How Long After Taking Naproxen Can I Drink Alcohol?

How Long After Taking Naproxen Can I Drink Alcohol
Frequently asked questions – What should I do if I have already mixed naproxen and alcohol? As naproxen is usually safe to take alongside alcohol, mixing both these substances in safe quantities should not be a cause for concern. However, if you are experiencing any of the side effects listed above or are finding it difficult to control your intake of alcohol or naproxen, we would strongly recommend contacting a health professional or local addiction treatment service to discuss your concerns.

Can I drink alcohol 4 hours after taking naproxen?

Can I drink alcohol while taking naproxen? Yes, you can drink alcohol while taking naproxen. But drinking too much alcohol may irritate your stomach.

Can I take naproxen 2 hours after drinking?

There are 4 alcohol/food/lifestyle interactions with naproxen. Ask your doctor before using naproxen together with ethanol. Do not drink alcohol while taking naproxen. Alcohol can increase your risk of stomach bleeding caused by naproxen. Call your doctor at once if you have symptoms of bleeding in your stomach or intestines.

How long does it take for naproxen to get out of your system?

How long it lasts – After you take a dose of naproxen, the drug may last as long as 4 days in your body. Depending on the condition you’re treating with naproxen, you may take a dose every 6 to 12 hours. Or you may take naproxen up to twice per day. Regardless of how often you take naproxen, you’ll likely only take it until your symptoms go away.

  1. Studies have determined the dosages that help keep an effective level of the drug in the body for the different conditions naproxen treats.
  2. Your doctor will recommend the right dosage of naproxen for your condition.
  3. After you stop taking naproxen, the drug should be fully gone from your body in about 4 days.

If you have questions about how long naproxen lasts in your body, ask your doctor or pharmacist.

How many naproxen can I drink?

Headaches – Using naproxen to relieve pain from headaches and migraine headaches is controversial. People can try taking 550 mg of naproxen sodium every 12 hours and may increase it to 825 mg if needed. The daily dose should not exceed 1,375 mg. Naproxen sodium is degraded more slowly than regular naproxen and other NSAIDs.

Can I go to bed after taking naproxen?

Do not lie down for at least 10 minutes after taking this drug. The dosage is based on your medical condition and response to treatment. To reduce your risk of stomach bleeding and other side effects, take this medication at the lowest effective dose for the shortest possible time.

Why was naproxen taken off the market?

The decision to discontinue production of Naprosyn (naproxen) suspension on a global basis was made because of the discontinuation of one of the flavouring agents. This meant extensive reformulation work, stability testing and then registering the new formulation on a worldwide basis.

How many hours does naproxen last for pain?

Typically, naproxen is taken every 8-12 hours, while ibuprofen (Advil) is taken every 4-6 hours.

Is 2 naproxen a day too much?

Dosing – The dose of this medicine will be different for different patients. Follow your doctor’s orders or the directions on the label. The following information includes only the average doses of this medicine. If your dose is different, do not change it unless your doctor tells you to do so.

For naproxen (eg, Naprosyn®) tablet and oral suspension dosage forms:

For rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis:

Adults—At first, 250 milligrams (mg) (10 milliliters (mL)/2 teaspoonfuls), 375 mg (15 mL/3 teaspoonfuls), or 500 mg (20 mL/4 teaspoonfuls) 2 times a day, in the morning and evening. Your doctor may adjust your dose as needed. However the dose is usually not more than 1500 mg per day. Children 2 years of age and older—Dose is based on body weight and must be determined by your doctor. The dose is usually 5 milligrams (mg) per kilogram (kg) of body weight 2 times a day. Children younger than 2 years of age—Use and dose must be determined by your doctor.

For acute gout:

Adults—750 milligrams (mg) for the first dose, then 250 mg every 8 hours until the attack is relieved. Children—Use and dose must be determined by your doctor.

For naproxen controlled-release tablet (eg, Naprelan®) dosage form:

For rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis:

Adults—At first, 750 milligrams (mg) (taken as one 750 mg or two 375 mg tablets) or 1000 mg (taken as two 500 mg tablets) once a day. Your doctor may adjust your dose as needed. However the dose is usually not more than 1500 mg (taken as two 750 mg or three 500 mg tablets) per day. Children—Use and dose must be determined by your doctor.

