Moduretic is used for treating fluid retention (edema) and high blood pressure. It may be used alone or with other medicines.
Other names for this medication:
Also known as: Amiloride hydrochlorothiazide.
Moduretic is a diuretic (water pill) and a combination of a potassium-sparing diuretic (amiloride) and a thiazide diuretic (hydrochlorothiazide). It works by making the kidneys eliminate sodium (salt) and water from the body, which helps to lower blood pressure. The amiloride component helps minimize potassium loss.
Brand name of Moduretic is Moduretic.
Take Moduretic by mouth with food.
Moduretic may increase the amount of urine or cause you to urinate more often when you first start taking it. To keep this from disturbing your sleep, try to take your dose before 6 pm.
If you want to achieve most effective results do not stop taking Moduretic suddenly.
If you overdose Moduretic and you don't feel good you should visit your doctor or health care provider immediately.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Do not freeze. Keep container closed tightly. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Moduretic are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Moduretic if you are allergic to Moduretic components or to any ingredient in Moduretic or any other sulfonamide (eg, sulfamethoxazole).
Be careful with Moduretic if you're pregnant or you plan to have a baby, or you are a nursing mother.
Be careful with Moduretic if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.
Be careful with Moduretic if you have allergies to medicines, foods, or other substances.
Be careful with Moduretic if you have cirrhosis or liver problems, diabetes, gout, kidney problems or kidney stones, asthma, heart problems, or systemic lupus erythematosus.
Be careful with Moduretic if you have elevated blood acid, low folic acid levels, or electrolyte problems, or are dehydrated.
Be careful with Moduretic if you take potassium-sparing diuretics (eg, spironolactone), potassium supplements, or salt substitutes containing potassium because high blood potassium levels may occur and cause listlessness, confusion, abnormal skin sensations of the arms and legs, heaviness of limbs, slowed heart rate, irregular heart rhythm, or stopping of the heart; cholestyramine or colestipol because they may decrease Moduretic 's effectiveness; nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, indomethacin) because they may decrease Moduretic 's effectiveness and risk of kidney problems may be increased; barbiturates (eg, phenobarbital), certain chemotherapy medicines, corticosteroids (eg, prednisone), digoxin, dofetilide, ketanserin, narcotic pain medicines (eg, codeine), or medicines for high blood pressure because the risk of their side effects may be increased by Moduretic; diazoxide, lithium, or nondepolarizing neuromuscular blockers (eg, pancuronium) because their actions and the risk of their side effects may be increased by Moduretic; angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril) because the risk of high blood potassium and kidney problems may be increased by Moduretic; diabetes medicines (eg, glipizide) or insulin because their effectiveness may be decreased by Moduretic.
Do not stop taking Moduretic suddenly.
A low-renin status characterized two-thirds of patients with treatment-resistant hypertension, who could be treated efficiently by aldosterone inhibition. Patients with an escape phenomenon (18%) could effectively be treated by increasing the aldosterone inhibitor. Low-renin hypertensives had high prevalence of adrenocortical adenomas and primary aldosteronism.
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Common carotid artery intima-media thickness (IMT) progression was compared between 4 years of treatment with nifedipine and diuretic.
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In a randomized double blind study 100 men (mean age 46 (22-64) years) with mild to moderate hypertension were followed every 3rd month for one year. Fifty were randomized to atenolol 50 mg and 50 to hydrochlorothiazide 25 mg+amiloride 5 mg (co-amiloride) once daily. The doses were doubled at 3 or 6 months if diastolic blood pressure (DBP) remained > or = 95 mmHg. If DBP was > or = 95 mmHg even at 6 or 9 months, patients were classified as non-responders, and nifedipine 20 mg b.i.d. was added. After one year 31/50 randomized to atenolol and 17/50 randomized to co-amiloride had responded to monotherapy (p < 0.05). Neither clinical findings nor haemodynamic measurements by Doppler at baseline could distinguish between co-amiloride responders and non-responders. Conversely, non-responders to atenolol as compared with atenolol responders had higher body weight (p = 0.02), higher systolic BP (p = 0.03), higher DBP (p = 0.009), stroke volume (p = 0.04), and cardiac output (p = 0.0002) combined with lower total systemic vascular resistance (p = 0.02). This suggests that some were apparent non-responders due to too low dosing of atenolol rather than true non-responders. Measurements of haemodynamics may be of importance in the assessment of optimal antihypertensive therapy according to baseline and follow-up haemodynamic aberrations.
