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Music Player
"What A Wonderful World"
Louis Armstrong
However, this song, sampled above, had something of an uncertain beginning, as an ABC Records executive was opposed to its release. More on that later. First, some background and context.
By the mid-1960s Louis Armstrong was already a music legend, having been one of the paramount names of American jazz since the 1920s. Known for his trumpet playing, scat singing, and irrepressible smile, Armstrong by the 1960s had compiled a long list of hits, and also some movie credits. In his early years, Armstrong was best known for his virtuosity with the cornet and trumpet, with notable jazz renditions from his early years on his Hot Five and Hot Seven recordings.A sample from that earlier era can be heard below in the second selection, a famous 1928 hit entitled "West End Blues" which also includes a bit of Armstrong scat vocals.
Music Player
"West End Blues"-1928
"West End Blues" was written by King Oliver as a blues song, named for the West End of New Orleans, Louisiana, a popular picnic and entertainment area on Lake Pontchartrain. But it was Armstrong's version of the song, made a few weeks after Oliver's, that made it a landmark jazz recording.
In liner notes for the Ken Burns CD, The Definitive Louis Armstrong, jazz historian and music critic Doug Ramsey says of "West End Blues":
"Mozart, Bartok, or Stravinsky would have been grateful for the inspiration to compose the nine-bar cadenza [Armstrong] improvised to open 'West End Blues.' In every element of conception and execution, the recording was a monumental achievement. It gave notice that jazz was capable of artistry at the highest level of human expression."
In 1928, "West End Blues" also captured a feel for the times — laid back a bit, pre-Great Depression. The song was later inducted into the Grammy Hall of fame in 1974.
Armstrong was considered a jazz innovator who pushed the boundaries of the genre and his craft, later passing the baton to Lester Young, Charlie Parker and others. Among Armstrong's hit recordings are: "Stardust", "When The Saints Go Marching In," "Dream a Little Dream of Me," "Ain't Misbehavin'," "You Rascal You," and "Stompin' at the Savoy." During his long career he played and sang with some of the most important instrumentalists and vocalists of the time; among them: Bing Crosby, Duke Ellington, Billie Holiday, Fletcher Henderson, Earl Hines, Jimmie Rodgers, Bessie Smith, and perhaps most famously, Ella Fitzgerald. Armstrong recorded three albums with Fitzgerald.But by the mid-1960s, rock 'n roll and groups like the Beatles were all the rage. Old line jazz performers had become somewhat less visible. Yet Armstrong, in the midst of the rock `n roll tsunami, was having something of a renaissance.
In December 1963, at the behest of his manager, Armstrong made a demo recording of "Hello, Dolly!" to promote the stage show which opened in New York in January 1964. Kapp Records released Armstrong's demo as a commercial single and it became a surprise pop hit reaching No. 1 on the U.S. Billboard Hot 100. He was 63 when "Hello, Dolly!" topped the charts the week of May 9, 1964.
Armstrong's "Hello, Dolly," in fact, ended The Beatles' streak of three No. 1 hits in a row over 14 consecutive weeks. It also spent nine weeks atop the adult contemporary chart. "Hello Dolly" became a giant hit for Armstrong, followed by a gold-selling album of the same name.
"Hello, Dolly!" also won the Song of the Year Grammy for 1965, and Armstrong received a Grammy for Best Vocal Performance. He would later perform the song in the popular 1969 film, Hello, Dolly!, which starred Barbra Streisand."What A Wonderful World" was a song that came a few years after the success of "Hello, Dolly!" However this song had a somewhat difficult road – both in its recording and finding its audience.
The song was written by Bob Thiele and George David Weiss. Thiele was a record producer, and earlier as head of Impulse Records, he had issued recordings for jazz artists such as John Coltrane, Charles Mingus, Dizzy Gillespie, and others. Weiss was a songwriter who wrote or co-wrote many songs, including the hit version of "The Lion Sleeps Tonight." Initially, Thiele and Weiss had pitched "What A Wonderful World" to Tony Bennett, who turned them down.
Then in the summer of 1967, another producer, Artie Butler, suggested the song might be offered to Louis Armstrong, who was then working on material for a prospective album. Armstrong agreed to do the song and in mid-August 1967, Thiele, Weiss and Butler traveled to Las Vegas where they would meet Armstrong for a late-night recording session.
Raucous Session
Armstrong was then appearing in performance at the Tropicana Hotel. After one of his midnight shows, a recording session was arranged at Bill Porter's United Studios in Las Vegas. Armstrong, Theile, Weiss and Butler all met there along with a group of studio engineers and musicians. By the time they began recording it was around 2 a.m.
