Aquazide

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What Is Aquazide?

Aquazide is an oral 12.5 / 25 mg hydrochlorothiazide tablet from Sun Pharma, supplied in 30-180 tablets. Hydrochlorothiazide was introduced in 1959 by Merck Sharp & Dohme as HydroDiuril — derived from sulfanilamide during the sulfonamide-antibiotic programme when its diuretic activity was noticed serendipitously. HCTZ became the reference thiazide and has been a first-line antihypertensive ever since.

How Hydrochlorothiazide Works

Hydrochlorothiazide inhibits the NCC (sodium-chloride cotransporter) in the distal convoluted tubule. The downstream effects:

• Reduced sodium reabsorption in the distal convoluted tubule — a modest (~5%) increase in urinary sodium excretion
• Volume contraction over the first 1-2 weeks — this is the dominant early BP-lowering mechanism
• Direct vasodilator activity developing over 2-6 weeks — the dominant long-term BP mechanism; thiazides at steady state reduce systemic vascular resistance independent of continued volume contraction
• Enhanced distal-tubule calcium reabsorption — modestly raises serum calcium and reduces urinary calcium (exploited in calcium stone prevention)
• Reduced free water clearance — can cause hyponatraemia in susceptible patients
• Activation of the renin-angiotensin-aldosterone system as a compensatory response — partially blunts the BP effect of monotherapy; neutralised by combining with an ARB or ACE inhibitor (the rationale for FDCs like Telma H, Cosart H)

Approved and Evidence-Based Uses

• Hypertension (first-line; guideline-recommended alongside ARB, ACEi, and CCB) — primary indication
• Mild heart failure oedema — step up to loop diuretic if not controlled
• Recurrent calcium-containing kidney stones — 12.5-25 mg reduces calcium excretion and stone recurrence by 30-50%
• Nephrogenic diabetes insipidus — paradoxical reduction in urine output at 25 mg BD
• Osteoporosis — modest benefit via reduced urinary calcium loss (adjunctive only)

Pivotal trial evidence: ALLHAT (2002) — chlorthalidone (a close thiazide analogue) non-inferior to amlodipine and lisinopril for fatal and nonfatal cardiovascular endpoints in >33,000 hypertensive patients; cemented thiazides as a first-line option. SHEP (1991) — chlorthalidone-based therapy reduced stroke by 36% in isolated systolic hypertension of the elderly. MRFIT, HDFP (1970s-80s) — earlier evidence base. HCTZ-specific large-scale hard-outcome data is weaker than chlorthalidone’s but class effect is presumed.

Aquazide Dosage

Hypertension dose: Start 12.5 mg once daily in the morning. Target 12.5-25 mg. Do not exceed 25 mg for hypertension — higher doses give diminishing returns on BP but worsen metabolic side effects (urate, glucose, lipids). Modern guidelines have moved away from the historical 50 mg antihypertensive dose.

Other indications: Mild heart failure oedema: 25-50 mg/day; escalate to loop diuretic (furosemide) if not controlled. Idiopathic hypercalciuria (recurrent calcium stones): 12.5-25 mg/day — thiazides promote distal-tubule calcium reabsorption and reduce stone recurrence by 30-50%. Nephrogenic diabetes insipidus: 25 mg twice daily paradoxically reduces urine output.

Administration: once daily (or twice daily for high-dose loop diuretics in HF), in the morning. Evening dosing causes nocturia and should be avoided when possible. Take at the same time each day. Food does not significantly affect absorption for any of these diuretics.

Monitoring schedule:

• Baseline: urea, electrolytes (especially potassium and sodium), creatinine, eGFR, glucose, serum urate. Home or clinic BP and daily weight for HF patients.
• 1-2 weeks after start or dose change: repeat U&E and creatinine. Expect mild electrolyte shifts; investigate substantial changes.
• 4-6 weeks: BP review and full metabolic panel.
• Ongoing: annual U&E, urate, glucose, and lipid panel once stable. More frequent in CKD, HF, or on combination therapy.
• Stop or dose-reduce on: sodium <130 with symptoms, potassium <3.0 or >5.5, creatinine rise >30%, new gout, severe dehydration symptoms.