To study the effect of a combination of amiloride, 5 mg, and hydrochlorothiazide, 50 mg (Moduretic), on plasma and skeletal muscle electrolytes in patients on long-term diuretic therapy (greater than 1 year) for arterial hypertension and/or congestive heart failure, 58 patients were recruited. Fifty-five patients completed the study, 27 controls and 28 in the treatment group. The Moduretic group demonstrated a significant increase in skeletal muscle potassium and magnesium values and a significant decrease in systolic blood pressure after 6 months on therapy. There was no significant change in these parameters in the control group. It is concluded that this combination of amiloride and hydrochlorothiazide is capable of preserving the internal and external balance of potassium and magnesium on a long-term basis in the patient categories studied.
In a double-blind parallel-group study 133 patients with mild to moderate essential hypertension were randomised to felodipine 5mg twice daily or Moduretic mite every morning after a run-in placebo period of 1 to 2 weeks. All previous antihypertensive therapy was withdrawn at the start of the run-in period. After 4 weeks the dose of felodipine was increased to 10mg twice daily, and Moduretic mite was replaced by Moduretic in patients with a diastolic blood pressure of greater than 80mm Hg. On the low dose, the supine blood pressure on felodipine was reduced by 24/14mm Hg from 174/105mm Hg, and on Moduretic mite by 19/11mm Hg from 171/103mm Hg. After the increase in dosage blood pressure was lowered further. There was no statistically significant difference in blood pressure reduction between the 2 groups. Severe adverse drug experiences (ADEs) were few and equally distributed. However, more felodipine patients were withdrawn because of ADEs. Potassium levels decreased and uric acid levels increased significantly in the Moduretic group.
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A double-blind randomized study comparing the effects of 1 year's treatment with atenolol (A) 50 mg or hydrochlorothiazide 25 mg plus amiloride 5 mg (Moduretic (M)) on the lipid profile was performed in 100 hypertensive men (mean age 47, range 22-64 years). After 4 weeks' wash-out and 4 weeks on placebo therapy subjects were randomized to either A or M therapy and followed up every third month for 1 year. If the diastolic blood pressure (DBP) was greater than or equal to 95 mmHg at a subsequent visit, the doses were doubled (n = 17 for A and n = 12 for M) and, if DBP was still greater than or equal to 95 mmHg on double dose, nifedipine 20 mg b.d. was added (n = 15 for A and n = 27 for M, p less than 0.05). The lowering of heart rate (p = 0.0001) and DBP (p = 0.005) was more pronounced with A after 1 year. During that time no significant treatment differences were noted for total cholesterol, low-density lipoprotein (LDL) cholesterol or apoproteins A and B. High-density lipoprotein (HDL) cholesterol decreased from a mean of 1.19 (+/- 0.36) mmol l-1 to 1.13 (+/- 0.35) with A, and increased from 1.14 (+/- 0.30) mmol l-1 to 1.22 (+/- 0.28) with M, and this treatment difference was significant (p = 0.0002). The triglycerides increased from 2.0 (+/- 1.2) mmol l-1 to 2.3 (+/- 1.6) in the A group and did not change with M treatment (p = 0.02) for treatment difference). In view of similar effects on cholesterol, LDL cholesterol and apoproteins, the prognostic importance of the observed treatment differences on HDL cholesterol and triglycerides remains to be established.
Three cases are presented which emphasize the importance of hyponatraemia as a cause of grand mal seizures. The combination of hydrochlorothiazide and amiloride appears to increase the risk of hyponatraemia. We discuss the aetiology and treatment of hyponatraemia and review the necessity for such combination therapy. We recommend caution in prescribing diuretics and preparations such as Moduretic should be used only in those few patients shown to need potassium supplementation.
