litters, 24 63% ; of 38 acidotic rats and 29 78% ; of 37 saline control rats survived to the conclusion of the study day 13 ; . No preretinal neovascularization was observed in either the low-dose acetazolamide rats or the saline control rats Table 2 ; . High-Dose Acetazolamide 200 mg kg ; . Of the 100 rats in 4 litters, 29 58% ; of 50 rats receiving high-dose acetazolamide 200 mg kg ; , and 44 88% ; of 50 saline control rats survived. Data from surviving rats were used for analysis. Preretinal neovascularization similar to ROP Fig. 2 ; occurred in 17 59% ; of 29 rats receiving high-dose acetazolamide vs. 0% of saline controls P 0.001; Table 2 ; . In affected rats, the median severity of neovascularization was 1 clock hour, with a range of up to clock hours. Rats receiving high-dose acetazolamide demonstrated growth retardation compared with saline controls at day 8 intermediate weight: 7.9 1.3 vs. 11.1 1.4 g, P 0.001 ; and at day 13 final weight: 13.0 2.2 vs. 18.2 2.2 g, P 0.001; Table 2 ; . Growth retardation was more severe in the high-dose than in the low-dose acetazolamide rats Table 2 ; . Ratios of the vascularized to total retinal areas were smaller in rats receiving high-dose acetazolamide compared with saline controls 94% 5% vs. 98% 1%, P 0.001; Table 2 ; . Low-dose acetazolamide rats had vascularized areas similar to those of saline controls. It should be noted that "vascularized retinal area" refers to the entire superficial retinal vasculature, normal and abnormal, from the optic nerve to the periphery. The vascularized retinal area is the converse of the peripheral avascular zone in immature retinas and actimmune.
Table 3 - Clinical evolution of patients and bacteria isolated per examination. Pathogen N of patients with isolated bacteria clinical classification of the evolution ; 1 2 3 Inclusion Day10 Day 30 Haemophilus influenzae 3 1 treatment failure ; treatment failure ; Haemophilus parainfluenzae 1 cured ; Klebsiella pneumoniae 1 7 2 cured ; 7 Moraxella catarrhalis 10 1 cured ; 3 4 improvements ; all cured ; 2 treatment failures ; Pseudomonas aeruginosa 2 3 1 cured ; cured ; 1 improvement ; Streptococcus pneumoniae 5 2 3 improvement ; 2 cured ; 1 treatment failure ; 1 treatment failure.
If acetazolamide fails after maximal dosage, it is appropriate to undertake a trial of dichlorphenamide, which in some patients can abolish hypokalemic attacks that acetazolamide is unable to prevent.
How does the hospice ensure that there is a valid order for all medications given to the patient? Rev. 265 12-94 M-58 and adefovir.
Background and Purpose--There is growing evidence that pharmacologic interference with the renin-angiotensin system may reduce risk of stroke, although the mechanism is unclear. Impaired reactivity of cerebral vessels has recently been recognized as a risk factor for stroke. We examined the effect of the angiotensin-converting enzyme ACE ; inhibitor perindopril on cerebral vasomotor reactivity to acetazolamide in patients with lacunar cerebral infarction. Methods--We studied a cohort of male patients between 3 and 12 months after lacunar infarction confirmed on computed tomography. Each patient received perindopril 4 mg daily or matching placebo for 2 weeks in a randomized, double-blind, placebo-controlled crossover fashion. A 1-week washout period was observed between dosing periods. Cerebral vasomotor reactivity increase in middle cerebral artery mean flow velocity in response to intravenous injection of 15 mg kg acetazolamide ; was measured before and after each dosing period using standard Doppler ultrasound techniques. Results--Twelve patients mean age 63.2 2.3 years ; completed the protocol. There was no treatment order effect. Cerebral vasomotor reactivity was significantly greater after perindopril treatment percent change from baseline 18.8 10.1% after perindopril, 4.6 4.1% after placebo; P 0.032 ; . Dosing with perindopril did not affect resting cerebral blood flow velocity percent change from baseline 3.1 9.5% after perindopril, 0.6 5.4% after placebo ; , nor was there a change in resting blood pressure 1.8 mm Hg 3.1 after perindopril, 1.4 mm Hg 2.5 after placebo ; . Conclusions--This study provides evidence of a significant improvement in cerebral vasomotor reactivity induced by perindopril, beyond any effect on blood pressure. The results suggest a possible mechanism for the beneficial effect of ACE inhibition on stroke risk observed in recent clinical trials, and suggest a role for the renin-angiotensin axis in the pathophysiology of subcortical small vessel disease. Stroke. 2004; 35: 1899-1902. ; Key Words: hemodynamics ultrasonography, Doppler, transcranial white matter.
