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Tus, body composition, dietary habits, and physical fitness levels VOzmax ; of the subjects to accurately determine the influence of primary aging on glucose metabolism. Hyperinsulinemia with or without noninsulin-dependent diabetes mellitus is associated with heightened risk of stroke and coronary artery disease in older individuals 50-52 ; . The possibility that the insulin resistance and glucose intolerance that commonly occur with aging in Western societies are modifiable is intriquing. While glucose tolerance and insulin sensitivity improve with aerobic exercise training and or weight reduction in young and middle-aged individuals, there are a limited number of longitudinal intervention studies that examine this possibility in the elderly 45, 46, 53 ; . The relationship of the improvement in glucose metabolism with these interventions to changes in the regional distribution of body fat is unclear. In the very old, cross-sectional data suggest that age is associated with a significant deterioration in glucose tolerance independent of body composition or physical activity status; however, at least up to age 60 yr, glucose tolerance was comparable to that in the younger subjects 54 ; . Further investigation is needed to determine whether exercise training and weight reduction can improve insulin sensitivity in the elderly as it does in young individuals.
Resistance will require the use of thirdline drugs such as clofazamine, linezolid, or macrolides. Potential crossresistance occurs between certain drug classes, for example between isoniazid and ethionamide and between amikacin and kanamycin as drug resistance is associated with the same mutation. In general, there is complete class effect or cross-resistance among the fluoroquinolones, though some activity has been described with more potent drugs, such as the newer quinolones moxifloxicin and gatifloxacin. As each regimen has to be individually tailored to available sensitivity patterns, predicting efficacy and length of treatment is based mainly on expert opinion rather than randomized clinical trials. All drug-resistant cases require directly observed therapy, particularly if secondary drug resistance resulted from prior poor compliance. High-level drug resistance requires 24 months of treatment beyond culture conversion, which is a considerable challenge for the patient and physician as many of these drugs are poorly tolerated. In cases that continue to be culture positive 4 to 6 months into treatment or if no suitable drug regimen is available, surgery should be considered if the disease is sufficiently localized to allow lobectomy or pneumonectomy. Successful lung resection does not preclude the completion of a full course of treatment, if available, nor does it allow shortening of the course. While the treatment of drug resistant disease presents major challenges, novel agents are currently being studied, which we hope will allow cure in almost all cases. --Richard K. Elwood, MB, BCh, MRCP UK ; , FRCPC --Victoria Cook, MD, FRCPC BC Centre for Disease Control.
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With isoniazid plus PAS or, indeed, with isoniazid alone. Moreover, of 22 patients who were prescribed their maximum tolerated dose that is, the maximum dose tolerated on four consecutive occasions ; for a period of eight weeks, 20 developed clear-cut intolerance during this period, 17 of them within two weeks. Indeed, nearly all had had symptoms of intolerance before they attained their maximum tolerated dose. These findings are discouraging for the long-term use of even a moderately high dosage of ethionamide on a twice-weekly basis in Madras patients. Fox and others 1969 ; studied, also in a `double-blind' investigation, acute intolerance to individual doses of ethionamide and prothionamide in East African patients who were under treatment with a daily regimen of isoniazid plus streptomycin. They concluded that in these patients, it would not be possible, as a routine, to increase the dosage of either ethionamide or prothionamide in intermittent regimens above the conventional dosages used in daily regimens. It has been reported by Prignot, Everaents and Tyberghein 1962 ; and Gyselen and others 1963 ; that vitamin B-complex preparations substantially reduce the frequency and severity of the side-effects of ethionamide. Later studies, however, have shown that this is not the case Verbist and others, 1967 ; Fox and others, 1969 ; . The design and conduct of this study merit special mention. The study was conducted `double-blind' with respect to ethionamide.
