Thiothixene

This leaflet answers some common questions about CHAMPIX. It does not contain all the available information. It does not take the place of talking to your doctor or pharmacist. All medicines have risks and benefits. Your doctor has weighed the risks of you taking CHAMPIX against the benefits they expect it will have for you. If you have any concerns about taking this medicine, ask your doctor or pharmacist. Keep this leaflet with the medicine. You may need to read it again. Navane: thiothixene : orap: diphenylbutylpiperidine: pimozide. Based on precipitation ofthe ape-B-containing lipoproteins. The quality of the precipitation often is questioned, whatever the agent. The critical studies need to be discussed in light of recent works in which more complicated methods such as ultracentrif# gation, cholesterol labeling, or electroiminunoassays 1-3 ; were used to validate these techniques. Elsewhere 4 ; , we correlated ultracentrifugation with polyacrylainide gel electrophoresis PAGE ; of lipoprothins, using a concentration and pH gradient and Sudan Black staining "Lipophor" tubes; Miles Labs, Elkhart, IN 46514 ; . We believed such an electrophoresis could be used to test the efficiency of the precipitation techniques. Thus we studied the method used most frequently in the U.S.A. 5 ; and Europe, a sodium phosphotungstate-MgCl2 NAP reagent ; , as well as a method involving polyethylene glycol 6000 at pH 10 PEG reagent ; , considered 6 ; to be very good technique. Experiments were performed either on 60 individual randomly selected sera from fasting normolipemic subjects [total cholesterol TC ; 3.39 to 6.12 mmol L; triglycerides TG ; 0.58 to 1.34 mmolJL; phospholipids PL ; 2.10 to 3.06 mmol L] or 40 individual sera covering a wide range of lipemia, from subjects with type Ha, llb, and JV according to Fredrickson's classification and from malnourished patients on total parenteral nutrition TC 0.61 to 9.23 mmolJL; TG 0.48 to 2.60 mmoIJL; PL 1.74 to 4.97 mmoIJL ; . We excluded from this study patients with types I, ifi, or V because the hypertriglyceridemia impedes HDL-C evaluation. Moreover, such sera represent 1% of all hyperlipemias in the population of our regions 7 ; . The precipitation techniques were used according to the authors' recommendations 8, 9 ; . CVs were 1.6% within-run and 4.2% between-run for the PEG technique, and 1.1% and 3.9%, respectively, for the NAP technique. Cholesterol was quantified by an enzymatic procedure Bio-M# rieux, Marcy l'Etoile, 69260, France ; . For electrophoretic control, we used the supernates and the precipitates redissolved in a sodium citrate 0.15 molJL ; -sodium chloride 0.11 moIIL ; solution. Each chromatogram was densitometrically measured to quantify the a and pref3 + 3 migrating material. Results were expressed as percentages. Then, from these percentages and TC, we evaluated each fraction in terms of millimoles of HDL-C per liter. The results, tabulated on the next page, show that a ; in PEG reagent, gains and losses were not negligible but counterbalanced each other; and b ; in NAP reagent, although the gains were similar to those found with PEG reagent, the losses were definitely greater, and this induced a consistent decrease in measured HDL-C. To assess our results, we took a methodological precaution to ensure that no significant variation in the results should be ascribable to changes of physicochemical conditions pH or PEG, phosphotungstic acid, and Mg concentrations ; with either precipitating reagent. Intragroup analysis of variance demonstrated that the concentration of cholesterol in the supernates was constant a ; in PEG reagent when the pH was varied from 9.00 to 10.50 and the PEG concentration from 80 to 120 gIL F 5.84, P 0.001 ; and b ; in NAP reagent when the pH ranged from 5.20 to 6.20, the Mg concentration from 1.00 to 2.50 mollL, and the phosphotungstic acid concentration from 35 to 50 8.29, P 0.001 ; . PAGE evidently is a suitable alternative to more-complicated methods for validating precipitation methods used to quantify HDL-C. Please see brief summary of navanex thiothixene thiothixene hci ; prescribing information on adjacent page.