80. 128 CONTINUED: BUTCH Be right back. Don't be stingy with that mustard now. Phillip nods and continues piling the yellow goop on each of the slices of bread. BUTCH walks ahead to the crest of the hill, the tallest hill in the county. He takes in the 360 degree view. His eyes settle on. LINE OF CARS IDLING as they wait their turn to pass a roadblock at the bottom of the hill. PHILLIP spreading even more mustard. Every so often he sneaks a peek back at the picnicing family. EMERGENCY BRAKE slips a little, then gives all at once. FORD starts to roll backwards. Whooaaa! BUTCH turns and sees the Ford rolling backwards, picking up steam back down the hill. BUTCH Step on the brake! Put your foot on the brake! The middle one!! PHILLIP panicked, slides over and grabs the wheel. Of course, he is too short to press on the brake and when he bends down. FORD swerves off the road and onto the shoulder. CONTINUED ; Butch! PHILLIP Butch!!! 128 and adriamycin.
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Amide and MPA studies.9, 12, 17 A possible explanation could be a different technique: measurement of the HVR at predrug Pco2 level resulted in an increased HVR12, 15, 19 instead of a decrease under lower postdrug Pco2 levels.9, 12, 17 The slope of P0.1 vs Sao2 was significantly increased by acetazolamide Fig 5 ; , but did not reach any significance with MPA. For MPA, this is in agreement of the observations of Schoene et al, 40 although this is inconsistent with the observed increase in HVR. This might be due to the large interindividual and intraindividual variability as mentioned by Whitelaw et al.24 Nocturnal Parameters Acetazolamide treatment significantly decreased nocturnal desaturation time the percentage of time with Sao2 90% ; . It is known that the respiratory stimulant may contribute to improvement of desaturation time by diminishing central sleep apnea and periodic breathing.41 This supports the opinion that acetazolamide augments the chemical drive, as was shown in those patients. This may also explain the decrease in Petco2, although occasional nocturnal hypoventilation may still be present. MPA has a beneficial effect on Petco2, as shown in Table 5. This is in agreement with others.42 Clinical Implications The current study showed that short-term acetazolamide treatment is more beneficial compared to short-term MPA treatment, as can be seen from a larger change in daytime Paco2 in hypercapnic patients with COPD. However, the long-term clinical benefit of acetazolamide and MPA treatment on patients with severe COPD remains to be investigated. The possible effect on survival of a modest increase in Pao2 and a decrease in Paco2 is not yet clear. Hypoxia and hypercapnia are both considered to be independent poor prognostic factors for survival, 2, 4, 43 yet others question the prognostic role of hypercapnia.3 If the role of Paco2 as an independent predictor for a prognostic poor prognosis will be and acetazolamide!
When Goldmann and Schmidt first described the applanation tonometer, they discussed the possible influence of corneal thickness on IOP as measured by the device. At the time, they assumed a normal corneal thickness of 500 m, and theorized variations in corneal thickness only occurred rarely in the face of significant corneal disease. As optical and later ultrasonic pachymeters came into widespread use, it became apparent that variations in corneal thickness are much more widespread than once believed. The OHTS confirmed that measurement of CCT is useful for all ocular hypertension patients to estimate their actual risk for progression to POAG. In a recent meta-analysis of the corneal thickness literature, Doughty and Zaman reported that the mean corneal thickness in eyes described as normal was 534 m, for slit-lamp-based optical pachymetry, mean corneal thickness was 530 m, and for ultrasonic pachymetry, 544 m.[Goldmann applanation tonometers assume a CCT of 500 m, and an algorithm for correction of corneal thickness variations has not been established. Several studies have suggested conversion factors, but they vary widely.The most conservative estimates suggest 2 mmHg for each 100 m change in corneal thickness, while other studies have suggested as much as 5 mmHg for each 70 m change. It is most likely that the relationship between CCT and true IOP measurement is complex and nonlinear, and cannot be corrected with a simple conversion factor and agenerase.
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Surgical transection of the optic nerve was performed on one eye of rabbits and a sham procedure on the fellow eye. The operative procedures, criteria for utilization, and techniques for measurement of intraocular pressure and outflow facility using topical anesthesia alone were previously described1. The blood supply to the extraocular muscles was not interrupted. Care was taken to avoid damaging neighboring vessels accompanying the optic nerve and the central retinal artery which enters the optic nerve close to the globe. Animals were not used until at least one month after transection. Several drugs were tested. Ethanol, 50 per cent, was administered by oral-gastric tube, in doses of 0.75, 1.5, and 2.0 ml. per kilogram of body weight. Schi0tz tonometry was done before and 1 and 2 hours after administration. Pilocarpine, 4 per cent drops, was applied topically to both eyes 4 times a day for 4 days, and tonography was carried out two hours after the last drop. Epinephrine hydrochloride, 2 per cent drops, was applied topically to both eyes 3 times a day for 2 days, and tonography was carried out 2 hours after the last drop. Acetazolamide Diamox ; , 50 mg. per milliliter, was administered intra.
