Postgraduate Medicine
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Propranolol-Induced Lupus Syndrome? Thurston Harrison, Thomas S. Sisca & William H. Wood To cite this article: Thurston Harrison, Thomas S. Sisca & William H. Wood (1976) Propranolol-Induced Lupus Syndrome?, Postgraduate Medicine, 59:1, 241-244, DOI: 10.1080/00325481.1976.11716542 To link to this article: http://dx.doi.org/10.1080/00325481.1976.11716542
Published online: 07 Jul 2016.
Submit your article to this journal
View related articles
Citing articles: 12 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [Australian Catholic University]
Date: 06 August 2017, At: 03:20
Downloaded by [Australian Catholic University] at 03:20 06 August 2017
• A 51-year-old man was admitted to Memorial Hospital, Easton, Maryland, for evaluation of sore muscles and a rash on his legs. He was known to have chronic essential hypertension and other problems, including gout and mild, diet-controlled diabetes, and had been treated with various antihypertensive agents for a number of years. At his an nuai checkup the previous year, the blood pressure had been 190/ Il 0 mm Hg. The physical examination was otherwise unremarkable, and laboratory data were ali within normallimits. At that time, the patient was taking guanethidine and chlorothiazide. The guanethidine dosage was gradually increased in an attempt to reduce the blood pressure, but the drug was discontinued when orthostatic hypotension developed. Hydralazine (25 mg four times daily) was started, and chlorothiazide (500 mg/day) was continued. After one month, during which the response to varying doses of hydralazine up to lOO mg four times a day had been inadequate, propranolol (20 mg four times a day) was added to the regimen. Two months after initiation of the hydralazine therapy and one month after initiation of the propranolol therapy, the patient be gan to complain of soreness in the calves and thighs. Propranolol was discontinued. The next day, a red papular rash appeared on both legs. The rash became somewhat violaceous, with several slightly raised areas, and later spread to the trunk and arms. Sorne areas became indurated, and one area was definitely tender. Because the patient was thought to have allergie vasculitis induced by hydralazine, the drug was discontinued and the patient was placed under continued observation. Muscle soreness persisted, and the right knee and right elbow became tender and sore, suggesting the possibility of arthritis. Aften ten days without im-
Vol. 59 • No. 1 • January 1976 • POSTGRADUAlE MEDICINE
case report PROPRANOLOL-INDUCED LUPUS SYNDROME? Thurston Harrison, MD Thomas S. Slsca, Pharm D William H. Wood, MD Memorial Hospital, Easton, Maryland
provement, the patient was admitted to Memorial Hospital. On admission, results of a complete clinical and laboratory workup were essentially normal. Three lupus erythematosus (LE) cell preparations and serologie tests for rheumatoid factor and antinuclear antibodies were negative. The serum complement (C'3) value was 30 IU/100 ml by the radioimmunodiffusion method, and the protein electrophoretogram showed no abnormalities. The white blood cell count (WBC) was 17 ,000/cu mm, with a normal differentiai count, and the erythrocyte sedimentation rate (Wintrobe method) was 35 mm/hr. Findings on urinalysis (on three occasions), kidney function studies, chest x-ray film, and a multichannel biochemical analysis (SMA-12) ali were normal. Values for lactic dehydrogenase (on three occasions), creatine phosphokinase, serum glutamic oxalacetic transaminase, and serum glutamic pyruvic transaminase were within normallimits. Two LE cell preparations made two weeks after the reaction were negative. A skin biopsy showed evidence of mild vasculitis, with nonspecific, diffuse, chronic inflammation in the dermis. Small arteries
241
Downloaded by [Australian Catholic University] at 03:20 06 August 2017
ca•~port
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..