Discontinuation: no withdrawal syndrome but abrupt stop can cause rebound volume retention in HF patients on chronic high-dose loop diuretics — taper where possible and monitor weight.

• Loses efficacy at eGFR <30. Switch to a loop diuretic (furosemide, torasemide) at advanced CKD — thiazides need functioning distal-tubule sodium delivery.
• Raises serum calcium (paradoxical: thiazides enhance distal calcium reabsorption). Useful in osteoporotic patients; problematic in hypercalcaemic conditions (primary hyperparathyroidism, sarcoidosis).
• Photosensitivity rash is a specific thiazide class effect — counsel sun protection in sunny regions.
• Sulfonamide cross-reactivity — avoid if severe sulfa allergy (rare; non-antibiotic sulfonamides rarely cross-react).

Παρενέργειες

Common (>1%):

• Hypokalaemia (3-5%) — more common at doses >25 mg; largely prevented when combined with an ACEi/ARB
• Hyponatraemia (2-5%) — especially in elderly women on low-salt diets; can be severe
• Υπερουριχαιμία and gout precipitation
• Modest worsening of glucose tolerance (fasting glucose +5-8 mg/dL average)
• Mild LDL and triglyceride rise
• Ανικανότητα στύσης in some men — dose-related
• Υπερκαλσιναιμία (usually mild)
• Photosensitivity rash

Uncommon but clinically important:

• Severe hyponatraemia — particularly in elderly on low-salt diets, SIADH-prone states, or combined with SSRIs. Can present as confusion, falls, or seizures.
• Pancreatitis — rare thiazide/loop class effect; stop immediately on upper abdominal pain with lipase rise
• Thrombocytopenia, leucopenia, agranulocytosis — rare hypersensitivity reactions (more common with thiazides than loop agents)
• Acute myopia and angle-closure glaucoma — rare sulfonamide-class reaction within hours to days of starting; stop immediately if sudden painful eye or vision change
• Stevens-Johnson syndrome / toxic epidermal necrolysis — extremely rare but reported

Αντενδείξεις

• Anuria or severe renal impairment (eGFR <30) — loses efficacy
• Sulfonamide (sulfa) hypersensitivity
• Symptomatic hyponatraemia (Na <130) or hypokalaemia (K <3.0) at baseline
• Υπερκαλσιναιμία
• Σοβαρή ηπατική δυσλειτουργία (Child-Pugh C)
• Addison disease (primary adrenal insufficiency)

Pregnancy: generally avoided — thiazides cross the placenta and can cause fetal or neonatal jaundice and thrombocytopenia. Use only if benefit clearly outweighs risk (resistant HTN in late pregnancy), under specialist care.

Breastfeeding: generally acceptable at low doses; high doses can suppress lactation (particularly thiazides). Alternative antihypertensives (propranolol, nifedipine) preferred when possible.

Αλληλεπιδράσεις Φαρμάκων

• Lithium — CRITICAL INTERACTION. Thiazide and loop diuretics reduce lithium renal clearance and can precipitate lithium toxicity. Avoid combination if possible; if unavoidable, monitor lithium levels weekly for the first month and reduce lithium dose by 25-50%.
• Μη στεροειδή αντιφλεγμονώδη φάρμακα (NSAIDs) — reduce diuretic effect (via prostaglandin blockade) and substantially raise AKI risk when combined with ACEi/ARB (the “triple whammy”). Use paracetamol preferentially for chronic pain.
• ACE inhibitors and ARBs — the combination is standard and beneficial in HTN; ACEi/ARB addition blocks compensatory RAAS activation and potentiates the diuretic effect. Monitor potassium and creatinine.
• Potassium supplements and potassium-sparing diuretics — often needed to offset loop/thiazide-induced hypokalaemia. Monitor potassium; avoid over-correction.
• Ντιγκοξίνη — hypokalaemia potentiates digoxin toxicity (loop and thiazide diuretics); spironolactone reduces digoxin clearance directly. Monitor digoxin levels and potassium when starting or changing diuretic.
• Oral corticosteroids, amphotericin B, stimulant laxatives — additive hypokalaemia (loop/thiazide) or masked potassium need (spironolactone).
• Oral antidiabetic drugs, insulin — thiazides and (less so) loops worsen glucose tolerance; may require dose adjustment.
• Cholestyramine / colestipol — reduce absorption of thiazides and loop diuretics by 40-85%. Separate dosing by 4 hours.
• Αλκοόλ — additive postural hypotension.