For bursitis, tendinitis, menstrual cramps, and other kinds of pain:

Adults—At first, 1000 milligrams (mg) (taken as two 500 mg tablets) once a day. Some patients may need 1500 mg (taken as two 750 mg or three 500 mg tablets) per day, for a limited period. However, the dose is usually not more than 1000 mg per day. Children—Use and dose must be determined by your doctor.

For acute gout:

Adults—1000 to 1500 milligrams (mg) (taken as two to three 500 mg tablets) once a day for the first dose, then 1000 mg (taken as two 500 mg tablets) once a day until the attack is relieved. Children—Use and dose must be determined by your doctor.

For naproxen delayed-release tablet (eg, EC-Naprosyn®) dosage form:

For rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis:

Adults—At first, 375 or 500 milligrams (mg) 2 times a day, in the morning and evening. Your doctor may adjust the dose as needed. However, the dose is usually not more than 1500 mg per day. Children—Use and dose must be determined by your doctor.

For naproxen sodium (eg, Anaprox®, Anaprox® DS) tablet dosage form:

For rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis:

Adults—At first, 275 or 550 milligrams (mg) 2 times a day, in the morning and evening. Your doctor may adjust the dose as needed. However, the dose is usually not more than 1500 mg per day. Children—Use and dose must be determined by your doctor.

For bursitis, tendinitis, menstrual cramps, and other kinds of pain:

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Adults—550 milligrams (mg) for the first dose, then 550 mg every 12 hours or 275 mg every 6 to 8 hours as needed. Your doctor may adjust the dose as needed. However, the dose is usually not more than 1375 mg per day. Children—Use and dose must be determined by your doctor.

For acute gout:

Adults—825 milligrams (mg) for the first dose, then 275 mg every 8 hours until the attack is relieved. Children—Use and dose must be determined by your doctor.

Can I drink 2 days after taking ibuprofen?

Frequently Asked Questions – 1. Can I drink alcohol after taking ibuprofen? Ibuprofen warns users, just like with any other NSAID medication telling them that taking ibuprofen and consuming an alcoholic beverage can increase your risk of gastrointestinal bleeding, which is bleeding that occurs inside of the digestive tract.

  1. The mouth, esophagus, stomach, and small intestine are all part of the upper GI tract, while the lower consists of the large intestine and the anus.
  2. A sore on the lining of the stomach is referred to as a stomach ulcer or peptic ulcer, which can be a risk increased by combining both alcohol and prescription medication.2.

How long should I wait to drink alcohol after taking medicine? If you are unsure about the details of any medication you take, it is best to speak with your healthcare provider or pharmacist. While a small amount of alcohol may be okay to consume around the same time as the medication, this can depend on factors like age and overall health.

  • Ask them when it is safe to consume alcohol again after taking ibuprofen.
  • You may need to wait up to 72 hours (3 days) after taking the medication to have a drink.3.
  • Is it safe to drink alcohol after taking ibuprofen? Generally, the two are safe to take together as long as a small number of alcoholic beverages such as a small glass of wine or a cold beer and you have a healthy liver and kidney and are a healthy person overall.

However, always consult your doctor when mixing any drug with alcohol, as doing so can often have harmful side effects and increase the risk of health problems such as kidney issues, heart attacks or strokes, and gastrointestinal bleeding. This is from the ibuprofen interacting with the alcohol increasing the usual side effects of the medication like bleeding, risk of ulcers, and increased heart rate.

Why can’t I sleep after taking naproxen?

Abstract – Previous studies have demonstrated that some nonsteroidal anti-inflammatory drugs (NSAIDs), specifically aspirin and indomethacin, have acute negative effects on sleep in humans and animals. Whether this finding can be replicated and extended to other NSAIDs, particularly the widely used over-the-counter drugs ibuprofen and acetaminophen, was the focus of the present investigation.

