Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

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An yearly reward for the best article authored can also incentivize the authors. Though the process of finding the best article will be not be very easy. I do not know how reviewing process can be improved. If an article is being reviewed by two reviewers, then opinion of one can be communicated to the other or the final opinion of the editor can be communicated to the reviewer if requested for. This will help one’s reviewing skills.
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Dr. Mamta Gupta
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Aug 2018

Dr. Rajendra Kumar Ghritlaharey

"I wish to thank Dr. Hemant Jain, Editor-in-Chief Journal of Clinical and Diagnostic Research (JCDR), for asking me to write up few words.
Writing is the representation of language in a textual medium i e; into the words and sentences on paper. Quality medical manuscript writing in particular, demands not only a high-quality research, but also requires accurate and concise communication of findings and conclusions, with adherence to particular journal guidelines. In medical field whether working in teaching, private, or in corporate institution, everyone wants to excel in his / her own field and get recognised by making manuscripts publication.

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Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
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Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
On May 11,2011

Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
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Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."

Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
On April 2011

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.

Dr. Anuradha
On Jan 2020

Important Notice

Letter to Editor
Year : 2007 | Month : June | Volume : 1 | Issue : 3 | Page : 205 - 208 Full Version

Phenytoin-Induced Toxicity Due To Drug Interactions

Published: June 1, 2007 | DOI:

Department of Clinical Pharmacology St. John’s Medical College and Hospital,Bangalore-560034, India E-mail :

Correspondence Address :
Dr. Chanda Kulkarni.
Department of Clinical Pharmacology
St. John’s Medical College and Hospital, Bangalore-560034, India
E-mail :


Phenytoin is effective against both partial and tonic-clonic seizures. It is said to act by limiting repetitive firing of action potentials evoked by sustained depolarization, mediated by slowing the rate of recovery of voltage activated sodium channels from inactivation. The optimal initial dose, suggested for phenytoin is 3 to 4 mg/kg, body weight /day, while the usual maintenance dose is 200 to 500 mg/day for an adult. Phenytion is completely absorbed from upper intestine and is metabolized by liver. It undergoes entero-hepatic recycling and is excreted in urine, either as free or conjugated form. It is widely distributed throughout the body and is extensively plasma protein bound (90%). The toxic effects of phenytoin depend upon the route of administration, duration of exposure and dosage. Its toxic manifestations present as a syndrome comprising of cerebellar, vestibular and ocular effects such as nystagmus, diplopia, slurred speech and ataxia. Mental confusion and exacerbation of seizure frequency have also been noted. Overdose leads to hypotension, coma and respiratory depression. The dosage adjustments of phenytoin are necessary, to achieve adequate control of seizures, along with monitoring of its plasma concentration. This is because it follows saturation kinetics such as the rate of elimination varies as a function of its concentration. The plasma half-life ranges from 6 to 24 hrs at plasma concentration below 10 mg/ml, but increases with higher concentration. As a result, even with small increments in it’s dosage to attain the levels towards therapeutic range, plasma drug concentration may increase disproportionately leading to toxicity. While, several reports are available indicating adverse drug reactions to phenytoin, the following case illustrates how phenytoin toxicity is affected by its interaction with other drugs especially in situations of polypharmacy.