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Sputum production on most days for at least 3 months of the year for at least 2 years, suspect chronic bronchitis, especially if the patient has a history of smoking or exposure to environmental irritants. Suspect bronchiectasis if the patient complains of the production of large amounts of sputum, weight loss, fever, and malaise. The chest x-ray usually shows findings consistent with bronchiectasis. Suspect tuberculosis if there is a cough associated with weight loss, fatigue, and possible night sweats. If the patient has cough with heartburn and a sour taste in the mouth, suspect GERD. There also may be evidence of reflux on upper GI studies, evidence of esophagitis on esophagogastroduodenoscopy, or episodic evidence of acid reflux on esophageal pH monitoring. Pulmonary embolism may be suggested by cough; tachypnea; tachycardia; diminished breath sounds; and adventitious sounds such as wheezes, crackles, or pleural friction. A chronic, dry, nonproductive cough that begins after the initiation of angiotensin-converting enzyme inhibitors may indicate a side effect to the medication and etidronate.
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References 1. Grlek A, Bayraktar M, Kirazli S: Increased plasminogen activator inhibitor-1 activity in offspring of type 2 diabetic patients: lack of association with plasma insulin levels. Diabetes Care 23: 8892, 2000 Mansfield MW Stickland MH, Grant PJ: , PAI-1 concentrations in first-degree relatives of patients with non-insulin-dependent diabetes: metabolic and genetic associations. Thromb Haemost 77: 357361, 1997 Medvescek M, Keber D, Stegnar M: Impaired fibrinolysis in offspring of parental pairs with type 2 diabetes mellitus Abstract ; . Diabetologia 38 Suppl. 1 ; : A52, 1995 4. Landin K, Tengborn L, Smith U: Elevated fibrinogen and plasminogen activator inhibitor PAI-1 ; in hypertension are related to metabolic risk factors for cardiovascular disease. J Intern Med 227: 273278, 1990 Potter van Loon BJ, Kluft K, Radder JK, Blankenstein MA, Meinders AE: The cardiovascular risk factor plasminogen activator inhibitor type 1 is related to insulin resistance. Metabolism 42: 945949, 1993 Juhan-Vague I, Alessi MC: Plasminogen activator inhibitor 1 and atherothrombosis. Thromb Haemost 70: 138143, 1993 Stiko-Rahm A, Wiman B, Hamsten A, Nilsson J: Secretion of plasminogen activator inhibitor-1 from cultured human umbilical vein endothelial cells is induced by very low density lipoprotein. Arteriosclerosis 10: 10671073, 1990 Grant PJ, Regg M, Medcalf RL: Basal expression and insulin-mediated induction of PAI-1 mRNA in Hep G2 cells. Fibrinolysis 5: 8186, 1991 Calles-Escandon J, Mirza SA, Sobel BE and etodolac.
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Recommendations for the treatment of pregnant women with pulmonary TB are provided by the New York City Department of Health2 and the American Thoracic Society.4 However, guidelines are not available for the treatment of patients with MDR-TB during pregnancy. The natural history of TB was studied in 250 pregnant women with 370 pregnancies prior to the advent of effective treatment.5 None of the women died during pregnancy, but 24 spontaneous abortions 6.5% ; occurred. None of the infants developed congenital TB, and cervical TB was diagnosed in one pregnant woman. Although the literature reports 176 cases of congenital TB, 6 the prevalence is 1% for the offspring of untreated mothers. In 1981, 16 pregnant women were reported to have isoniazid-resistant TB.7 All were treated with first-line medications and para-aminosalicylic acid during pregnancy. One patient had a spontaneous abortion after 4 months of pregnancy. After birth, one infant died of miliary TB at 3 months, and one infant died of meningeal TB. Another infant developed pulmonary TB from inhalation at 6 months. The 12 remaining pregnancies had positive outcomes. However, none of the isoniazidresistant isolates was tested for rifampin resistance. Five cases of documented MDR-TB in pregnant women were located in the literature.8, 9 Only one of these five patients was treated with a second-line drug ethionamide ; , in addition to pyrazinamide and rifampin. This patient did not develop adverse effects from three-drug therapy, and the neonate was healthy. Two patients were untreated during gestation. One patient had a therapeutic abortion, and the other received therapy with rifampin and isoniazid for MDR-TB so-called "holding therapy" ; . An additional sixth pregnant woman with isoniazid pyrazinamide-resistant Mycobacterium bovis infection was treated with rifampin, isoniazid, and ethambutol only.10 Therapy with streptomycin was added after delivery, and a second-line medication was not administered. The treatment for our patient was more complicated. The patient refused therapeutic abortion. Her cavitary TB worsened on chest radiograph, and her sputum smears remained strongly positive for TB, suggesting MDR-TB. Treatment was clearly indicated to curtail weight loss; to terminate a source of transmission; to avoid dissemination, mycobacteremia, meningitis, or death for the mother; to decrease the risk of congenital TB; to protect the healthcare workers in the delivery room; and to decrease the separation time between mother and newborn. The so chestjournal.