Among 54 patients attending a hospital hypertension clinic and receiving the fixed-combination diuretic Moduretic (hydrochlorothiazide 50 mg, amiloride 5 mg), there was a 44.4% incidence of hypokalaemia. The mean drop in plasma potassium level was 0.69 mmol/L (P less than 0.0001), the mean low level being 2.81 mmol/L. Seventy-four per cent of falls occurred within 52 weeks of the start of therapy, 19.5 weeks being the average period between a normal and a low plasma potassium level. There was no difference in the fall in potassium level between male and female subjects, and beta-blockers were not obviously protective, although there was a statistically significant smaller fall in potassium level in females treated with them. The clinical significance of the unexpected hypokalaemia is uncertain; but even with fixed-combination diuretics, it remains necessary to monitor the plasma potassium level regularly in order to avoid complicating situations. The results of the present study would cast doubt on the efficacy of 5 mg of amiloride with 50 mg of hydrochlorothiazide in fixed-combination form in preventing hypokalaemia in this clinical situation.
Three patients with impaired renal function suffered complications of hyperkalaemia within 10 days of beginning therapy with hydrochlorothiazide and amiloride combination (Moduretic). The possible relationship between hyperkalaemia and this diuretic is discussed.
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A cross-over study, comparing the effects of doxazosin, moduretic and amlodipine on plasma lipid and lipoprotein levels in 9 hypertensive Nigerians aged 35 to 65 years is presented. Doxazosin therapy had favourable lipid changes characterized by a statistically significant reduction in total cholesterol (TC) at 6 months. Though consistent reduction was observed in total triglycerides (TG) low density lipoprotein cholesterol (LDL-C), very low density lipoprotein-cholesterol (VLDLC) upto 6 months, no effect was seen on high density lipoprotein cholesterol (HDLC). This is against unfavourable increments in the mean values of TC, VLDLC, LDLC/HDLC and decrease in HDLC/TC during moduretic treatment phase. Amlodipine therapy did not alter the lipid and lipoprotein levels. The non-significant variation in the mean high density lipoprotein-cholesterol (HDLC) level observed with these agents, seem to suggest that HDL-cholesterol metabolism may be maintained during antihypertensive pharmacotherapy.
A cross-over study comparing the effects of doxazosin, moduretic and amlodipine on fasting blood glucose and blood pressure levels in 9 adult hypertensive Nigerians is presented. The results showed that doxazosin, moduretic and amlodipine were effective in reducing diastolic blood pressure and thus confirmed our previous observation of blood pressure reduction during the monotherapies of these antihypertensive agents. The study further indicated the effectiveness of doxazosin in the management of severe essential hypertension in Nigerian patients. Fasting blood glucose level significantly decreased during doxazosin treatment phase and increased during moduretic phase, while amlodipine treatment did not have any effect on blood glucose level. In conclusion, the cross-over study seem to confirm the effectiveness of doxazosin therapy and its antidiabetic effect in hypertensive patients. The effectiveness of amlodipine therapy in controlling blood pressure was also observed, but no effect on blood glucose level, while moduretic therapy has hyperglycemic effect despite its effectiveness in blood pressure control in African patients.
Twenty patients with essential hypertension aged 39-70 years, underwent 20 weeks (short-term) and 30 weeks (long-term) lipid and lipoprotein assessment following moduretic (combination of hydrochlorothiazide and amloride) therapy. Moduretic caused adverse alterations in plasma lipid and lipoprotein concentrations at 20 weeks, characterized by increases in total cholesterol (TC) (9-23%), low-density lipoprotein-cholesterol (LDL-C) (18-42%), Triglycerides (TG) (12-26%) and LDL-C/HDL-C (36-92%), as well as decreases in high density lipoprotein-cholesterol (HDL-C) (-14 to -26%) and HDL-C/TC (-23 to -39%). For 12 patients who were continued on the same therapy for the longer period of 30 weeks, the adverse effects were less pronounced when compared with the short-term effects. The increases in TC (9.6%), in LDL-C (21%), and in LDL-C/HDL-C (48%), and the decreases in the mean HDL-C (-20%), and in HDL-C/TC (-25%), were all significant. In contrast, the slight increase in TG noted during the long-term moduretic therapy was not significant. Our data suggest that moduretic therapy induces altered lipid-lipoprotein patterns in hypertensive patients. However, the possible influence of baseline cholesterol concentration and the duration of therapy, may be important factors in the lipid response to moduretic therapy.