  • Thirty-seven male and female subjects slept in the sleep laboratory on 2 consecutive nights; sleep was polygraphically recorded on the second night.
  • Three doses of a prostaglandin-inhibiting drug (i.e., aspirin, acetaminophen, or ibuprofen) or placebo were administered, one each at 2300 h on the day prior to sleep recording, and at 0815 h and 2300 h on the day sleep was recorded.

Subjects slept from 2400-0800 h both nights. Aspirin and ibuprofen disrupted sleep in comparison to placebo by increasing the number of awakenings and percentage of time spent in stage wake, and by decreasing sleep efficiency. Ibuprofen also delayed the onset of the deeper stages of sleep.

Is naproxen hard on your system?

– Long-term use of Aleve can make your heart work harder. Aleve makes you retain water, which increases the load on your heart. This extra work can cause pressure on your cardiovascular system and can sometimes lead to a heart attack or stroke. These risks are even greater at higher dosages, even if you don’t have any heart conditions or risk of heart disease.

chest painshortness of breathslurred speechweakness in your arms or legs

These are signs of a stroke or heart attack, If you take Aleve and have unexplained weight gain or swelling, especially in your legs and feet, talk to your doctor right away. These may be signs of heart failure. To lower your risk of heart problems, use the lowest dosage for the shortest amount of time.

Is naproxen hard on the liver or kidneys?

Naproxen Induced Acute Interstitial Nephritis with Renal Cortical Necrosis Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by 1 Department of Pathology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India Find articles by Department of Nephrology, Aster Medcity Hospital, Kochii, Kerala, India 1 Department of Pathology, Aster Medcity Hospital, Kochii, Kerala, India Address for correspondence: Dr.V.

  • Narayanan Unni, Lead Senior Consultant, Nephrology, Aster Medcity Hospital, Kuttisahib Road, Near Kothad Bridge, South Chittor P.
  • O, Cheranelloor, Kochi – 682 027, Kerala, India.
  • E-mail: Received 2019 Feb 25; Revised 2019 Aug 2; Accepted 2019 Sep 9.
  • © 2020 Indian Journal of Nephrology This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

Drug induced acute interstitial nephritis is an idiosyncratic reaction following a drug exposure. The commonest drugs implicated are nonsteroidal anti-inflammatory drugs (NSAIDs), antibiotics and proton pump inhibitors. Renal cortical necrosis is a rare cause of acute kidney injury caused by severe and sustained vasoconstriction of small renal vessels.

There is a change in the epidemiology of acute kidney injury especially in developing countries where drug induced acute kidney injury is becoming increasingly common. Naproxen is known to cause renal failure by renal papillary necrosis, tubular damage and acute interstitial nephritis. We present a case of Naproxen induced acute interstitial nephritis with acute cortical necrosis.

Naproxen Review 💊 Uses, Dosage, Interactions, Warnings, Side Effects and Alcohol

To the best of our knowledge this is the first documented case of Naproxen induced renal cortical necrosis. Keywords: Renal cortical necrosis, Naproxen, NSAIDs Significant changes are observed in the epidemiology of acute kidney injury (AKI) in the past decade.

  • Sepsis and shock is the commonest cause of AKI, especially in developing countries.
  • With better health care and quality of life, now there is a change in epidemiology; more cases of drug induced renal injury are being reported.
  • Incidence of renal cortical necrosis (RCN) is 1.9-2% of all AKI, the commonest cause being obstetric complications.
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Drugs especially non-steroidal anti-inflammatory drugs (NSAID’s) are very rarely described in the literature to cause cortical necrosis. A 62-year-old gentleman, presented with fever, nausea, vomiting and bilateral flank pain for 2 days. He had bilateral pedal oedema and was breathless.

He is known to have Type 2 diabetes mellitus for 30 years, with poorly controlled blood sugars (HbA1c – 10%), bilateral non-proliferative diabetic retinopathy and sub-nephrotic range proteinuria with normal serum creatinine. He had systemic hypertension for ten years and was on Losartan (50 mg once daily) for control of blood pressure.