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Because of the role of sympathetic activation in adverse perioperative cardiac outcomes, -adrenergic receptor blocking drugs have been proposed as a means for providing cardioprotection. Potential cardioprotective mechanisms of -blockers include a ; reduced heart rate and contractility and subsequently lower myocardial oxygen demand; b ; a shift in energy metabolism from free fatty acids to the more energy efficient glucose; c ; antiarrhythmic effects; d ; anti-renin angiotensin properties; and e ; antiinflammatory effects possibly promoting plaque stability 79 ; . The effects on heart rate, contractility, and energy substrate shift occur almost instantly, whereas the antiinflammatory effects may be observed only after prolonged use of -blockers.
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Results for ethionamide are within acceptable range in 7H10 agar 2.5-10.0 ug ml ; with 50% of the isolates having MIC's 2.5 ug ml. Cycloserine, is inhibitory to 50% of the isolates tested with MIC 25 ug ml. Ofloxacin has been one of the potential antimycobacterial drugs. MIC in 7H10 agar ranged from 0.12 to 2.0 ug ml. 6 ; Our results showed the MIC of the tested isolates fall within the range of .031 - 8.0 ug ml. Ofloxacin has been shown to be more active than ciprofloxacin against M. tuberculosis.7 Kanamycin, an aminoglycoside, has undesirable side effects, such as nephrotoxicity and ototoxicity. Our result shows that 50% of isolates have MIC levels within .078-5.0 ug ml of kanamycin. Interest in ofloxacin's potential in treating MDR-TB is based on its potent antimycobacterial activity as reflected in very low in vitro MICs against the wild and resistant strains of Mycobacterium tuberculosis 2mg l ; . This concentration is achievable in serum and tissue levels following recommended therapeutic doses of ofloxacin. In vivo, animal studies demonstrate the significantly lower mortality rates in TB-infected mice treated with ofloxacin when used in combination with at least two or more anti-TB drugs to which the isolates have demonstrable susceptibility. In addition, INH may be retained in the regimen to provide coverage against subpopulations of susceptible mycobacteria. It has been demonstrated that the ofloxacin's antibacterial effect correlates with the dose concentration. This concentration-dependent bacterial killing favors the use of the 800 mg daily dose to optimize the bactericidal effect. A lower dose of 600 mg may also be acceptable provided initial in vitro studies on Philippine TB strains show susceptibility to levels that can be attained after administration of this dose. The use of the 400 mg, while economically more viable, has been shown to result in diminished efficacy. The optimum dose probably has to balance efficacy with cost considering the predominantly low-income status of majority of Filipino TB patients and that ofloxacin is not included in the current anti-TB formulary of the government. CONCLUSION Almost 50% of MDR-TB isolates studied have developed resistance to cycloserine and kanamycin. The sensitivity to ofloxacin at the time of study is 80% but with over-usage of the drug for other clinical indications, this rate might now be lower. Monitoring of resistance to ofloxacin should be done on MDR-TB isolates. To date, there is still no national program on multi-drug resistant TB. This study strives to bridge this gap in the most systematic way possible by bringing together experts to work in collaboration with industry, which will commit resources to address the problem of multi-drug resistant tuberculosis. REFERENCES and exenatide.
Or manufacture with intent to deliver, drug paraphernalia, knowHistor y: 1989 a 121 ; 1991 a 140 ing that it will be primarily used to plant, propagate, cultivate, 161 .677 Municipal ordinances. Nothing in this subgrow, harvest, manufacture, compound, convert, . produce ; process, prepare, test analyze, pack, cepack, store, contain, conceal, chapter precludes a city, village or town from prohibiting conduct inject, ingest, inhale or otherwise introduce into the human body that is the same as that prohibited by s . 161 573' 2 ; , 161, 574 2 ; a controlled substance in violation of this , chapter Any person or, 161, 575 2 ; . ; Histor y : 1989 a 121 who, violates this section may be fined not more than , 000 or imprisoned for': not more than 90 days or both.
