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LETTER
Year : 2015  |  Volume : 61  |  Issue : 2  |  Page : 149

Authors' reply


1 Department of Pharmacology, Maharishi Markandeshwar College of Pharmacy, Mullana, Ambala, Haryana, India
2 Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, Punjab, India
3 Department of Medicine, Maharishi Markandeshwar Institute of Medical Sciences, Maharishi Markandeshwar University, Mullana, Ambala, Haryana, India
4 Department of Molecular Biology and Biochemistry, Guru Nanak Dev University, Amritsar, Punjab, India

Date of Web Publication13-Mar-2015

Correspondence Address:
S Gupta
Department of Pharmacology, Maharishi Markandeshwar College of Pharmacy, Mullana, Ambala, Haryana
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Gupta S, Goel R K, Agrawal B K, Chattopadhyaya I, Sehajpal P K. Authors' reply. J Postgrad Med 2015;61:149

How to cite this URL:
Gupta S, Goel R K, Agrawal B K, Chattopadhyaya I, Sehajpal P K. Authors' reply. J Postgrad Med [serial online] 2015 [cited 2023 Jun 1];61:149. Available from: https://www.jpgmonline.com/text.asp?2015/61/2/149/153132


Sir,

We appreciate Dr. Raina's interest in our article. [1] His letter raises certain pertinent issues that we had not elaborated on so as to stay focused on our objective. In most of the cases of hypertension in adults, the etiology is not clear and it is categorized as essential hypertension. The prevalence of secondary hypertension is reported to be about 5%. [2] It remains a dilemma as to how much further we should investigate such cases. In the absence of guidelines, most experts opine that only those cases that have some clues in history, examinations, or routine laboratory tests can be explored further. Snoring, obesity, fatigue, and daytime somnolence suggest obstructive sleep apnea. History of headache, flushing, palpitation, sweating, and fluctuating blood pressure may be due to pheochromocytoma. Patients with clinical features suggestive of Cushing's syndrome and hypo/hyperthyroidism should be evaluated along those lines. Raised creatinine is indicative of renal disease, and aldosteronism should be considered in the presence of hypokalemia. However, secondary hypertension can occur even in the absence of any such clue, though such instances are rare.

In our study we had included patients with stage 1 hypertension without any target organ damage and with the absence of any signs, clinically or on routine investigation, suggestive of secondary causes. The usual daily dose of ramipril has been variably mentioned as 2.5-20 mg and 5-10 mg per day. [3],[4] Pharmacological treatment may be started at a threshold of >140 mmHg systolic and/or >90 mmHg diastolic blood pressure, with any of the first-line drugs in the absence of any comorbidity. [5] We had initiated treatment at a dose of 1.25 mg per day, along with advice regarding diet and other lifestyle measures. There are various options regarding dose titration, i.e., maximizing the first drug or adding a second drug before reaching the target blood pressure. [5] For the study's purpose, we had classified responders and nonresponders at the dose of 5 mg per day and tried to correlate gene polymorphism with drug response. We had added a second drug in nonresponders so as to achieve the target blood pressure.

Lifestyle changes should be initiated in all patients and continued indefinitely. This is an ever evolving subject, with the latest concern being the role of sugar in causing hypertension. Experts are still unresolved on whether we are unduly targeting salt and ignoring sugar. It may be prudent to put more emphasis on sugar over salt. [6] We advised lifestyle modifications to all patients and had reemphasized the same in all subsequent visits.

 
 :: References Top

1.
Raina SK. Establishing correlation between genetics and nonresponse. J Postgrad Med 2015;61:148.  Back to cited text no. 1
  Medknow Journal  
2.
Mayet J, Coats AJ. Diagnosis and investigation of essential and secondary hypertension. Eur Heart J 1998;19:372-7.  Back to cited text no. 2
    
3.
Kotchen TA. Hypertensive vascular disease. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18 th ed. New York: McGraw-Hill; 2012:2042-59.  Back to cited text no. 3
    
4.
Weber MA, Schiffrin EL, White WB, Mann S, Lindholm LH, Kenerson JG, et al. Clinical practice guidelines for the management of hypertension in the community a statement by the american society of hypertension and the international society of hypertension. J Hypertens. 2014 Jan; 32(1):3-15.  Back to cited text no. 4
    
5.
James PA, Oparil S, Carter BL, Cushman WC, Dennison-Himmelfarb C, Handler J, et al. 2014 Evidence-based guideline for the management of high blood pressure in adults. Report from the panel members appointed to the Eighth Joint National Committee (JNC 8). JAMA 2014;311:507-20.  Back to cited text no. 5
    
6.
DiNicolantonio JJ, Lucan SC. The wrong white crystals: Not salt but sugar as aetiological in hypertension and cardiometabolic disease. Open Heart 2014;1:e000167. doi:10.1136/openhrt-2014-000167.  Back to cited text no. 6
    




 

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