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binding to GABA receptors.[4] Impairment in active transport of cephalosporins from cerebrospinal fluid to blood due to competitive inhibition by accumulated toxic organic acids in patients with renal failure may account for the susceptibility to neurotoxicity.[5] Drug‑induced myoclonus usually resolves after withdrawal of the offending drug. In this patient, the temporal association of the development of myoclonus after starting ceftazidime, and resolution following the discontinuation strongly suggests a causal relationship.
a dihydropyridine calcium channel blocker. Compared to the racemic amlodipine, S‑amlodipine has 1000‑fold stronger affinity to the L‑type calcium channels.[1] The use of racemic amlodipine is commonly associated with adverse events like peripheral edema headache, dizziness, flushing and abdominal pain, gingival overgrowth or enlargement.[2] Controlled clinical trials showed that S‑amlodipine is rarely associated with these side effects.[1]
Due to the uncommon nature of the movement disorders induced by ceftazidime, which is commonly used in dialysis patients closer monitoring is advisable.
Gingival hyperplasia has potential cosmetic implications and provids new niches for the growth of microorganisms. Although the incidence of nifedipine‑induced gingival hyperplasia is about 10%, there are few reports of amlodipine‑related gingival hyperplasia. [3‑5] We encountered two patients with this complication.
J. Joseph, A. Vimala Department of Nephrology, SMCSI Medical College, Karakonam, Trivandrum, Kerala Address for correspondence: Dr. Jigy Joseph, Department of Nephrology, SMCSI Medical College, Karakonam, Trivandrum, Kerala. E‑mail: [email protected]
References 1. Gordon MF. Toxin and drug‑induced myoclonus. Adv Neurol 2002;89:49‑76. 2. Jiménez‑Jiménez FJ, Puertas I, de Toledo‑Heras M. Drug‑induced myoclonus: Frequency, mechanisms and management. CNS Drugs 2004;18:93‑104. 3. Slaker RA, Danielson B. Neurotoxicity associated with ceftazidime therapy in geriatric patients with renal dysfunction. Pharmacotherapy 1991;11:351‑2. 4. Sugimoto M, Uchida I, Mashimo T, Yamazaki S, Hatano K, Ikeda F, et al. Evidence for the involvement of GABA (A) receptor blockade in convulsions induced by cephalosporins. Neuropharmacology 2003;45:304‑14. 5. Richet G, Lopez de Novales E, Verroust P. Drug intoxication and neurological episodes in chronic renal failure. Br Med J 1970;2:394‑5.
A 37‑year‑old man with a case of chronic kidney disease (CKD) stage III was on 5 mg daily dose of S‑amlodipine for the past 1.5 years. He developed swelling of gums and was diagnosed S‑amlodipine‑induced gingival enlargement [Figure 1a]. S‑amlodipine was substituted with metoprolol and moxonidine. Discontinuation of S‑amlodipine and dental toileting led to resolution at 6 months [Figure 1b]. A 62‑year‑old woman with a case of CKD stage V was on 10 mg daily dose of S‑amlodipine for 1 year. She developed swelling of gums, which used to bleed while eating or cleaning and was diagnosed with S‑amlodipine‑induced gingival enlargement [Figure 1c]. She refused dental treatment but S‑amlodipine was changed to moxonidine. Six months later, she had regression of the gingival enlargement [Figure 1d].
Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.144426
S‑amlodipine‑induced gingival enlargement Sir, S‑amlodipine is the chirally pure, single, pharmacologically active enantiomer of amlodipine, 62
Jan 2015 / Vol 25 / Issue 1
a
b
c
d
Figure 1: (a) Gingival enlargement due to S-amlodipine and (b) resolution of the gingival enlargement at 6 months after discontinuation of the S-amlodipine; (c) gingival enlargement due to S-amlodipine and (d) resolution of the gingival enlargement at 6 months after discontinuation of the S-amlodipine
Indian Journal of Nephrology
Letters to Editor
Phenytoin, calcium channel blockers and cyclosporine commonly cause gingival overgrowth. [3‑5] Gingival overgrowth may be due to a direct effect of the drug that regresses upon interruption of drug therapy.[5] However, it is generally accepted that the inflammatory changes caused by the bacteria biofilm synergize with the drug effect to cause overgrowth of the soft tissues. Treatment includes mechanical and chemical plaque (bacterial biofilm) control. Gingivectomy of the overgrown tissue is often needed. If the offending drug cannot be replaced, dental prophylaxes (dental cleaning) at 3‑month intervals is recommended.[5]
References 1. ASOMEX (S‑amlodipine) Product Monograph. Pune, India: Emcure Pharmaceuticals Ltd.; 2006. 2. Norvasc (amlodipine) Package Insert. New York: Pfizer Labs; 2013. 3. Steele RM, Schuna AA, Schreiber RT. Calcium antagonist‑induced gingival hyperplasia. Ann Intern Med 1994;120:663‑4. 4. Ellis JS, Seymour RA, Thomason JM, Monkman SC, Idle JR. Gingival sequestration of amlodipine and amlodipine‑induced gingival overgrowth. Lancet 1993;341:1102‑3. 5. Srivastava AK, Kundu D, Bandyopadhyay P, Pal AK. Management of amlodipine‑induced gingival enlargement: Series of three cases. J Indian Soc Periodontol 2010;14:279‑81. Access this article online
S. Vikrant Department of Nephrology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India Address for correspondence: Dr. Sanjay Vikrant, Department of Nephrology, Indira Gandhi Medical College, Shimla ‑ 171 001, Himachal Pradesh, India. E‑mail: [email protected]
Indian Journal of Nephrology
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Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.144428
Jan 2015 / Vol 25 / Issue 1
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Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
binding to GABA receptors.[4] Impairment in active transport of cephalosporins from cerebrospinal fluid to blood due to competitive inhibition by accumulated toxic organic acids in patients with renal failure may account for the susceptibility to neurotoxicity.[5] Drug‑induced myoclonus usually resolves after withdrawal of the offending drug. In this patient, the temporal association of the development of myoclonus after starting ceftazidime, and resolution following the discontinuation strongly suggests a causal relationship.