showed hypertrophy of the tunica media. In a small segment of one artery, a fibrinoid lesion replaced a portion of the internai elastic membrane of the tunica intima. Surrounding the artery were mixed inflammatory cells, including eosinophils, neutrophils, histiocytes, and monocytes. The pathologie diagnosis was subacute vasculitis of the small arteries of the dermis, with platelet thrombi. A muscle biopsy showed minimal to mild chronic interstitial inflammation, probably secondary to vasculitis. Prednisone therapy (60 mg/day) was begun, and within 36 hours the symptoms were dramatically reduced. The patient continued to improve and was soon discharged on an antihypertensive regimen of triamterene and hydrochlorothiazide and tapering-off doses of steroid. The consensus was that this patient bad a late toxic reaction to hydralazine that resembled the systemic lupus erythematosus (SLE) syndrome. For three weeks after steroid bad been discontinued, the patient continued to improve, with complete resolution of the myositis syndrome. Then severe left-sided chest pain developed suddenly, and the patient was readmitted to Memorial Hospital. On initial examination, a loud friction rub and coarse raies were audible at the base of the left lung. There was no hemoptysis. A presumptive diagnosis of left lower lobe pulmonary embolus with infarction was made. On the basis of the clinical symptoms, the patient was immediately given intravenous heparin therapy. The chest pain persisted for 48 hours. The lung scan showed minimal abnormal perfusion, which conceivably could have been secondary to pulmonary embolism without infarction. Laboratory values were the same as those from the first admission, except for increased serum (C'3) (160 IU/100 ml, radio immunodiffusion method) and erythrocyte sedimentation rate (45 mm/br, Wintrabe method), decreased WBC (Il ,000/cu mm, with 9% eosinophils), and positive LE cell preparations. Because the blood pressure was significantly elevated, propranolol was administered. It was selected because of the patient's previous resistance to other agents and presumed reaction to hydralazine.
On the first day of propranolol therapy ( 10 mg every six hours), mild pruritus developed. Therapy was suspended for 48 hours, and the pruritus cleared. On the sixth day, the propranolol dosage was increased to 20 mg every six hours. Mild pruritus developed, and after the dosage was increased on the eighth day to 40 mg every eight hours, low-grade fever and severe myalgias developed. These symptoms were identical to those of the previous episode. At this time, however, three LE cell preparations were positive. Propranolol was immediately discontinued and prednisone was started. Within 48 hours, the patient showed dramatic improvement. After one week of steroid therapy, the LE cell preparations were negative. Steroid dosage was tapered off within three weeks, with total resolution of symptoms. At follow-up examinations, the LE cell preparations have been negative. Results of renal function studies, including 24-hour creatinine clearance and determinations of serum creatinine and blood urea nitrogen, have ali been within normallimits. This finding is consistent with the drug-induced SLE syndrome, in which renal involvement is not usually manifest.
Vot 59 • No. 1 • January 1976 • POSTQAADUATE MEDICINE
243
Discussion
A syndrome similar to SLE (fever, myalgias, and skin rash) developed in this patient during therapy with hydralazine and propranolol. Hydralazine is known to induce such a syndrome; more than 140 cases have been reported in the literature. 1 • 2 Thus, the symptoms in this patient were initially thought to be hydralazine-induced. However, a second episode of identical symptoms occurred after therapy with propranolol alone. LE cell preparations made during the first episode were negative; those made during the second episode were positive. Steroid, in addition to propranolol withdrawal, was effective in controlling symptoms. The clinical association of the described signs and symptoms with positive LE cell preparations in this patient defines the first reported case of apparent induction of an SLE-like syndrome by propranolol. Ali medications used in treating this patient, except hydralazine and propranolol, bad been
a...iihw.... SA (pentaerythritol tetrooitrotel 80mg
Downloaded by [Australian Catholic University] at 03:20 06 August 2017
case r e p o r t • • • • • • • • • • • administered at !east s1x months before the syndrome occurred and were continued without exacerbation of symptoms; therefore, they were not felt to be implicated. Raftery and Denman 3 described three patients in whom practolol induced an SLE-like syndrome. Practolol, like propranolol, is a beta-adrenergic-blocking drug. These patients had positive LE cell preparations, but unlike our patient, they also had positive tests for antinuclear antibodies. Withdrawal of the drug gave sorne relief, but steroid was required for adequate improvement. These investigators have suggested that practolol selectively inactivates the thymus-lymphocyte populations that control the emergence of the SLE-like syndrome. Further studies are needed, however, to defi ne the exact mechanism. There is a remote possibility that hydralazine induced the SLE-like syndrome in our patient and that propranolol reactivated it. The ultimate test would have been to rechallenge the patient, but this was not done. It is hoped that the report of this case will aid in the recognition of similar cases. Betaadrenergic-blocking agents are commonly used in combination with hydralazine and procainamide, drugs that are known to induce the SLE-like syn~rome; thus, propranolol may be overlooked as a causative agent. • Address reprint requests to Thomas H. Sisca, Pharm D, Memorial Hospital, S Washington St. Easton, MD 21601.