Shed in excreta and oroprahyngeal fluids in the ELS, as has been demonstrated in multiple other species Komar et al., 2003 ; . Contact transmission of WNV has been reported in several bird species maintained under laboratory conditions McLean et al., 2002; Komar et al., 2003 ; and may occur when ELS are housed together. Furthermore, as a carnivore, the ELS may be susceptible to WNV infection if it consumes infected prey Komar et al., 2003 ; . After vaccination, WNV neutralizing antibodies were demonstrated in 84% of the birds, which suggests that vaccination may protect ELS against WNV infection. The protective antibody level is largely unknown, but, in experimentally infected rock doves Columba livia ; , titers ranged from 10 to 640, 29 wk after inoculation Komar et al., 2003 ; . Because ELS appears to be exquisitely susceptible to WNV, vaccination may be an important tool in the preservation of the species, at least in captivity. We thank the staff at the Toronto Zoo for handling of and care for the shrikes, and the Histopathology Section, Animal Health Laboratory, Laboratory Services Division, University of Guelph, Guelph, Ontario, for carrying out the immunohistochemistry and tiagabine. Fig. 7G-I ; , suggesting that the muscarinic receptors couple in jejunum smooth muscle to the Cav1.2 channel and a member of the SOC family. To further prove this possibility, contractions were induced by capacitative Ca2 re-entry, which is supposed to be carried mainly by store-operated channels 23 ; . Surprisingly, the responses to capacitative Ca2 entry were much larger in jejunum muscles from Cav1.2SMACKO than from CTR mice Fig. 7JL ; . In addition, activation of Ca2 -entry by thapsigargin induced also larger contractions in muscles from Cav1.2SMACKO than from CTR mice 0.40 0.04 vs. 0.22 0.03 N g; n 35 44; P 0.001 ; , which were abolished by the putative SOC inhibitor Gd3 not shown ; . The contractions induced by capacitative Ca2 re-entry were concentration-dependently blocked by SKF96365 in both muscles from CTR and Cav1.2SMACKO mice Fig. 7J, K ; with IC50's of 12 and 14 M, respectively. These results indicate that, in jejunum muscle, muscarinic receptor activation can maintain a "normal" contraction in the Cav1.2SMACKO mice by switching from L-type calcium channel to a SOC-like channel 24. UMAN isolated cleft palate, which has an incidence of about 1 in 2500 human births, is an important clinical problem. Steroid-induced cleft palate in mice has been a popular model of the etiology of cleft palate FRASER and FAINSTAT1951 ; . It has been established that genetically different mouse strains exhibit different degrees of susceptibility to steroid-induced cleft palate FRASERand FAINSTAT1951; FRASER, WALKERand TRASLER 1957; KALTER 1954 ; . Genetic analyses have shown that the differences between inbred strains of mice with respect to their incidences of steroid-induced cleft palate cannot be explained by only one or two genetic factors KALTER1954; FRANCIS1973; BIDDLEand FRASER 1976, 1977 ; . A factor influencing this variable is the major histocompatibility locus, H-2. This was identified by the use of congenic strains and timolol. Pharmaceutical Research and Manufacturers of America QT Statistics Expert Working Team * Washington, District of Columbia Key Words QTc prolongation; Statistics; Design; Analysis; Interpretation Correspondence Address Scott D Patterson, Biomedical Data Sciences, GlaxoSmithKline Pharmaceuticals, 1250 South Collegeville Road, Collegeville, PA 19426 e-mail: scott.d.patterson gsk ; . The Drug Information Association is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The Drug Information Association designates this educational activity for a maximum of 1 category 1 credit toward the AMA Physician's Recognition Award. Each physician should only claim those credits that he she actually spent in the activity. The Drug Information Association is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education. This program is designated for a maximum of 1 contact hour or .1 continuing education units CEUs ; . 