He had taken Naproxen 500 mg twice daily (for migraine) for one week prior to admission. He had no myalgia, icterus, skin or mucosal bleeds, rash, or arthritis. He had no dysuria, haematuria, or lower abdominal pain. No history of haemoptysis or blood in stools, chest pain or hypotensive episodes.

He did not have productive cough, sore throat, skin lesions or other focus of infections; no abdominal pain radiating to back. On examination, he was febrile, tachypneic with a blood pressure of 170/90 mmHg. He had bilateral pedal oedema and bilateral basal coarse crepitations on auscultation of chest.

Investigations revealed serum creatinine of 3.1 mg/dl, serum Sodium: 127 meq/L, serum potassium: 5.4 meq/L, metabolic acidosis (pH 7.28, HCO3 18.9, pCO2 35.7, Lactate 1.93); random blood sugar was 200 mg/dl. His haemoglobin was 10.1 g/dL, total count 19,800/Cu.

Mm with neutrophils 75%, lymphocytes 2.9%, eosinophils 14.5% and platelet count 1.8 L/cu mm. He had eosinophilic leucocytosis with absolute eosinophil count of 2800/Cu. mm (normal 20-500/Cu mm) and eosinophiluria (urine eosinophils 39%). Liver function test and Creatinine phosphokinase levels (65.6 mg/dl) were normal.

Ultrasonogram of abdomen showed mildly enlarged kidneys (right kidney 12.5 cm and left kidney 12 cm); both kidneys were hyperechoeic in echotexture with normal pelvicalyceal system. X ray chest was normal and echocardiogram did not show any vegetations.

  • Plain CT abdomen showed mildly enlarged kidneys and normal collecting system.
  • With the above clinical picture, a provisional diagnosis of acute pyelonephritis was considered and broad-spectrum parenteral antibiotics started.
  • However, there were no urinary tract symptoms, ultrasonogram of abdomen ruled out obstructive uropathy or any collection or abscess.

Meanwhile, urine microscopy showed 3 + albumin, RBC 1/hpf, and WBC 24/hpf. There were no cast or crystals; blood and urine cultures were sterile. C reactive protein was only mildly elevated (55.75 mg/dl). Stool routine and microscopy did not show any ova or cysts.

Peripheral blood smear was negative for haemoparasites, atypical cells or schistocytes. There were no features of hemolysis on blood smear. Other infective causes like Leptospirosis, Dengue fever and Malarial illness were ruled out with appropriate tests. There were no features of Raynaud’s phenomenon, livedo reticularis, rash or Hollerhorst plaque on ophthalmic fundus examination.

History was reviewed and there was no history of ingestion of any other medications (other than Naproxen and Losartan), native medicines, and poisonous substances. There was no history of animal, insect or snake bite, and no recent severe physical exertion either.

  1. There was no evidence of acute pancreatitis on blood tests or on abdominal imaging.
  2. Renal failure worsened over a period of two days and he became oligoanuric with severe uremic symptoms and worsening breathlessness.
  3. He was initiated on haemodialysis via non-tunneled internal jugular venous catheter.
  4. The patient had persistent fever spikes in spite of broad-spectrum antibiotic and his urine culture and blood cultures were sterile, with no other evidence of sepsis.

Serial blood counts showed a progressive increase in eosinophils from 18.7 to 35.7% (AEC 2880 to 6450 cells/cubic mm). In view of eosinophilia, drug induced fever was considered, and antibiotics were stopped. Renal functions did not improve over a period of ten days and a renal biopsy was done, which showed patchy cortical necrosis and dense eosinophilic infiltrate admixed with lymphoplasmacytic inflammatory infiltrates and focal interstitial edema, suggestive of acute interstitial nephritis.

  1. There was no interstitial granuloma seen.
  2. There was no endocapillary proliferation or crescents.
  3. There was no evidence of capillary thrombi suggestive of hemolytic uremic syndrome or any features of vasculitis.
  4. However, afferent and efferent arterioles showed medial hypertrophy and hyaline arteriosclerosis.

Immunofluorescence test was negative for IgG, IgA, IgM, C3, C1q, kappa, lambda light chains and fibrinogen. There were no intra-parenchymal crystals seen. Doppler of renal vessels was normal and did not show any thrombus that could embolise to kidneys.