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1. Donnan GA, O'Malley HM, Quang L, Hurley S, Bladin PF. The capsular warning syndrome: pathogenesis and clinical features. Neurology. 1993; 43: 957-962. Waterston JA, Brown MM, Butler P, Swash M. Small deep cerebral infarcts associated with occlusive internal carotid artery disease: a hemodynamic phenomenon? Arch Neurol. 1990; 47: 953-957. Becker K, Skalabrin E, Hallam D, Gill E. Ischemic stroke during sexual intercourse: a report of 4 cases in persons with patent foramen ovale. Arch Neurol. 2004; 61: 1114-1116. Jackson M, Lennox G, Jaspan T, Jefferson D. Migraine angiitis precipitated by sex headache and leading to watershed infarction. Cephalalgia. 1993; 13: 427-430. Chang GY, Ahn PC. Postcoital vertebral artery dissection. Fam Physician. 1996; 54: 2195-2196. Benninger DH, Georgiadis D, Kremer C, Studer A, Nedeltchev K, Baumgartner RW. Mechanism of ischemic infarct in spontaneous carotid dissection. Stroke. 2004; 35: 482-485. Kondoh R, Utsugisawa K, Obara D, Mizuno M, Yonezawa H, Terayama Y. Striatocapsular infarction caused by middle cerebral artery dissection. Eur Neurol. 2004; 51: 120-121. Lin CH, Jeng JS, Yip PK. Middle cerebral artery dissections: differences between isolated and extended dissections of internal carotid artery. J Neurol Sci. 2005; 235: 37-44. Fahey CD, Alberts MJ, Bernstein RA. Oral clopidogrel load in aspirin-resistant capsular warning syndrome. Neurocrit Care. 2005; 2: 183-184 and exjade.
REFERENCES 1. Ahmad, S., and E. Mokaddas. 2004. Contribution of AGC to ACC and other mutations at codon 315 of the katG gene in isoniazid-resistant Mycobacterium tuberculosis isolates from the Middle East. Int. J. Antimicrob. Agents 23: 473478. 2. Ahmad, S., and E. Mokaddas. 2005. The occurrence of rare rpoB mutations in rifampicin-resistant clinical Mycobacterium tuberculosis isolates from Kuwait. Int. J. Antimicrob. Agents 26: 205212. 3. Banerjee, A., E. Dubnau, A. Quemard, V. Balasubramanian, K. S. Um, T. Wilson, D. Collins, G. de Lisle, and W. R. Jacobs, Jr. 1994. inhA, a gene encoding a target for isoniazid and ethionamide in Mycobacterium tuberculosis. Science 263: 227230. 4. Banerjee, A., M. Sugantino, J. C. Sacchettini, and W. R. Jacobs, Jr. 1998. The mabA gene from the inhA operon of Mycobacterium tuberculosis encodes a 3-ketoacyl reductase that fails to confer isoniazid resistance. Microbiology 144 Pt. 10 ; : 26972704. 5. Bartfai, Z., A. Somoskovi, C. Kodmon, N. Szabo, E. Puskas, L. Kosztolanyi, E. Farago, J. Mester, L. M. Parsons, and M. Salfinger. 2001. Molecular characterization of rifampin-resistant isolates of Mycobacterium tuberculosis from Hungary by DNA sequencing and the line probe assay. J. Clin. Microbiol. 39: 37363739. 6. Cavusoglu, C., S. Hilmioglu, S. Guneri, and A. Bilgic. 