286-000-05-412-H04. Release Date: August 2005 Expiration Date: August 31, 2006 Estimated time to complete the activity: 1 hour * The Pharmaceutical Research and Manufacturers of America QT Statistics Expert Working Team is composed of: Scott Patterson, PhD Chair ; , GlaxoSmithKline; Marilyn Agin, PhD Chair ; Pfizer; Rich Anziano, PhD, Pfizer; Tracy Burgess, Roche; Christy ChuangStein, PhD, Pfizer; Alex Dmitrienko, PhD, Eli-Lilly; Georg Ferber, PhD, Novartis; Margarida Geraldes, PhD, Bristol-Myers Squibb; Kalyan Ghosh, PhD, Merck; Ron Menton, PhD, Wyeth; Jaya Natarajan, PhD, Johnson & Johnson; Walt Offen, PhD, EliLilly; Jay Saoud, PhD, Aventis; Brian Smith, PhD Eli-Lilly; Ram Suresh, PhD, Schering Plough; and Nvine Zariffa, MMath, GlaxoSmithKline. Plan B is a form of emergency contraception. Emergency contraception is a way to help prevent pregnancy after unprotected sex. Because emergency contraception prevents pregnancy before it begins, it is not the same as an abortion and ting.

A Dose of Prevention Toolkit, Community Anti-Drug Coalitions of America and Consumer Healthcare Products Association: D OSEO FPREVENTI O N.O RG What Every Parent Needs to Know about Cough Medicine Abuse, Partnership for a Drug-Free America and Consumer Healthcare Products Association: CH PA-I N FO.O RG PU BS Stopping Cough Medicine Abuse, Consumer Healthcare Products Association: CH PA-I N FO.O RG CH PAPO RTAL FO RCO NSU M ERS CO U G ABUSE STO P CO U ABUSE Intelligence Bulletin: DXM, U.S. Department of Justice: USD OJ.G OV N D BS1111563 I N D What Every Parent Needs to Know about Cough Medicine Abuse, Partnership for a Drug-Free America and Consumer Healthcare Products Association: CH PA-I N FO.O RG PU BS Battling The Over-The-Counter High, Substance Abuse and Mental Health Services Administration: S: N CAD ISTO RE.SAM HSA.G OV CATALO G M ED IAD ETAI LS X?I D 371 Teens: Make Up Your Own Mind About DXM, Partnership for a Drug-Free America: DXMSTO RI ES.CO M.

Williams or Broughton are Commission-authorized physicians, and the Claimant is not requesting that the Commission order UAPB to pay for the services that he has received from them. He is asking, however, that UAPB compensate him for the additional maladies that he has suffered in the aftermath of his compensable eye injury and for future medical treatment. Following a hearing on March 20, 2003, the Administrative Law Judge in an opinion filed July 12, 2003 made the following findings of fact and conclusions of law: 1. 2. 3. The employee-employer-carrier relationship existed at all relevant times. The Claimant sustained a compensable injury to his right eye on June 28, 1995. The Claimant's average weekly wage is 5.20. The Respondents paid permanent partial disability from May 20, 1996 to June 13, 1998. The Respondents paid for Claimant's glaucoma surgery. The Claimant petitioned the Workers' Compensation Commission and received an order changing physicians. The preponderance of the evidence reflects that the Claimant is not entitled to medical treatment for alleged compensable consequences of his compensable eye injury and tinzaparin.