Lytic activity and demonstrated that inhibitors of leukocyte elastase24, 42, 43 were able to inhibit the caseinolytic activity of activated PMN-conditioned medium, to limit fibronectin degradation, and to prevent SMC retraction and anoikis, suggesting that leukocyte elastase is the main molecular effector of the phenomenon. Nevertheless, other agents, such as external superoxide anion O2 can induce apoptosis in some cultured cells, eg, arabidopsis mutants 44 and cardiomyocytes.45 Finally, we tested the hypothesis that ANP potentiation by NEP inhibition was able to prevent SMC anoikis induced by activated PMN supernatant. Preconditioning PMNs with ANP and NEP inhibition limited the ability of this supernatant to generate caseinolytic activity, to solubilize fibronectin fragments, and to induce SMC anoikis. Recently, it has been shown that ANP overexpression in SMCs reduces cell growth and induces apoptosis.46 Of interest, exogenous ANP did not induce SMC apoptosis in that study, in accordance with our results, and the authors suggested that the ANP accumulation within the cell triggered apoptosis. In conclusion, the present study confirms that natriuretic peptide and NEP inhibition can limit PMN activation. We demonstrated that ANP potentiation by NEP inhibition was able to inhibit PMN adhesion to hypoxic endothelial cells and the subsequent release of latent MMP-9, suggesting that latent MMP-9 could be used as an intermediate marker of PMN activation. The present study demonstrates, for the first time, that leukocyte elastase released by activated PMNs induces SMC anoikis, which is due, at least in part, to pericellular proteolysis of fibronectin. This phenomenon is also limited by ANP and by NEP inhibition. These data suggest that pathological conditions involving activated PMNvascular cell interactions could be interesting therapeutic targets for NEP inhibition in vivo and aggrenox.
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The available data on solubility, on oral absorption and permeability are not sufficiently conclusive to classify acetazolamide with certainty and acidophilus!
Antihistamine Decongestants ALLEGRA-D * promethazine w codeine promethazine w dm Antitussive & Expectorants benzonatate hydrocodone w guaifenesin promethazine w codeine TUSSIONEX Beta-2 Adrenergics OBSTETRICAL & albuterol GYNECOLOGICAL FORADIL MEDICATIONS metaproterenol PROAIR HFA PROVENTIL HFA Androgen Drugs SEREVENT DISKUS ANDRODERM terbutaline sulfate ANDROGEL VENTOLIN HFA Contraceptives XOPENEX, HFA NOTE: All generic Leukotriene Modifiers contraceptives are considered formulary, unless SINGULAIR excluded by benefit design. Methyl Xanthines ORTHO TRI-CYCLEN LO * aminophylline YASMIN theophylline, anhydrous, er YAZ UNIPHYL [G] Estrogen Drugs Other Drugs For Asthma estradiol, tds ADVAIR DISKUS, HFA VAGIFEM COMBIVENT cromolyn sodium Estrogen Progestin EPIPEN, JR [INJ] Combinations FLOVENT DISKUS, HFA CLIMARA PRO INTAL inh COMBIPATCH ipratropium bromide Prenatal Vitamins ipratropium-albuterol NOTE: All oral prescription PULMICORT generic prenatal vitamins are QVAR formulary. SPIRIVA Progestin Drugs SYMBICORT medroxyprogesterone acetate TILADE PROMETRIUM TWINJECT [INJ] Specialized OB GYN Drugs UROLOGICAL MEDICATIONS leuprolide acetate [INJ] OPHTHALMIC MEDICATIONS Anticholinergic Antispasmodics ENABLEX Antibacterial Drugs oxybutynin, er ciprofloxacin OXYTROL erythromycin VESICARE gentamicin sulfate ofloxacin Drugs Used For BPH polymyxin b sul trimethoprim finasteride sulfacetamide sodium FLOMAX tobramycin sulfate UROXATRAL VIGAMOX ZYMAR WEIGHT MANAGEMENT Antiglaucoma Drugs NOTE: Coverage based on acetazolamide benefit design. ALPHAGAN P brimonidine tartrate Appetite Suppressants COSOPT * phentermine hcl LUMIGAN pilocarpine hcl DIABETIC SUPPLIES timolol maleate TRUSOPT * NOTE: Coverage based on XALATAN benefit design. Corticosteroid Drugs Meters & Strips LOTEMAX ASCENSIA AUTODISC, prednisolone acetate BREEZE 2 ASCENSIA CONTOUR SYSTEM Other Ophthalmic Drugs ACULAR excluding LS & PF ; ASCENSIA DEX2, ELITE XL ASCENSIA MICROFILL atropine sulfate GLUCOMETER DEX, ELITE, PATADAY ENCORE PATANOL ONETOUCH II, BASIC, PROFILE VOLTAREN ophthalmic ONETOUCH FASTTAKE ZYLET ONETOUCH INDUO RESPIRATORY MEDICATIONS ONETOUCH SURESTEP ONETOUCH ULTRA, -2, -SMART ONETOUCH ULTRAMINI Antihistamines PRECISION XTRA fexofenadine Miscellaneous Supplies promethazine NOVOFINE 30 PRECISION SURE DOSE and alefacept.
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