2002. Characterization of rpoB mutations in rifampin-resistant clinical isolates of Mycobacterium tuberculosis from Turkey by DNA sequencing and line probe assay. J. Clin. Microbiol. 40: 44354438. 7. Cirillo, D. M., F. Piana, L. Frisicale, M. Quaranta, A. Riccabone, V. Penati, P. Vaccarino, and G. Marchiaro. 2004. Direct rapid diagnosis of rifampicinresistant M. tuberculosis infection in clinical samples by line probe assay INNO LiPA Rif-TB ; . New Microbiol. 27: 221227. 8. Davies, P. D. 2003. The worldwide increase in tuberculosis: how demographic changes, HIV infection, and increasing numbers in poverty are increasing tuberculosis. Ann. Med. 35: 235243. 9. de Oliveira, M. M., A. da Silva Rocha, M. Cardoso Oelemann, H. M. Gomes, L. Fonseca, A. M. Werneck-Barreto, A. M. Valim, M. L. Rossetti, R. Rossau, W. Mijs, B. Vanderborght, and P. Suffys. 2003. Rapid detection of resistance against rifampicin in isolates of Mycobacterium tuberculosis from Brazilian patients using a reverse-phase hybridization assay. J. Microbiol. Methods 53: 335342. 10. Edwards, K. J., L. A. Metherell, M. Yates, and N. A. Saunders. 2001. Detection of rpoB mutations in Mycobacterium tuberculosis by biprobe analysis. J. Clin. Microbiol. 39: 33503352. 11. Ferrara, G., L. Richeldi, M. Bugiani, D. Cirillo, G. Besozzi, S. Nutini, L. Casali, F. Fiorentini, L. R. Codecasa, and G. B. Migliori. 2005. Management of multidrug-resistant tuberculosis in Italy. Int. J. Tuberc. Lung Dis. 9: 507 513. Heep, M., B. Brandstatter, U. Rieger, N. Lehn, E. Richter, S. Rusch-Gerdes, and S. Niemann. 2001. Frequency of rpoB mutations inside and outside the cluster I region in rifampin-resistant clinical Mycobacterium tuberculosis isolates. J. Clin. Microbiol. 39: 107110. 13. Herrera-Leon, L., T. Molina, P. Saiz, J. A. Saez-Nieto, and M. S. Jimenez. 2005. New multiplex PCR for rapid detection of isoniazid-resistant Mycobacterium tuberculosis clinical isolates. Antimicrob. Agents Chemother. 49: 144147. 14. Hillemann, D., M. Weizenegger, T. Kubica, E. Richter, and S. Niemann. 2005. Use of the genotype MTBDR assay for rapid detection of rifampin and isoniazid resistance in Mycobacterium tuberculosis complex isolates. J. Clin. Microbiol. 43: 36993703. 15. Hirano, K., C. Abe, and M. Takahashi. 1999. Mutations in the rpoB gene of rifampin-resistant Mycobacterium tuberculosis strains isolated mostly in Asian countries and their rapid detection by line probe assay. J. Clin. Microbiol. 37: 26632666. 16. Iwamoto, T., and T. Sonobe. 2004. Peptide nucleic acid-mediated competitive PCR clamping for detection of rifampin-resistant Mycobacterium tuberculosis. Antimicrob. Agents Chemother. 48: 40234026. 17. Kapur, V., L. L. Li, S. Iordanescu, M. R. Hamrick, A. Wanger, B. N and ethionamide.