Pathway enzymes. Examples of these include pinoresinol lariciresinol reductases 13, 14 ; , secoisolariciresinol dehydrogenase 15-17 ; , phenylcoumaran benzylic ether reductase 14, 18 ; , isoflavone reductase 14 ; , cinnamyl alcohol dehydrogenases 19, 20 ; , chavicol p-anol and eugenol isoeugenol synthases 21, 22 ; , as well as dirigent proteins in the presence of auxiliary oxidative capacity ; 23-25 ; . These studies are part of broader goals aimed towards i ; systematically engineering selected enzyme substrate binding pockets in terms of potentially modifying them to be more specific for a particular metabolite metabolic pathway, and ii ; better understanding how these pathways in plants have evolved. The objective of the study herein is to determine the mechanism and structures of the enzyme involved in formation of medicinally promising dihydrophenylpropanoid derivatives, such as dihydroconiferyl alcohol 1 ; . In the Pinaceae, e.g. loblolly pine Pinus taeda ; , various dihydrophenylpropanoids accumulate as heartwood-forming constituents which contribute to the color, quality, and durability of its woody tissues; these can have either propanol, propionic acid or propanaldehyde side-chains [e.g. p-dihydrocoumaric 4 ; dihydroferulic 3 ; acids and p-dihydrocoumaryl 2 ; dihydroconiferyl 1 ; alcohols in Picea glauca 26 ; ]. Interestingly, their amounts e.g. 1 and 2 ; are known to increase in the galls of P. glauca upon aphid attack e.g. by Adelges abietis ; 26 ; , in further support of roles in plant defense. In 2001, we reported the discovery of a P. taeda phenylpropenal , double bond ; reductase PtPPDBR1 ; see Fig. 1A ; , whose encoding gene see Fig. 2 ; was cloned with the functionally recombinant protein obtained and preliminarily characterized 27 ; . This enzyme, which is a member of the Zn-independent medium chain dehydrogenase reductase MDR ; superfamily, catalyzes the NADPH-dependent conversion of various monomeric and dimeric phenylpropenalaldehydes e.g. 6 7, Fig. 1A ; into the corresponding phenylpropanaldehydes e.g. 8 9 ; . terms of its amino acid similarity identity, PtPPDBR has the closest homology to the Arabidopsis thaliana At5g16970 AtDBR1 ; , as well as to a gene encoding + ; -pulegone reductase PulR ; from Mentha piperita 28 ; , i.e!

Side effects common side effects associated with the use of thiothixene are abnormal muscle movements and muscle stiffness, muscle tremors, weight gain, sleepiness, dry mouth, dry eyes, difficulty urinating, constipation, and sudden decreases in blood pressure that cause dizziness when standing up suddenly and tobi. 2345-2346 3. Otto, K. 1965 ; 2. Phys. Chem. 341, 99-104 Lopes-Vieira, O., and Walker, B. 1967 ; 4. WiIliamson, D. H., Biochem. J. 104, 497-502 weight ml ; were incubated in Krebs-Ringer bicarbonate buffer, equil5. Brosnan, J. T., Krebs, H. A and Williamson, D. H. 1970 ; ibrated with an Oz C02mixture 95: 5 ; at 36.5 "C, in the presence of Biochem. J. 1 91-96 1 m pyruvate as substrate and the indicated L-cycloserine to pyruM 6. Wong, D. T., Fuller, R. W., and Molloy, B. B. 1973 ; Adu. Enzyme vate ratios.Samples were processed as described under "Experimental Regul. 11, 139-154 Procedures." Rates were calculated for the incubation interval be7. Barbieri, P., Di Marco, A., Fuoco, L., Julita, P., Migliacci, A., and tween 0 and 30 min. Rusconi, A. 1960 ; Biochern. Phrmacol. 3, 264-271 8. Braunstein, A. E. 1961 ; Proc. Int. Congr. Biochern. 4, 280-294 on products or substrates removal becomes available. 