Authors' reply.

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.[34] 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.