The patient was started on oral Prednisolone (1 mg/Kg) and he was continued on dialysis. His urine output steadily increased, serum creatinine improved to 2.6 mg/dL and he was off dialysis after 6 weeks. Steroid was tapered and stopped. The incidence of AKI has been increasing recently and significant changes are observed in the past decade.

There is a change in epidemiology of AKI – the shift of etiology from infectious causes, sepsis and obstetric causes to non-infectious causes like drugs. In a study conducted in Eastern India (1996-2008), in an analysis of 2405 cases, there has been significant increase in drug induced renal failure, mostly caused by NSAIDs and Rifampicin.

  1. NSAIDs are one of the most abused drugs in the community and in a hospital setting that can cause significant renal injury.
  2. Acute interstitial nephritis (AIN) accounts for 15-27% of patients with acute kidney injury, whereas renal cortical necrosis is much rarer entity accounting for only 1.9%-2% of all patients with AKI.

Acute interstitial nephritis is caused by drugs, infections and toxins. It is more common with antibiotics, NSAIDs and proton pump inhibitors. It was classically described with Methicillin as a triad of fever, eosinophilia and skin rash which is present in less than 10% of cases.

  1. NSAID induced acute interstitial nephritis can have more prominent renal failure and proteinuria in the absence of skin rash or other systemic symptoms and can have arthralgia and microscopic haematuria.
  2. Our patient had most features of AIN – fever, eosinophilic leucocytosis, eosinophiluria, and AKI with fever responding to stopping of offending drug.
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The presence of concomitant patchy renal cortical necrosis in a case of acute interstitial nephritis due to NSAIDs is an unusual and unexpected finding. Renal cortical necrosis is caused by intense, severe and sustained vasoconstriction of small renal vessels like afferent arteriole, renal artery thrombosis causing embolic showers or endothelial damage or coagulopathy causing thrombosis that results in severe ischaemic necrosis of patches of glomeruli and tubules.

It is a rare cause of AKI (1.9%-2%). Obstetric complications were the main causes (60-70%) of RCN in developing countries. The remaining cases of RCN caused by non-obstetric causes were mostly due to sepsis and haemolytic uremic syndrome. It generally has a poor prognosis. However, with improvement in healthcare, the epidemiology is slowly changing.

The non-obstetric conditions leading to acute cortical necrosis include snake bite (sea snake, green pit viper, Russell viper) (14.2% of all cases of acute renal cortical necrosis in the study), Haemolytic Uremic Syndrome (11.5%), hyper acute kidney rejection in transplant recipients, acute gastroenteritis (4.4%), acute pancreatitis (3.5%), septicemia (2.7%) and drugs (0.9%).

Other causes of ACN include shock, extensive burns, diabetic keto-acidosis, multiple fractures, haemorrhage, other infections like Leptospirosis, Plasmodium falciparum, Meningococcal meningitis, Acquired anti protein S deficiency, post Varicella infection, SLE related and primary anti-phospholipid antibody syndrome, wasp sting, dehydration in infancy or childhood, intra-abdominal procedures, sickle cell crisis and cryoglobulinemia.

Drug-induced cortical necrosis is very rare (0.9% of acute cortical necrosis). Many toxins and drugs are implicated in causing cortical necrosis like hypophosphatemia and myoglobinuria in rhabdomyolysis (severe physical exertion), Tranexamic acid, ethanol and contrast dye.

  1. NSAID induced cortical necrosis is even rarer.
  2. In our case no other cause of acute cortical necrosis could be found except NSAIDs.
  3. NSAIDs cause both immune mediated damage and non-immune mediated damage to the kidneys.
  4. Immune mediated damage is due to immunological reaction against endogenous nephritogenic antigens or exogenous antigens processed by tubular cells with cell mediated immunity having a pathogenic role.

Mechanism of non-immune mediated damage is by various mechanisms mostly by non-selective Cyclooxygenase inhibition. NSAID is hypothesised to have caused this intense vasoconstriction by release of cytokines like Endothelin 1 and blocking prostaglandins.