9. Williamson, 3. R., Meijer, A. J., and Ohkawa, K. 1974 ; in Regulation of Hepatic Metabolism Lundquist, F., and Tygstrup, The usefulness of t-cycloserine asa metabolic inhibitor lies N., eds ; pp. 457-479, Munksgaard, Copenhagen entirely on its ability to inhibit aminotransferases. L-CycloGimpel, J. Deleeuw, Tischler, M. E., Tager, serine has been utilized in two main ways: first, t o study 10. Meijer, A. J., Williamson, A., R. 1978 ; G., Biol. Chem. 253, 2308J. M., and J. J. amino acid production and or removal under several meta2320 biological 11. Lardy, M. A., Paetkan, V., and Walter, P. 1965 ; Proc. Natl. bolic or nutritional conditions 4-5 ; , or to study the Acad. Sci. U. S. A. 53, 1410-1415 effects of certain aminoacids when theirmetabolic conversion was prevented 25, 26 second, it hasbeen used as a selective 12. Krebs, H. A., Gascoyne, T., and Notton, B. M. 1967 ; Bwchem. J. 102, 275-282 inhibitor of hepatic gluconeogenesisfrom substrates more 13. and reduced than glucose 10 ; . From stoichiometric evaluations of 14. Berry, M . N., Friend, D. S. 1969 ; J. Cell Biol. 43, 506-520 . Seglen, P. 0 1976 ; Methods Cell Biol. 13, 29-83 carbon andhydrogen balances, it was postulated 1 1-12 ; that, 15. Girbes, T., Susin, A., Ayuso, M. S., and Parrilla, R. 1983 ; Arch. during gluconeogenesis fromsubstrates yielding pyruvate, Biochem., Biophys. 226, 37-49 intramitochondriallyformed oxaloacetate, would leave the 16. Bergemeyer, H. V. ed ; 1965 ; Methods of Enzymatic Analysis, Academic Press, New York mitochondria predominantly as aspartate or as malate when the substrate was morereduced lactate ; or more oxidized 17. Cer&n, S., Subramanian, V. H., Hiberman, M., Cone, J., Egan, J., Chance, E., and Williamson, J. R. 1986 ; Magn. Reson. pyruvate ; than glucose, respectively. If oxaloacetate leaves Med. 3, 432-439 the mitochondria as aspartate, then transamination is essen- 18. Cerdan., S: , Parrilla, R., Santoro, J., and Rico, M. 1985 ; FEBS tial toform aspartate in the mitochondrial matrix and to yield LRtt. 187, 167-172 oxaloacetate in the cytosol. The observation that t-cycloser- 19. Segal, H. L., Beattie, E. S., and Hopper, S. 1962 ; J. Biol. Chem. 23`7, 1914-1920 ine inhibited only gluconeogenesis from lactate with no de20. Ojelund, G., and Wadso, I. 1967 ; Acta Chem. S c a 21, 1408tectable effectswhen pyruvate was the carbon sourcewas 1414 utilized in support of this hypothesis 10 ; . The results pre- 21. Griffiths, V. S., and Socrates, G. 1967 ; Trans. Faraday SOC. 20, sented seriously question thevalidity o f these arguments. The 673-677 inhibitory effect of L-cycloserine on gluconeogenesis from 1 22. Turchin, K. F. 1971 ; Zh. Strukt. Khim. 12, 996-1000 mM pyruvate Fig. 7 ; suggests that its inhibitory effect on 23. Meijer, A. J., Gimpel, J. A., Deleeuw, G.A., Tager, J. M., and Williamson, J. R. 1975 ; J . Biol. Chem. 250, 7728-7739 lactate to glucose flux could probably be explained solely on the basis of its ability to remove pyruvate.When 10 mM 24. Dieterle, P., Brawand, F., Moser, V. K., and Walter, P. 1978 ; Eur. J. Biochem. 88, 467-473 lactate is utilized as a substrate, the expected intracellular 25. Tischler, M. E., Desautels, M., and Goldberg, A. L. 1982 ; J. Biol. concentration of pyruvate should be approximately 0.3 mM. Chern. 257, 1613-1621 According to the data presented Figs. 1and 7, L-cycloserine 26. P6rez-Sala, M. D., Parrilla, R. 1985 ; XI1 Congress of The in and Spanish Biochemical Society, Valencia Abstr. 167 ; concentrations above 1 mM 10 ; would cause an inhibition of gluconeogenesis whether or not the transamination steps were 27. Goodman, L. S., and Gilman, A. 1970 ; The Pharmacological Basis of Therapeutics, McMillan Co. New York inhibited. Failure to previously observe an inhibition of glu28. Solokoff, L. 1960 ; in Handbook of Physiology Section I, Neuroconeogenesisfrom pyruvatecanbeexplainedtakinginto physiology, pp. 1483, American Physiological Society, Bethesda, account thatlarge supraphysiological concentrations of pyruMD vate lo mM ; were utilized 10, 24 ; . 29. Cahill, G. F., J. R., and Owen, 0.E. 1967 ; Trans. An. Clin. Cli?7ZQtOl.ASSOC. 