a dihydropyridine calcium channel blocker. Compared to the racemic amlodipine, S‑amlodipine has 1000‑fold stronger affinity to the L‑type calcium channels.[1] The use of racemic amlodipine is commonly associated with adverse events like peripheral edema headache, dizziness, flushing and abdominal pain, gingival overgrowth or enlargement.[2] Controlled clinical trials showed that S‑amlodipine is rarely associated with these side effects.[1]
Due to the uncommon nature of the movement disorders induced by ceftazidime, which is commonly used in dialysis patients closer monitoring is advisable.
Gingival hyperplasia has potential cosmetic implications and provids new niches for the growth of microorganisms. Although the incidence of nifedipine‑induced gingival hyperplasia is about 10%, there are few reports of amlodipine‑related gingival hyperplasia. [3‑5] We encountered two patients with this complication.
J. Joseph, A. Vimala Department of Nephrology, SMCSI Medical College, Karakonam, Trivandrum, Kerala Address for correspondence: Dr. Jigy Joseph, Department of Nephrology, SMCSI Medical College, Karakonam, Trivandrum, Kerala. E‑mail: [email protected]
References 1. Gordon MF. Toxin and drug‑induced myoclonus. Adv Neurol 2002;89:49‑76. 2. Jiménez‑Jiménez FJ, Puertas I, de Toledo‑Heras M. Drug‑induced myoclonus: Frequency, mechanisms and management. CNS Drugs 2004;18:93‑104. 3. Slaker RA, Danielson B. Neurotoxicity associated with ceftazidime therapy in geriatric patients with renal dysfunction. Pharmacotherapy 1991;11:351‑2. 4. Sugimoto M, Uchida I, Mashimo T, Yamazaki S, Hatano K, Ikeda F, et al. Evidence for the involvement of GABA (A) receptor blockade in convulsions induced by cephalosporins. Neuropharmacology 2003;45:304‑14. 5. Richet G, Lopez de Novales E, Verroust P. Drug intoxication and neurological episodes in chronic renal failure. Br Med J 1970;2:394‑5.
A 37‑year‑old man with a case of chronic kidney disease (CKD) stage III was on 5 mg daily dose of S‑amlodipine for the past 1.5 years. He developed swelling of gums and was diagnosed S‑amlodipine‑induced gingival enlargement [Figure 1a]. S‑amlodipine was substituted with metoprolol and moxonidine. Discontinuation of S‑amlodipine and dental toileting led to resolution at 6 months [Figure 1b]. A 62‑year‑old woman with a case of CKD stage V was on 10 mg daily dose of S‑amlodipine for 1 year. She developed swelling of gums, which used to bleed while eating or cleaning and was diagnosed with S‑amlodipine‑induced gingival enlargement [Figure 1c]. She refused dental treatment but S‑amlodipine was changed to moxonidine. Six months later, she had regression of the gingival enlargement [Figure 1d].
Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.144426
S‑amlodipine‑induced gingival enlargement Sir, S‑amlodipine is the chirally pure, single, pharmacologically active enantiomer of amlodipine, 62
Jan 2015 / Vol 25 / Issue 1
a
b
c
d
Figure 1: (a) Gingival enlargement due to S-amlodipine and (b) resolution of the gingival enlargement at 6 months after discontinuation of the S-amlodipine; (c) gingival enlargement due to S-amlodipine and (d) resolution of the gingival enlargement at 6 months after discontinuation of the S-amlodipine
Indian Journal of Nephrology
Letters to Editor
Phenytoin, calcium channel blockers and cyclosporine commonly cause gingival overgrowth. [3‑5] Gingival overgrowth may be due to a direct effect of the drug that regresses upon interruption of drug therapy.[5] However, it is generally accepted that the inflammatory changes caused by the bacteria biofilm synergize with the drug effect to cause overgrowth of the soft tissues. Treatment includes mechanical and chemical plaque (bacterial biofilm) control. Gingivectomy of the overgrown tissue is often needed. If the offending drug cannot be replaced, dental prophylaxes (dental cleaning) at 3‑month intervals is recommended.[5]
References 1. ASOMEX (S‑amlodipine) Product Monograph. Pune, India: Emcure Pharmaceuticals Ltd.; 2006. 2. Norvasc (amlodipine) Package Insert. New York: Pfizer Labs; 2013. 3. Steele RM, Schuna AA, Schreiber RT. Calcium antagonist‑induced gingival hyperplasia. Ann Intern Med 1994;120:663‑4. 4. Ellis JS, Seymour RA, Thomason JM, Monkman SC, Idle JR. Gingival sequestration of amlodipine and amlodipine‑induced gingival overgrowth. Lancet 1993;341:1102‑3. 5. Srivastava AK, Kundu D, Bandyopadhyay P, Pal AK. Management of amlodipine‑induced gingival enlargement: Series of three cases. J Indian Soc Periodontol 2010;14:279‑81. Access this article online
S. Vikrant Department of Nephrology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India Address for correspondence: Dr. Sanjay Vikrant, Department of Nephrology, Indira Gandhi Medical College, Shimla ‑ 171 001, Himachal Pradesh, India. E‑mail: [email protected]
Indian Journal of Nephrology
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Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.144428
Jan 2015 / Vol 25 / Issue 1
63
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