Naproxen is a non-selective Cyclooxygenase inhibitor, known to cause renal failure by renal papillary necrosis, tubular damage and interstitial nephritis. To the best of our knowledge, this is the first reported case of Naproxen-induced renal cortical necrosis. The presence of renal cortical necrosis and acute interstitial nephritis due to NSAIDs in the same patient is very rare.

A high index of suspicion is essential to detect this condition early as it has prognostic implications. The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given his consent for his images and other clinical information to be reported in the journal.

  1. The patient understands that his name and initials will not be published and due efforts will be made to conceal his identity, but anonymity cannot be guaranteed.
  2. There are no conflicts of interest.1.
  3. Hoste EAJ, Kellum JA, Katz NM, Rosner MH, Haase M, Ronco C.
  4. Epidemiology of acute kidney injury.
  5. Contrib Nephrol.2010; 165 :1–8.2.

Awdishu L. Drug-induced kidney disease in the ICU: Mechanisms, susceptibility, diagnosis and management strategies. Curr Opin Crit Care.2017; 23 :484–90.3. Prakash J, Vohra R, Wani IA, Murthy AS, Srivastva PK, Tripathi K, et al. Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing countries: A single-centre experience of 22 years from Eastern India.

  • Nephrol Dial Transplantat.2007; 22 :1213–7.4.
  • Chugh KS, Jha V, Sakhuja V, Joshi K.
  • Acute renal cortical necrosis-A study of 113 patients.
  • Ren Fail.1994; 16 :37–47.5.
  • Schneider PD.
  • Nonsteroidal anti-inflammatory drugs and acute cortical necrosis.
  • Ann Intern Med.1986; 105 :303–4.6.
  • Ravnskov U.
  • Glomerular, tubular and interstitial nephritis associated with non-steroidal antiinflammatory drugs.

Evidence of a common mechanism. Br J Clin Pharmacol.1999; 47 :203–10.7. Kumar V, Nada R, Kumar S, Ramachandran R, Rathi M, Kohli HS, et al. Acute kidney injury due to acute cortical necrosis following a single wasp sting. Ren Fail.2013; 35 :170–2.8. Odabaş AR, Cetinkaya R, Selçuk Y, Kaya H, Coşkun U.

  • Tranexamic-acid-induced acute renal cortical necrosis in a patient with haemophilia.
  • A Nephrol Dial Transplant.2001; 16 :189–90.9.
  • Jung YS, Shin HS, Rim H, Jang K, Park MH, Park J-S, et al.
  • Bilateral renal cortical necrosis following binge drinking.
  • Alcohol Alcohol.2012; 47 :140–2.10.
  • Abuelo JG.
  • Abuelo JG, editor.

Vascular causes of renal failure. Renal Failure Developments in Nephrology.1995; 37 :55–6.11. Baumgartner H, Scheitlin W, von Rechenberg HK. Bilateral renal cortical necrosis following pyrazolone treatment. Dtsch Med Wochenschr.1967; 92 :1075–7.12. Segre EJ.

Can I take paracetamol 4 hours after naproxen?

Taking naproxen with other painkillers – Do not take naproxen with ibuprofen or other non-steroidal anti-inflammatory drugs ( NSAIDs ). But it’s OK to take naproxen with paracetamol or co-codamol that you buy over the counter. This should just be for short periods of time.

If you often need to take extra painkillers with naproxen or for more than a few days, talk to your doctor. Sometimes, taking different painkillers together is a good way to relieve pain, but there may be other treatments you can try. It’s OK to take other painkillers with naproxen for longer if your doctor has given them to you on prescription and told you to take them together.

If you’re unsure, talk to your doctor.

Can I take another naproxen after 5 hours?

Naproxen, depending on the strength and type, can be taken as often as every eight to 12 hours. Products marked ‘extra strength’ or ‘all-day relief’ should not be taken as often. You don’t have to adjust your doses of either drug or take them at different times if you take both drugs.

What happens if I take 4 naproxen in 24 hours?

Symptoms of naproxen sodium overdose include: Agitation, confusion, incoherence (the person is not understandable) Blurred vision. Coma.

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