13-18 79, The well-known pharmacological actions of t-cycloserine. In SHR maintained on the high compared to basal ; NaCl diet for 2 weeks, basal levels of MOPEG in the AHN were approximately 60% lower and arterial pressure was approximately 12 mm Hg higher, as previously reported Peng et al., 1995; Fig. 2 ; . The microperfusion of SCH 32615 into AHN elicited no significant decrease in AHN MOPEG in the SHR on the high NaCl diet. This contrasts with the large decrease in AHN MOPEG elicited in the SHR on the basal NaCl diet Fig. 1 ; . Despite this difference in MOPEG responses, the SCH 32615 microperfusion caused a similar increase in arterial pressure in SHR on the two diets. In WKY, the SCH 32615 microperfusion elicited no significant change in extracellular MOPEG concentra and tolcapone. Concentrate 5 mg mI periods ; . Blood dyscrasias agranulocytosts, pancytopenia, thrombocytopenic purpura ; . and liver damage jaundice. biNary stasis ; have been reported with related druQs. Undue exposure to sunlight should be avoided. Photosensttive reactions have been reported in patients on Navane thiothixene ; . lntramusculaMdministration-As with all intramuscularpreparations, Navane Intramuscular should be injected well within the body of a relatively large muscle. The preferred sites are the upper outer quadrant of the buttock i.e. gluteus maximus ; and the mid-lateral thigh. The deltoid area should be used only if well developed, such as in certain adults and older children, and then only with caution to avoid radial nerve intury. Intramuscular injections should not be made into the lower and mid-thirds of the upper arm. As with all intramuscular injections, aspiration is necessary to help avoid inadvertent injection into a blood vessel. Neuroleptic drugs elevate prolactin levels; the elevation persists during chronic administration. Tissue culture experiments indicate that approximately one third of human breast cancers are prolactin-dependent in vitro, a factor of potential importance ifthe prescription ofthese drugs is contemplated in a patient with a previously detected breast cancer. Although disturbances such as galacforrhea, amenorrhea, gynecomastia, and impotence have been reported, the clinical significance of elevated serum prolactin levels is unknown for most patients. An increase in mammary neoplasms has been found in rodents after chronic administration of neuroleptic drugs. Neither clinical studies nor epidemiologic studies conducted to date, however, have shown an association between chronic administration ofthese drugs and mammary tumorgenesis; the available evidence is considered too limited to be conclusive at this time. Information forPatients-Given the likelihood that some patientsexposed chronicallyto neurolepticswill develop tardive dyskinesia, it is advised that all patients in whom chronic use is contemplated be given, it possible, full information about this risk The decIsion to inform patients and or their guardians must ohviotisfy take into account the clinical circumstances and the competency of the patientto understand the information provided. Adverse ReactIons: Note: Not all of the following adverse reactions have been reported with Navane thiothixene ; . However, since Navane has certain chemical and pharmacoloqlc similanties to the phenothiRiflC5, all of the known side effects and toxicity associated with phenothiazine therapy should be borne in mind when Navane is used. Cardiovascular effects: Tachycardia, hypotension, lightheadedness, and syncope. In the event hypolension occurs, epinephrine should not be used as a pressoragentsince a paradoxicalfurther lowering of blood pressure may result. Nonspecific EKG changes have been observed in some patients receiving Navane thiothixene ; . These changes are usually reversible and frequently disappear on continued Navane therapy. The incidence of these changes is lower than that observed with some phenothiazines. The clinical significance otthese changes is not known. CNS effects: Drowsiness, usualfy mild, may occur although it usually subsides with