However, another person, ABC Records President Larry Newton, had also come to Las Vegas to meet with Armstrong, who had just signed with ABC Records. Newton had come to Las Vegas to have some publicity photos taken of his new star. Newton had high hopes for Armstrong's music, as "Hello, Dolly!" had stormed the pop charts two years earlier, and Newton expected more of the same.
But Newton was not very excited about the slow-tempo ballad that was "What A Wonderful World." Newton was opposed to Armstrong doing the song. In fact, he came to the late night recording session and tried to stop it – to the point where he had to be locked out of the studio while the session proceeded.
Recordings in those days were done "live" – with vocalist, band or orchestra, and any background vocals all recorded at the same time. A recording session could run through dozens of takes to get everything just right. Overdubbing was still rare then. That night in Las Vegas, however, proved to be very challenging as the session was interrupted twice by the sounds of a coming and going Union Pacific freight train near the studio, blowing its horn. And fuming ABC exec Larry Newton was still locked outside the studio, but making his presence known. The session could have gone bad at the point, given all the interruptions and tension with Newton. But according to one account, Armstrong himself lightened the load, by shaking his head at one point and laughing at the craziness involved, with others joining in. The work then proceeded with renewed determination.
Despite the interruptions, Armstrong and group eventually got the song they wanted, finishing their work around 6 a.m. Since the session had run longer than planned the musicians were due extra pay, and Armstrong only accepted the basic scale of $250 to make sure the orchestra members were paid.
Artie Butler, the arranger and composer who was also at the session, is shown in the two photos here at work with Armstrong that night. Butler, at the invitation of Theile, wrote the arrangement for "A Wonderful World." Butler recalls that at the end of the late night session, "we were all starving so we went for breakfast," during which they exchanged stories about their music and life experiences, and also shared a few jokes. Butler adds of that evening and the breakfast session:
…At the end of our breakfast, Louis grabbed me by my shoulders and pulled me over and kissed me on the head and said "Artie its been a real pleasure working with you and a gas laughing with you. Let's do more."
I will never ever forget the few hours I got to spend with Louis Armstrong. Every time I hear "What A Wonderful World" on the radio or TV it truly brings a warm feeling all over me as I reflect back to that special recording session and breakfast. These photos were taken at the recording session in Las Vegas … sometime between freight trains.
Song Held Back
Meanwhile, ABC's Larry Newton – the guy who was locked out of the studio – would have his revenge apparently. The tapes for the recording of "What A Wonderful World" languished at ABC Records in New York for months, only being released in the U.K. in early 1968 to ABC Records' partner there, EMI. "What A Wonderful World" came out there on one of EMI's record labels named "His Masters Voice" (HMV), as shown in the photo at left.
The song first charted in the U.K. in February 1968 at No. 45, rising to No. 1 by April, staying there for four weeks. In fact, "What A Wonderful World" became the top-selling UK single in 1968. Back in the states, ABC's Larry Newton refused to promote the song, and it reportedly sold only 1,000 copies.
But 1968 in the U.S. was turning out to be a very tumultuous year, with racial and political havoc added to the Vietnam War. It was also a presidential election year. Martin Luther King, Jr. and Robert Kennedy were both assassinated that spring and summer, and there was growing civil and racial unrest with urban riots and Viet Nam War protests.Some thought Armstrong's song could be a positive antidote for the troubled world of 1968. In the midst of all this, songwriters Thiele and Weiss saw Armstrong as "the perfect ambassador to restore race relations" during America's tumultuous summer. Yet since the 1950s, Armstrong had been charged by some as being an "Uncle Tom," catering to white America with his music. But Armstrong's appeal at the time extended to all races, and the hope was that a 66-year-old singing a tune of goodwill on the airwaves might make a difference. Armstrong also felt the song needed to be heard in the country to promote a sense of hope and optimism. He loved the song and performed it everywhere, including numerous television appearances, and its popularity began to grow. At one performance, he reportedly introduced the song with this explanation:
"Some of you young folks been saying to me: 'Hey, Pops – what do you mean, what a wonderful world? How about all them wars all over the place, you call them wonderful?' …But how about listening to old Pops for a minute? Seems to me it ain't the world that's so bad but what we're doing to it, and all I'm saying is: see what a wonderful world it would be if only we'd give it a chance. Love, baby, love. That's the secret…"
In October 1968, EMI forced ABC to release a U.S. album with the recording, but like the original single, it was never promoted for radio or retail, and did not do well. After Armstrong passed away in July 1971, dying of heart failure at the age of 69, the record was re-released and enjoyed modest success. But it wasn't until 1988, more than 20 years after its first recording, that the song found a bigger audience and grew in stature.