Case Report

A 50-year-old woman was brought with a history of diabetes of 2 yrs duration, treated with insulin. She was also reported to be on antihypertensive medication, atenolol 50 mg, once daily, for 17 yrs and aspirin 75 mg, once daily for prophylaxis of myocardial infraction.Patient gave history of periodic consumption of ibuprofen 200 mg and combination of calcium carbonate and vitamin D3 (shelcal ) 500mg, for her osteoarthritis of 20 yrs duration.
The patient was admitted with a provisional diagnosis of chronic renal failure as a result of non-steroidal anti-inflammatory drugs (NSAID) abuse, along with seizure disorder. Diagnosis of myoclonic jerks secondary to metabolic factors was made and she was advised additional treatment with phenytoin 100 mg, thrice daily along with clonazepam 0.5 mg, once daily. As thepatient had symptoms of peptic ulcer she was prescribed pantoprazole 40 mg, once daily. Patient was subsequently discharged a week later with a note to continue the above medications and was asked to come for a follow-up visit to the out-patient department after 15 days.
However, the patient developed symptomsof inability to coordinate voluntary movements and excessive weakness ten days after starting phenytoin for metabolic seizures along with pantoprazole for peptic ulcer. However patient sought admission two days later. A diagnosis of ataxia, secondary to phenytoin toxicity was then made. Her hemoglobin was 10.2 g/dl and HBsAg was negative. Serum sodium 128mEq/L, potassium 3.9 mEq/L and chloride 97 mEq/L. Fasting blood sugar was 159 mg/dl and her serum phenytoin level was > 40 μg/ml (normal range = 10-20μg/ml) at the time of admission and 30 > μg/ml, two days after the admission.
On the day of admission, the patient was treated with amlodipine 2.5 mg, once daily and combined vitamin B1, B6 and B12 (Neurobion) 5000 units, intramuscularly. She also received hepatitis B (Shanvac) 1 ml IM and oral salt 5-6 gm/day, in addition to the previous treatment regimen for diabetes, hypertension and peptic ulcer. Hepatitis B vaccine was found to have been given as a part of protocol defined for the treatment of chronic kidney disease to prevent hepatitis infection during the course of dialysis and oral salt to compensate for low sodium level i.e. 125 mEq/L (135-145 mEq/L). Since her serum phenytoin level was high, the drug was withheld for one day and she was prescribed clonazepam 2mg intravenously as needed, if she had a seizure. After a 24-hr break her blood sample was sent for estimation of phenytoin levels and was restarted on 100 mg of phenytoin once a day, along with clonazepam 0.5 mg once daily. During her stay in the hospital ataxia was reported to be less severe and her phenytoin level was 30 mg/ml two days after the admission.


In this patient, ataxia was identified to be secondary to phenytoin toxicity, as a result of pharmacokinetic drug interactions which may be due to multiple medications she received.
Pantoprazole an anti-peptic ulcer agent, inhibits oxidative hepatic metabolism of phenytoin(2), decreases it’s plasma clearance by 15% and increases it’s elimination half life by 27%, resulting in higher serum levels. Ibuprofen is an anti-inflammatory drug and when co-administered with phenytoin is known to inhibit hepatic metabolism of phenytoin and also displace phenytoin from albumin binding sites (3), which may increase the levels of phenytoin. Amlodipine is a calcium channel blocker and phenytoin when co-administered is known to induce the cytochrome P450 3A4 system and is reported to reduce bioavailability of calcium channel blockers (4). Salicylates can also affect the serum levels of phenytoin by increasing the plasma-free phenytoin fraction (5). Further, there is evidence for phenytoin-induced hyperglycemia and hypocalcemia, which deserves a careful consideration of using these drugs along with phenytoin, as she is a known diabetic. Also, the decrease in serum calcium concentration to hypocalcemic values, along with significant reduction in 25 hyroxy-cholecalciferol concentration and increase in alkaline phosphatase, by phenytoin may worsen osteoarthritis (1).

Suggestions for safer medications
In the present patient, a H2 (histamine) receptor blocking agent can be substituted to treat peptic ulcer in place of pantoprazole. The NSAIDS such as aspirin and ibuprofen may be avoided or given as and when required because they have a tendency to produce gastrointestinal damage, bleeding and interactions altering blood phenytoin levels. . As the patient was already receiving atenolol for blood pressure control, the use of a calcium channel blocker should be reassessed.


Thus, the increased serum levels of phenytoin in this patient appear to be due to drug-drug interactions and clinicians should pay special attention to the usage of drugs such as pantoprazole, NSAIDs and Calcium channel blockers when a patient is receiving phenytoin for seizure disorder.

Conflict of Interest: None declared


Sean C Sweetman; The Martindale : The Complete Drug Reference; 33rd (Ed): Pharmaceutical Press; London. Chicago 2002: 357.
Prichard PJ, et al, Oral phenytoin pharmacokinetics during omeprazole therapy. Br. Jr. Clin. Phramacol 1987; 24: 543-5.
Dasgupta, et al, In vitro displacement of phenytoin from protein binding by nonsteroidal antiinflammatory drugs tolmetin, ibuprofen, and naproxen in normal and uremic sera. Ther Drug Moint 1996; 18(1):97-99.
Cachat F, Turfro A, Phenytoin/Isradipine interaction causing severe neurologic toxicity. Ann Pharmacother. 2002; 36(9): 1399-402
Paxton JW. Effects of aspirin on salivary and serum phenytoin Kinetics in healthy subjects. Clin Pharmacol Ther. 1980; 27: 170.

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