References 1. Perry HM Jr: Late toxicity to hydralazine resembling systemic lupus erythematosus or rheumatoid arthritis. Am J Med 54:58-71. 1973 2. Alarcon-Segovia D: Drug-induced lupus syndrome. Mayo Clin Proc 44:664, 1966 3. Raftery EB. Denman AM: Systemic lupus erythematosus syndrome induced by practolol. Br Med J 26:452-456. 1973
PosTGRADUATE MEDICINE invites submission of brief reports for earl y publication. Illustrations and references should be included only when essential.
244
lldian
CAUTION: FederoiJow prohibits dispensing without prescription. Description: Eoch ta blet of Peritrote SA Sustoined Action contoins: pentoerythritol tetronitrote 80 mg (20 mg in immediate releose loyer and 60 mg in sustoined releose bose}. Peritrote • ( pentoerythritol tetroni· trote} iso ni tric a cid ester of o tetrohydric olcohol (pentoerythritol}. Indications: 8osed on o review of this drug by the National Acodemy of SciencesNational Reseorch Council and/or other information. FDA hos clossified the indice· fions os follows: "Possibly" effective· Peritrote (penta· erythritol tetronitrote}. is indicoted for the relief of angine pectoris (pain ossocioted with coroner y ortery di seo se}. lt is not intended to a bort the ocute onginol episode but it is widely regorded os use· fui in the prophyloctic treotment of angine pectoris. Final classification of the less-thon· effective indications requires further investigation. Contraindications: Peritrote SA Sustoined Action (pentoerythritol tetronitrote} 80 mg is controindicoted in patients who hove o history of sensitivity to the drug. Warning: Dota supporting the use of Peritrote (pentoerythritol tetronitrote} during the earl y doy_s of the ocute phase of myocordiol inforction (the period during which clinicol and loborotory findings ore unstoble} ore insufficient ta estoblish sofety. This drug.con oct os o physiologicol ontogonist to norepinephrine, acetylcholine, histamine. and many other agents. Precautions: Should be used with caution in patients who hove glaucome. Tolerance to this drug, and cross-tolerance to other nitrites and nitrates moy occur. Adverse Reactions: Side effects reported to dote hove been predominontly reloted to rosh (which requires discontinuotion of medication} and heodoche and gostrointestinal di stress, which ore usuolly mild and tronsient with con· tinuotion of medication. ln sctme cases severe persistent heodoches moy occur. ln addition, the following adverse reactions to nitrates such os pentoerythritol tetronitrote hove been reported in the literoture: (a} Cutoneous vasodilatation with flushing. (b} Tronsient episodes of dizziness and weokness, os weil os other signs of cerebral ischemie ossocioted with postural hypotension, moy occosionolly develop. (c} An occosionol individuel exhibits morked sensitivity to the hypotensive effects of nitrite and severe responses (nausee, vomiting, weokness, restlessness, pollor, perspiration and collopse} con occur, even with the usuel theropeutic doses. Alcohol moy enhonce this effect. Dosage: Peritrote SA Sustoined Action (pentoerythritol tetronitrote} 80 mg (b.i.d. on onempty stomoch}, 1 toblet immediotely on orising and 1 toblet 12 hours loter. Toblets should not be chewed. Supplied: Peritrote SA Sustoined Action (pentoerythritol tetronitrote} 80 mg, double loyer, biconvex, dork green/light green fa blets in botties of 100 (N 0047-0004-51} and 1000 (N 0047-0004-60}. A Iso in unit dose- package of 10 x 10 strips (N 0047-0004·11 }. Additional Dosage Forma: Peritrote 20 mglight green, scored ta blets in botties of 100 (N 0047-0001-51} and 1000 (N 0047-0001·60}. Also in unit dose- package of 10 x 10 strips (N 0047-0001-11}. Peritrote 10 mg -light green, unscored toblets in botties of 100 (N 00470007·51} and 1000 (N 0047-0007-60}. Full information ls available on request.
ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20
Propranolol-Induced Lupus Syndrome? Thurston Harrison, Thomas S. Sisca & William H. Wood To cite this article: Thurston Harrison, Thomas S. Sisca & William H. Wood (1976) Propranolol-Induced Lupus Syndrome?, Postgraduate Medicine, 59:1, 241-244, DOI: 10.1080/00325481.1976.11716542 To link to this article: http://dx.doi.org/10.1080/00325481.1976.11716542
Published online: 07 Jul 2016.
Submit your article to this journal
View related articles
Citing articles: 12 View citing articles
Full Terms & Conditions of access and use can be found at http://www.tandfonline.com/action/journalInformation?journalCode=ipgm20 Download by: [Australian Catholic University]
Date: 06 August 2017, At: 03:20
Downloaded by [Australian Catholic University] at 03:20 06 August 2017
• A 51-year-old man was admitted to Memorial Hospital, Easton, Maryland, for evaluation of sore muscles and a rash on his legs. He was known to have chronic essential hypertension and other problems, including gout and mild, diet-controlled diabetes, and had been treated with various antihypertensive agents for a number of years. At his an nuai checkup the previous year, the blood pressure had been 190/ Il 0 mm Hg. The physical examination was otherwise unremarkable, and laboratory data were ali within normallimits. At that time, the patient was taking guanethidine and chlorothiazide. The guanethidine dosage was gradually increased in an attempt to reduce the blood pressure, but the drug was discontinued when orthostatic hypotension developed. Hydralazine (25 mg four times daily) was started, and chlorothiazide (500 mg/day) was continued. After one month, during which the response to varying doses of hydralazine up to lOO mg four times a day had been inadequate, propranolol (20 mg four times a day) was added to the regimen. Two months after initiation of the hydralazine therapy and one month after initiation of the propranolol therapy, the patient be gan to complain of soreness in the calves and thighs. Propranolol was discontinued. The next day, a red papular rash appeared on both legs. The rash became somewhat violaceous, with several slightly raised areas, and later spread to the trunk and arms. Sorne areas became indurated, and one area was definitely tender. Because the patient was thought to have allergie vasculitis induced by hydralazine, the drug was discontinued and the patient was placed under continued observation. Muscle soreness persisted, and the right knee and right elbow became tender and sore, suggesting the possibility of arthritis. Aften ten days without im-
Vol. 59 • No. 1 • January 1976 • POSTGRADUAlE MEDICINE
case report PROPRANOLOL-INDUCED LUPUS SYNDROME? Thurston Harrison, MD Thomas S. Slsca, Pharm D William H. Wood, MD Memorial Hospital, Easton, Maryland
provement, the patient was admitted to Memorial Hospital. On admission, results of a complete clinical and laboratory workup were essentially normal. Three lupus erythematosus (LE) cell preparations and serologie tests for rheumatoid factor and antinuclear antibodies were negative. The serum complement (C'3) value was 30 IU/100 ml by the radioimmunodiffusion method, and the protein electrophoretogram showed no abnormalities. The white blood cell count (WBC) was 17 ,000/cu mm, with a normal differentiai count, and the erythrocyte sedimentation rate (Wintrobe method) was 35 mm/hr. Findings on urinalysis (on three occasions), kidney function studies, chest x-ray film, and a multichannel biochemical analysis (SMA-12) ali were normal. Values for lactic dehydrogenase (on three occasions), creatine phosphokinase, serum glutamic oxalacetic transaminase, and serum glutamic pyruvic transaminase were within normallimits. Two LE cell preparations made two weeks after the reaction were negative. A skin biopsy showed evidence of mild vasculitis, with nonspecific, diffuse, chronic inflammation in the dermis. Small arteries
241
Downloaded by [Australian Catholic University] at 03:20 06 August 2017
ca•~port
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ..