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We here showed that F may be administered to a patient with previous AmHTZ induced hyponatremia without risk for recurrent hyponatremia.
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In 75 patients with circulatory insufficiency of various degree the diuretic effect of moduretic was studied. In 25 of them besides the potassium and sodium metabolism and in 33 others, with a background of chronic ischemic disease of the heart and hypertensive disease, the state of the hemocoagulation system was investigated in the moduretic medication. In 24 patients with hypertensive disease of the I--IIA stage subject to study was the effect of moduretic on the arterial pressure, with this drug administered by mouth in doses of 3 to 1/2 tablet a day. The drug proved to have a marked duretic effect in patients with different degree of circulatory insufficiency. It increases sodium excretion with urine and retains potassium in the organism, without causing hyperkaliemia. In patients with circulatory insufficiency of the I degree the drug can provoke thrombogenesis and in cases of the IIA, IIB and III degree may be considered a drug of choice. Moduretic brings down the systolic and diastolic pressure in patients with hypertensive disease of the I and II stages.
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The purpose of this study was to identify the frequency of cardiac dysrhythmias in two similar groups of hypertensive middle-aged males (age 45-66). They had previously been randomized either to a diuretic treatment (n = 42), or a beta-blocking agent (n = 41). A 24-hour ambulatory Holter monitoring, and serum potassium, was obtained in all patients, serum magnesium was measured in 35 patients. The mean number of ventricular premature beats (VPBs) and the frequency of complex arrhythmias (19 vs. 5) was significantly higher in the diuretic group (p less than 0.01). The serum potassium was significantly lower (p less than 0.001) in the diuretic group, and there was a significant (p less than 0.005) inverse correlation between the number of VPBs and the serum potassium in all treated patients. The patients with complex arrhythmias were older (p less than 0.01) than the remainder of the patients. No correlation between serum magnesium and VPBs or complex arrhythmias was found. This study demonstrates increased frequency of VPBs in older hypertensive males, treated with diuretics, and that hypokalaemia predisposes to increased cardiac arrhythmias. We conclude that in older mildly hypertensive men hypokalaemia should be avoided.
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27 patients with essential hypertension received placebo for 2 weeks, then 1 Moduretic tablet (50 mg hydrochlorothiazide and 5 mg amiloride) daily for 4 weeks, followed by 2 Moduretic tablets daily for a further 10 weeks. The average systolic and diastolic reductions were 26.3/14.0 mm Hg standing and 27.8/19.7 mm Hg lying. 17 of the 27 patients were treated before the beginning of the study with 100 mg hydrochlorothiazide or an equivalent preparation. After 14 weeks' therapy with Moduretic the average systolic/diastolic fall in pressure in these 17 patients was 18.5/9.9 mm Hg standing and 21.6/14.3 mm Hg lying, which was lower than with a thiazide monotherapy. No cases of hyperkalemia or hypokalemia were observed. Moduretic lowers the blood pressure considerably more than thiazide alone and without any concomitant danger of hypokalemia.
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Thiazide diuretics frequently cause a decrease in serum potassium levels. In this study, 34 percent of patients taking hydrochlorothiazide had serum potassium levels below 3.5 meq/liter. The response of the serum potassium level was studied after treatment in 56 patients was switched from 50 mg of hydrochlorothiazide daily to either two capsules of hydrochlorothiazide/triampterene (Dyazide), or one tablet of hydrochlorothiazide/amiloride (Moduretic) daily, over nine to 15 months. The 24 patients whose treatment was changed to Dyazide had a rise in serum potassium levels from a mean of 3.56 meq/liter to 4.17 meq/liter in two to three weeks. The 32 patients whose treatment was changed to Moduretic had a rise in serum potassium levels from a mean of 3.76 meq/liter to 4.14 meq/liter in two to three weeks. The resultant rise in potassium levels was stable throughout the follow-up period in both groups. Patient acceptance of this change was excellent.