continuation of Navanetherapy. The incidence of sedation appears similar to that ofthe piperazine group of phenothiazines, but less than that of certain aliphatic phenothiazines. Restlessness, agitation and insomnia have been noted with Navane. Seizures and paradoxical exacerbation of psychotic symptoms have occurred with Navane infrequently. Hyperreflexia has been reported in infants delivered from mothers having received structurally related drugs. In addition, phenothiazine derivatives have been associated with cerebral edema and cerebrospinal fluid abnormalities. Extrapyramidal symptoms, such as pseudo-parkinsonism, akathisia, and dystonia have heart reported. Management of these extrapyramidal symptoms depends upon the type and severity. Rapid relief of acute symptoms may requirethe use of an injectable antiparkinson agent. More slowly emerging symptoms may be managed by reducing the dosage of Navane and or administering an oral antiparkinson agent. Persistent Tardive Dyskinesia: As with all antipsychotic agents tardive dyskinesia may appear in some patients on long-term therapy or may occur after drug therapy has been discontinued. The syndrome is characterized by rhythmical involuntary movements ofthetorigue, face, mouth orjaw e.g. , protrusion of tongue, puffing of cheeks, puckenng of mouth, chewing movements ; . Sometimes these may be accompanted by involuntary movements of extremities. Since early detection of tardive dyskinesia is important, patients should be monitored on an ongoing hesis. It has been reported that finevermicular movement of the tongue may be an early sign of the syndrome. If this or any other presentation of the syndrome is observed, the clinician should consider possible discortinuation of neuroleptic medication. See Warntn9s section. ; Hepatic Effects: Elevations of serum transaminase and alkaline phosphatase, usually transient, hat been infrequently observed in some patients. No clinically confirmed cases otjaundice attributable to Navane have been reported. Hematologic Effects: As is true with certain other psychotropic drugs, leukopenia and leukocytosis. which are usually transient, can occur occasionally wtth Navane. Other antipsychotic drugs have been associated with agranulocytosis, eosinophilia, hemolytic anemia, thrombocytopenia and pancytopenia. Allergic Reactions: Rash, pruritus, urticana, photosensitivity and rare cases of anaphylaxis have been reported with Navane. Undue exposure to sunliqht should be avoided. Although not experienced with Navane, extoliative dermatitisand contact dermatitis in nursing personnel ; have been reported with certain phenothiazines. Endocrine Disorders: Lactation, moderate breast enlargement and amenorrhea have occurred in a small percentage of females receiving Navane. If persistent, this may necessitate a reduction in dosage or the discontinuation of therapy. Phenothiazines have been associated with false positive pregnancy tests, gynecomastia, hypoglycemia, hyperglycemia, and glycosuria. Autonornic Effects: Dry mouth, blurred vision, nasal congestion, constipation, increased sweating, increased salivation, and impotence have occurred infrequently with Navane therapy Phenothiazines have been associated with miosis, mydriasis, and adynamic ileus. Other Adverse Reactions: Hyperpyrexia, anorexia, nausea, vomiting, diarrhea, increase in appetite and weight, weakness or fatigue, polydipsia and peripheral edema. Although not reported with Navane. evidence indicates there is a relationship between phenothiazine therapy and the occurrence of a systemic lupus erythematosus-like syndrome. Neuroleptic Malignant Syndrome NMS ; : Please refer to the text regarding NMS in the WARNINGS and thorazine.
Navane thiothixene hydrochloride ; Concentrate is available in 120 cc. 4 oz. ; bottles with an accompanying dropper calibrated at 2 mg., 4 mg., 5 mg., 6 mg., 8 mg. and 10 mg. Each cc and tolmetin.