Where Aquazide Fits in the Diuretic Class

Αποθήκευση

Store Aquazide below 25°C in the original blister pack. Keep out of reach of children.

Συχνές Ερωτήσεις

When should I take Aquazide — morning or evening?

Morning in almost all cases. The diuretic effect produces increased urine output for 2-4 hours after dosing. Evening dosing causes nocturia and disrupts sleep. Patients on twice-daily loop diuretics typically dose at breakfast and early afternoon (not bedtime).

Is Aquazide a first-line blood-pressure drug?

Yes — thiazides (HCTZ, chlorthalidone) and thiazide-like agents (indapamide) are one of the four first-line antihypertensive classes alongside ARBs, ACE inhibitors, and calcium-channel blockers. For most newly diagnosed hypertensive patients, a thiazide is a reasonable first or second agent, and nearly all patients on a multi-drug regimen include one.

Will Aquazide affect my potassium?

Yes — Aquazide lowers potassium by increasing distal-tubule potassium excretion. Monitor at baseline, 1-2 weeks, and periodically. Hypokalaemia risk is minimised by combining Aquazide with an ARB or ACE inhibitor — which is the standard combination in hypertension anyway. If potassium drops below 3.5 in isolated diuretic use, add potassium supplementation, a potassium-rich diet, or a small dose of a potassium-sparing agent (spironolactone, eplerenone, or an amiloride-containing combination).

I have gout — can I take Aquazide?

With caution. Thiazides and (less so) loop diuretics raise serum uric acid by competing for proximal-tubule excretion. In gout-prone patients: prefer losartan-based combinations (Cosart H, Cozartan H) whose losartan component is uniquely uricosuric and offsets the thiazide urate rise. If Aquazide is already in use and gout flares, add or continue urate-lowering therapy (allopurinol) rather than stopping Aquazide outright.

I’m diabetic — is Aquazide safe?

Mostly yes, but be aware that thiazides and (to a lesser extent) loop diuretics modestly worsen glucose tolerance (average fasting glucose rise 5-8 mg/dL, HbA1c 0.1-0.3%). The BP benefit outweighs this in most diabetics. If you want a more metabolically neutral combination, ARB+CCB is an alternative (Olmezest AM).

Can I take ibuprofen with Aquazide?

Occasional short-term use is usually fine. Chronic daily NSAIDs (ibuprofen, diclofenac, naproxen) reduce the diuretic and antihypertensive effect of Aquazide (prostaglandin blockade) and substantially raise the AKI risk when combined with an ACE inhibitor or ARB — the “triple whammy.” Use paracetamol preferentially for chronic pain.

Will I urinate more at night?

Usually no, if you take Aquazide in the morning. The diuretic effect peaks 2-4 hours after dosing and has mostly worn off by evening. Nocturia is a common complaint when patients switch to evening dosing; switch back to morning dosing and nocturia resolves within 1-3 days.

Can I take Aquazide in pregnancy?

Routinely avoided. Thiazides cross the placenta and can affect the fetus. For hypertension in pregnancy, switch to labetalol, methyldopa, or nifedipine. Diuretics are used in pregnancy only for specific indications (pulmonary oedema, resistant HF) under specialist supervision.

Τι γίνεται αν χάσω μια δόση;

Take it as soon as you remember, unless it is nearly time for your next dose — in that case skip the missed dose. Do not double up. A single missed dose does not meaningfully affect long-term BP or fluid control.

Where can I buy Aquazide online?

You can buy Aquazide (12.5 / 25 mg hydrochlorothiazide, 30-180 tablets) from MedsBase with discreet packaging and worldwide shipping.

Related Antihypertensives & Diuretics on MedsBase

• Aldactone — Spironolactone 25 mg (aldosterone antagonist)
• Cosart H — Losartan + HCTZ fixed combination
• Dytor — Torasemide (loop, more predictable bioavailability)
• Hydrocl — Hydrochlorothiazide (HCTZ)
• Losar — Losartan (ARB partner for diuretic)
• Telma H — Telmisartan + HCTZ fixed combination
• Browse all High Blood Pressure Medications

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