showed hypertrophy of the tunica media. In a small segment of one artery, a fibrinoid lesion replaced a portion of the internai elastic membrane of the tunica intima. Surrounding the artery were mixed inflammatory cells, including eosinophils, neutrophils, histiocytes, and monocytes. The pathologie diagnosis was subacute vasculitis of the small arteries of the dermis, with platelet thrombi. A muscle biopsy showed minimal to mild chronic interstitial inflammation, probably secondary to vasculitis. Prednisone therapy (60 mg/day) was begun, and within 36 hours the symptoms were dramatically reduced. The patient continued to improve and was soon discharged on an antihypertensive regimen of triamterene and hydrochlorothiazide and tapering-off doses of steroid. The consensus was that this patient bad a late toxic reaction to hydralazine that resembled the systemic lupus erythematosus (SLE) syndrome. For three weeks after steroid bad been discontinued, the patient continued to improve, with complete resolution of the myositis syndrome. Then severe left-sided chest pain developed suddenly, and the patient was readmitted to Memorial Hospital. On initial examination, a loud friction rub and coarse raies were audible at the base of the left lung. There was no hemoptysis. A presumptive diagnosis of left lower lobe pulmonary embolus with infarction was made. On the basis of the clinical symptoms, the patient was immediately given intravenous heparin therapy. The chest pain persisted for 48 hours. The lung scan showed minimal abnormal perfusion, which conceivably could have been secondary to pulmonary embolism without infarction. Laboratory values were the same as those from the first admission, except for increased serum (C'3) (160 IU/100 ml, radio immunodiffusion method) and erythrocyte sedimentation rate (45 mm/br, Wintrabe method), decreased WBC (Il ,000/cu mm, with 9% eosinophils), and positive LE cell preparations. Because the blood pressure was significantly elevated, propranolol was administered. It was selected because of the patient's previous resistance to other agents and presumed reaction to hydralazine.
On the first day of propranolol therapy ( 10 mg every six hours), mild pruritus developed. Therapy was suspended for 48 hours, and the pruritus cleared. On the sixth day, the propranolol dosage was increased to 20 mg every six hours. Mild pruritus developed, and after the dosage was increased on the eighth day to 40 mg every eight hours, low-grade fever and severe myalgias developed. These symptoms were identical to those of the previous episode. At this time, however, three LE cell preparations were positive. Propranolol was immediately discontinued and prednisone was started. Within 48 hours, the patient showed dramatic improvement. After one week of steroid therapy, the LE cell preparations were negative. Steroid dosage was tapered off within three weeks, with total resolution of symptoms. At follow-up examinations, the LE cell preparations have been negative. Results of renal function studies, including 24-hour creatinine clearance and determinations of serum creatinine and blood urea nitrogen, have ali been within normallimits. This finding is consistent with the drug-induced SLE syndrome, in which renal involvement is not usually manifest.
Vot 59 • No. 1 • January 1976 • POSTQAADUATE MEDICINE
243
Discussion
A syndrome similar to SLE (fever, myalgias, and skin rash) developed in this patient during therapy with hydralazine and propranolol. Hydralazine is known to induce such a syndrome; more than 140 cases have been reported in the literature. 1 • 2 Thus, the symptoms in this patient were initially thought to be hydralazine-induced. However, a second episode of identical symptoms occurred after therapy with propranolol alone. LE cell preparations made during the first episode were negative; those made during the second episode were positive. Steroid, in addition to propranolol withdrawal, was effective in controlling symptoms. The clinical association of the described signs and symptoms with positive LE cell preparations in this patient defines the first reported case of apparent induction of an SLE-like syndrome by propranolol. Ali medications used in treating this patient, except hydralazine and propranolol, bad been
a...iihw.... SA (pentaerythritol tetrooitrotel 80mg
Downloaded by [Australian Catholic University] at 03:20 06 August 2017
case r e p o r t • • • • • • • • • • • administered at !east s1x months before the syndrome occurred and were continued without exacerbation of symptoms; therefore, they were not felt to be implicated. Raftery and Denman 3 described three patients in whom practolol induced an SLE-like syndrome. Practolol, like propranolol, is a beta-adrenergic-blocking drug. These patients had positive LE cell preparations, but unlike our patient, they also had positive tests for antinuclear antibodies. Withdrawal of the drug gave sorne relief, but steroid was required for adequate improvement. These investigators have suggested that practolol selectively inactivates the thymus-lymphocyte populations that control the emergence of the SLE-like syndrome. Further studies are needed, however, to defi ne the exact mechanism. There is a remote possibility that hydralazine induced the SLE-like syndrome in our patient and that propranolol reactivated it. The ultimate test would have been to rechallenge the patient, but this was not done. It is hoped that the report of this case will aid in the recognition of similar cases. Betaadrenergic-blocking agents are commonly used in combination with hydralazine and procainamide, drugs that are known to induce the SLE-like syn~rome; thus, propranolol may be overlooked as a causative agent. • Address reprint requests to Thomas H. Sisca, Pharm D, Memorial Hospital, S Washington St. Easton, MD 21601.