The clinical pharmacology of the diuretic amyloride was studied in 60 patients suffering from circulatory insufficiency of various origin. Midamor and moduretic of the "Merck" firm (USA) were used in a dose of 1 to 4 tablets. The duration of treatment was from 3 days to 18 months. It was found that under the effect of amyloride natriuresis increases moderately in patients with circulatory insufficiency with no simultaneous increase in the loss of potassium with the urine. As the circulatory insufficiency becomes more severe, the natriuretic and potassium-saving effect of the drug diminishes. Amyloride potentiates the diuretic and natriuretic effect of furosemide and hydrochlorothiazide well without increasing kaliuresis. In patients in whom the disease is less severe, two-week treatment with amyloride leads to an authentic increase in the total metabolic potassium in the organism. The patients tolerate the drug well. It is recommended for wide clinical use.
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Therapy resistance is an enduring problem in clinical hypertension. Our aims were to estimate: (1) the contribution of a low-renin status in therapy resistance; (2) whether such status could give a clue to more successful treatment; and (3) the contribution by adrenal cortical adenomas and by primary aldosteronism.
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Simultaneous administration of indomethacin and Moduretic (Merck Sharp & Dohme, USA, 5 mg of amiloride HCl, 50 mg hydrochlorothiazide) to a 78-yr-old patient resulted in severe hyperkalemia twice. When administered alone, neither drug significantly changed the normal serum potassium levels. Laboratory findings suggest an alteration of the internal balance of potassium as the main mechanism of this particular drug-induced hyperkalemia.
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After a run-in period of 8 weeks on a regimen of hydrochlorothiazide (HCT, median dosage 75 mg/day), patients with essential hypertension were randomly allocated to continued hydrochlorothiazide therapy (Group I) or additional treatment with amiloride (Group II, median dosage 15 mg/day, or 5 mg per 25 mg hydrochlorothiazide) for the following 12 weeks. Thereafter all the patients were changed to treatment with a fixed combination tablet containing 5 mg amiloride and 50 mg hydrochlorothiazide (Moduretic), keeping the thiazide dosage unchanged for an additional 12 weeks. In Group I patients there was no change in plasma potassium, total body potassium content or the renin-angiotensin-aldosterone system during the 12 weeks on HCT. When the treatment was changed to Moduretic, significant increases were found of 10% in plasma potassium and 3% in total body potassium content. No important stimulation of the renin-angiotensin-aldosterone system was found. In Group II patients addition of an average of 15 mg amiloride to the hydrochlorothiazide treatment led to significant increases in plasma potassium and total body potassium content of approximately 15% and 4%, respectively. There was also a significant increase in the plasma concentrations of renin, angiotensin II and aldosterone. Reducing the average dose of amiloride to 7.5 mg/day by use of Moduretic did not lead to decrease in plasma potassium or total body potassium content. Plasma concentrations of renin, angiotensin II, and aldosterone were decreased, but the individual changes varied markedly and no significant overall change was found.
Rapid, precise, accurate and specific ratio spectra derivative spectrophotometry and high-performance liquid chromatographic procedures were described for the simultaneous determination of hydrochlorothiazide and amiloride hydrochloride in combined pharmaceutical dosage forms. For the first method, ratio spectra derivative spectrophotometry, the signals were measured at 285.7 nm for hydrochlorothiazide and at 302.5 nm for amiloride hydrochloride in the mixture, in the first derivative of the ratio spectra. The second method is based on high-performance liquid chromatography (HPLC) on LiChrosorb RP-C18 column (5 microm, 20 cm x 4.6 mm) using 0.025 M orthophosphoric acid (adjusted to pH 3.0 with triethylamine (TEA)), acetonitrile (84:16 v/v) as a mobile phase at a flow rate of 1.2 ml/min(-1). Detection was carried out using a UV detector at 278.0 nm. Commercial sugar-coated and laboratory-prepared mixtures containing both drugs in different proportions were assayed using the developed methods.