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Cross-examination may have revealed Rams used other information sources besides defendant. Finally, she argues cross-examination may have shown Rams coerced her into making involuntary admissions. Recently, in People v. Ramos 2004 ; 34 Cal.4th 494, 525-526 Ramos ; , the Supreme Court rejected claims similar to those lodged here. In Ramos, the defendant sought disclosure of a newsreporter's unpublished information concerning the reporter's interview of defendant. Specifically, defendant sought the reporter's interview notes to "validate [defendant's] psychiatric disorder." The court concluded defendant failed to meet Delaney's threshold test, concluding his showing rested on "mere speculation" and the evidence "does not suggest the notes contain anything of substance that the jury had not already heard." Id. at p. 527. ; [5] Defendant's assertions parrot those the defendant lodged in Sanchez and Ramos, and amount to nothing more than rank speculation. Much of the information she sought to elicit was cumulative of other admitted evidence. Rams recounted defendant's statements describing her fear of Godley and his violent conduct. Other witnesses corroborated Godley's violent character and defendant's expert explained her battered women's syndrome defense. Defendant never claimed Rams's account of his interview with her was untruthful or inaccurate. Thus, defendant's argument, stripped of its gloss, is merely a request to elicit additional corroborating information from Rams. As in Sanchez, defendant failed to explain how this information would have assisted her defense, or how it differed from other mitigating evidence presented at trial. Finally, we note defendant filed no declarations or investigative reports to support her Delaney showing. We also reject the notion a lengthy list of detailed questions amounts to an offer of proof, or satisfies defendant's burden "to make the required showing." Delaney, supra, 50 Cal.3d at p. 809; see also In re Mark C. 1992 ; 7 Cal.App.4th 433, 444 [offer of proof must set forth the substance and purpose of the evidence]; People v. Allen 1986 ; 42 Cal.3d 1222, 1270, fn. 30 [general rule offer of proof not required for cross-examination does not apply where trial court has overlooked the question's probable relevance or invites counsel to suggest a theory of relevance]. ; [131 Cal.App.4th 156] Measured under the Sanchez standard, defendant failed to show a reasonable possibility the unpublished information would materially assist her defense. Consequently, we need not consider the second Delaney prong requiring a balancing of factors to determine whether disclosure of the unpublished information was required. Sanchez, supra, 12 Cal.4th at p. 58, fn. 4; Ramos, supra, 34 Cal.4th at p. 527. ; D. The Remedy of Excluding or Striking the Newsreporter's Testimony When Shield Law Immunity Is Validly Asserted During Cross-Examination Alternatively, defendant contends the trial court erred by failing to strike Rams's direct testimony or exclude him from testifying altogether. Where a criminal defendant fails to satisfy Delaney's threshold test, the Attorney General argues the appropriate remedy is to limit the newsperson's testimony to published information, as in Sanchez. Before turning and ezetimibe.
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Worldwide, including within the United States, where 74 culture-confirmed cases of TB disease reported during 1993-2004 met the criteria for XDR-TB. Most recently, a cluster of XDR-TB cases was reported among primarily HIV-infected individuals in a South African hospital; 52 of 53 patients died within an average of 25 days after XDR-TB was first suspected. Because of the extent of drug resistance, treatment options for persons with XDR-TB are not likely to meet the World Health Organization WHO ; 's standard of treatment i.e., treatment with at least four drugs to which the organism is known to be susceptible ; . Treatment outcomes for XDR-TB are worse than for MDR-TB; patients from the United States with XDR TB were reported as 64% more likely to die during treatment than patients with MDR-TB. The potential public health impact of XDR-TB is enormous, greatly surpassing that of MDR-TB. A case of XDR-TB was reported to the Minnesota Department of Health MDH ; in the summer of 2006. The case-patient originally came from China on an employment visa and had lived in the Twin Cities area for several months before presenting to a clinic with TB-related symptoms and a noncavitary chest radiograph consistent with active TB disease. The patient was referred to a public health TB specialty clinic for further diagnostic evaluation and treatment and began a standard course of four-drug TB therapy administered by directly observed therapy DOT ; , consistent with national TB treatment guidelines. Public health measures were implemented to limit transmission and a contact investigation was coordinated by the local health department. When first-line drug susceptibility results were reported as resistant to all four first-line TB medications i.e., INH, RIF, pyrazinamide, and ethambutol ; , second-line testing was ordered and the regimen was revised to include moxifloxicin, amikacin, cycloserine, ethionmide, and PAS. Second-line drug susceptibility testing revealed resistance to many additional TB medications i.e., capreomycin, kanamycin, amikacin, PAS, and levofloxacin ; and sensitivity to only ethionamide and cycloserine. The patient was hospitalized to address major adverse reactions to second-line medications and to again revise the treatment regimen. The patient showed some clinical and 56.
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Hand r card #20 ; read if necessary: medications to treat, control, or prevent mac mycobacterium avium complex ; clarithromycin biaxin, klacid ; azithromycin zithromax ; clofazimine lamprene ; ethambutol myambutol ; ciprofloxacin cipro ; rifabutin mycobutin ; rifampin sparfloxacin ethionamide trecator ; medications to treat, control, or prevent tb tuberculosis ; isoniazid inh ; rifampin rifamate inh rifampin ; ethambutol myambutol ; pyrazinamide pza ; circle one and detrol and ethosuximide.
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