References 1. Perry HM Jr: Late toxicity to hydralazine resembling systemic lupus erythematosus or rheumatoid arthritis. Am J Med 54:58-71. 1973 2. Alarcon-Segovia D: Drug-induced lupus syndrome. Mayo Clin Proc 44:664, 1966 3. Raftery EB. Denman AM: Systemic lupus erythematosus syndrome induced by practolol. Br Med J 26:452-456. 1973
PosTGRADUATE MEDICINE invites submission of brief reports for earl y publication. Illustrations and references should be included only when essential.
244
lldian
CAUTION: FederoiJow prohibits dispensing without prescription. Description: Eoch ta blet of Peritrote SA Sustoined Action contoins: pentoerythritol tetronitrote 80 mg (20 mg in immediate releose loyer and 60 mg in sustoined releose bose}. Peritrote • ( pentoerythritol tetroni· trote} iso ni tric a cid ester of o tetrohydric olcohol (pentoerythritol}. Indications: 8osed on o review of this drug by the National Acodemy of SciencesNational Reseorch Council and/or other information. FDA hos clossified the indice· fions os follows: "Possibly" effective· Peritrote (penta· erythritol tetronitrote}. is indicoted for the relief of angine pectoris (pain ossocioted with coroner y ortery di seo se}. lt is not intended to a bort the ocute onginol episode but it is widely regorded os use· fui in the prophyloctic treotment of angine pectoris. Final classification of the less-thon· effective indications requires further investigation. Contraindications: Peritrote SA Sustoined Action (pentoerythritol tetronitrote} 80 mg is controindicoted in patients who hove o history of sensitivity to the drug. Warning: Dota supporting the use of Peritrote (pentoerythritol tetronitrote} during the earl y doy_s of the ocute phase of myocordiol inforction (the period during which clinicol and loborotory findings ore unstoble} ore insufficient ta estoblish sofety. This drug.con oct os o physiologicol ontogonist to norepinephrine, acetylcholine, histamine. and many other agents. Precautions: Should be used with caution in patients who hove glaucome. Tolerance to this drug, and cross-tolerance to other nitrites and nitrates moy occur. Adverse Reactions: Side effects reported to dote hove been predominontly reloted to rosh (which requires discontinuotion of medication} and heodoche and gostrointestinal di stress, which ore usuolly mild and tronsient with con· tinuotion of medication. ln sctme cases severe persistent heodoches moy occur. ln addition, the following adverse reactions to nitrates such os pentoerythritol tetronitrote hove been reported in the literoture: (a} Cutoneous vasodilatation with flushing. (b} Tronsient episodes of dizziness and weokness, os weil os other signs of cerebral ischemie ossocioted with postural hypotension, moy occosionolly develop. (c} An occosionol individuel exhibits morked sensitivity to the hypotensive effects of nitrite and severe responses (nausee, vomiting, weokness, restlessness, pollor, perspiration and collopse} con occur, even with the usuel theropeutic doses. Alcohol moy enhonce this effect. Dosage: Peritrote SA Sustoined Action (pentoerythritol tetronitrote} 80 mg (b.i.d. on onempty stomoch}, 1 toblet immediotely on orising and 1 toblet 12 hours loter. Toblets should not be chewed. Supplied: Peritrote SA Sustoined Action (pentoerythritol tetronitrote} 80 mg, double loyer, biconvex, dork green/light green fa blets in botties of 100 (N 0047-0004-51} and 1000 (N 0047-0004-60}. A Iso in unit dose- package of 10 x 10 strips (N 0047-0004·11 }. Additional Dosage Forma: Peritrote 20 mglight green, scored ta blets in botties of 100 (N 0047-0001-51} and 1000 (N 0047-0001·60}. Also in unit dose- package of 10 x 10 strips (N 0047-0001-11}. Peritrote 10 mg -light green, unscored toblets in botties of 100 (N 00470007·51} and 1000 (N 0047-0007-60}. Full information ls available on request.