The efficacy and biochemical effects of two low-dose thiazide plus potassium-sparing diuretic preparations were compared in the treatment of elderly patients with stable, mild to moderate congestive heart failure. Sixty patients (mean age 80 years) were randomly allocated to treatment with 1 tablet daily of either 25 mg hydrochlorothiazide/2.5 mg amiloride or 25 mg hydrochlorothiazide/50 mg triamterene. The dose was increased to 2 tablets daily if necessary, after 2 weeks, for a further 6 weeks. Patients' response to treatment was assessed at 2, 4 and 8 weeks using a simple clinical scoring system for signs and symptoms of their condition, and routine biochemical analysis was carried out at baseline and the end of treatment. One patient was withdrawn from the study due to a rash which was probably related to hydrochlorothiazide/amiloride treatment. A further 11 patients were excluded from the analysis because of intercurrent illness or inadequate records. Analysis of the results from 48 patients showed that both treatments resulted in an improvement in clinical score and weight reduction, with more than three-quarters of the patients responding to treatment. No serious biochemical disturbances occurred; in particular, no new cases of hyponatraemia (serum sodium less than 130 mmol/l) developed. Both preparations, therefore, were effective and tolerated forms of treatment for mild to moderate congestive heart failure in the elderly and there were no significant differences between them.
Medical treatment of the disease improved the dilation in all cases, preventing its potential complications. Regardless of the good outcome of our patients, periodic urologic follow-up is recommended in NDI patients.
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Patients were diagnosed at a median age of 1.6 years (range, 0.16-6.33 years) and treated with a low osmotic diet, hydrochlorothiazide-amiloride and indomethacin, which decreased the diuresis from a median of 10.5 ml/kg/h to 4.4 ml/kg/h (p < 0.001). Three patients showed normal renal ultrasound before treatment until last control, while the remaining seven showed urinary tract dilation. In this second group, dilation was reduced with treatment in four patients and disappeared in the remaining three. Children without dilation or in whom the dilation disappeared were diagnosed and treated earlier than those with persistent dilation (median 1.66 versus 4.45 years, respectively). After a median of 10.4 (range, 2.3-20.3) years of follow-up, no patients showed urological complications.
The Authors have studied the effects of fenquizone compared to those of hydrochlorothiazyde-amyloride therapy. They have found a good activity in hypertension and a powerful diuretic action, besides fenquizone has no remarkable side-effect.
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73% (138) of the patients were on anti-hypertensive drug combinations, comprising 71.7% (99), 24.4% (34) and 3.6% (5) on combinations of two, three and four drugs respectively. Overall, Thiazide diuretic consisting mainly of fixed dose combination of Amiloride and Hydorchlorothiazide (Moduretic(r)) was the most frequently prescribed drug class in anti-hypertensive combination therapy (83.3%). ACE inhibitor, Lisinopril (Zestril(r)), was prescribed in combination with Moduretic(r), Calcium channel blocker and beta-blocker in 6.5%, 8.5% and 0.7% respectively. Blood pressure control was adequate in only 29% (40) of patients, though adherence with therapy was documented as adequate in 77.5% (107). Type-2 diabetes mellitus (32.7%) and osteoarthritis (21.8%) were the most frequent co-morbidities. Potentially harmful drug-drug interactions in the study sample were identified in 17.5% (46) of patients. Physician documentation of adverse drug reactions among patients was done in only 10.9% of cases. There appear to be no institutionalised system in place to monitor, detect and document adverse drug reactions among patients on anti-hypertensive drug therapy.
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We report a case of lithium overdose in a patient who presented in non-convulsive status epilepticus. The lithium toxicity was probably due to interaction with Moduretic. The diagnosis was not suspected until electroencephalography was performed. This case underscores the importance of therapeutic drug level monitoring of lithium, especially where toxicity is suspected, and the indispensable role electroencephalography plays by allowing a correct diagnosis to be made promptly.
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In patients with ISH, nifedipine GITS and co-amilozide had similar effects on clinical outcomes and BP lowering. They lend support to international guidelines for the treatment of hypertension recommending the use of long-acting dihydropyridine calcium-channel blockers as one treatment option for patients with ISH.
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