"Good Morning, Vietnam"
In Hollywood, director Barry Levinson was then working on Good Morning, Vietnam, a film that would star Robin Williams as Airman Second Class Adrian Cronauer, a military disc jockey who comes to work for the Armed Forces Radio Service in Saigon during the war. Levinson needed a song to use as a musical backdrop for a montage of Vietnam War images. He considered dozens of songs, but when he heard Armstrong's version of "What A Wonderful World," he found it to be the perfect choice for the counterpoint he had in mind. The poignant lyrics and Armstrong's gravelly voice stood in stark contrast to the images of war Levinson would screen, a paradox of sight and sound – not exactly the imagery Thiele, Weiss, and Armstrong had in mind at the song's creation. Still, the music made its political points in the film, but the song also struck an emotional chord with audiences.
As a result of this exposure, Armstrong's 20 year-old recording of "What A Wonderful World" was re-released as a single, hitting No. 32 on the Billboard chart in February 1988. In Australia, the single charted at No. 1 for a brief period in late June 1988.Since then, the song has also found its way into other film and television uses. In 1989, Armstrong's version of "What a Wonderful World" was used as a theme song for the opening credits of the first five episodes of the ABC-TV show Family Matters. And according to Thiele and Weiss credits listed at the Internet Movie Database, the song has also been used variously in at least 50 other TV shows and films.
In 1999, Armstrong's recording of "What A Wonderful World" was inducted in the Grammy Hall of Fame. In December 2011, a BBC promotion celebrating its many years of Natural History on BBC with David Attenborough, offered a collage of footage from Attenborough's shows as his spoken-word recording of "What a Wonderful World" ran behind it.
Fan Favorite
To this day, Armstrong's version of "What A Wonderful World" remains a popular fan favorite. Although regarded by some critics as overly sentimental, an internet query using the song's title plus "my favorite song" on any of the search engines will usually yield postings from folks who have kind things to say about the song. Family historians crafting slide shows and video remembrances use the song in their home-made soundtracks. It's also popular at weddings, especially for the father-daughter dance. And it is valued generally for its upbeat and optimistic outlook. In 2012, Neil McCormick, chief rock music critic at The Telegraph in London, writing about the song in a piece entitled "What Is the Happiest Song of All Time?," had this say:
"…My vote, although it seems almost too obvious, would go to 'What A Wonderful World,' performed by Louis Armstrong. It's got a beautiful rolling melody, and simple, life-affirming lyrics, but what makes it so powerful is Armstrong's vocal, which is not smug or avuncular, his voice is so old and cracked that it contains a sense of loss within it, the bittersweet tinge of a man looking back, who has already lived a long life and is acutely aware of how precious it is. So, curiously, it seems to me there is an almost invisible shadow of melancholia in the song that actually magnifies its happiness. You can put that song on in any context, and people stop and smile."
What A Wonderful World
I see trees of green, red roses too
I see skies of blue, and clouds of white
The colors of the rainbow, so pretty in the sky
I hear babies cry, I watch them grow
Yes I think to myself, what a wonderful world.
Armstrong himself stated in the late 1960s that he recalled "three generations" of children he watched growing up in his own Corona/Queens, NY neighborhood where he lived with his wife Lucille for 28 years — part of his own "life reservoir" that he brought to the song.
Add to that the "slings and arrows" suffered by a black man in America over decades during segregation and the civil rights struggle, and Armstrong's singing of this song takes on even more depth.
Of course, every listener brings their own life experience to the song. Yet it is Armstrong's rendition that provides the powerful starting point. And given the song's simple yet enduring sentiments, it is likely one that will live for the ages.
Throughout his career, and after his passing, Louis Armstrong was recognized for his musical contributions. In 1972, he was posthumously awarded the Grammy Lifetime Achievement Award by the Academy of Recording Arts and Sciences – issued to performers who have made creative contributions of outstanding artistic significance to the field of recording. In 2002, his Hot Five and Hot Seven recordings from 1925–1928 were selected for the National Recording Registry at the Library of Congress.At least ten of Armstrong's recordings – some performed with other artists such as Bessie Smith, Earl Hines and Ella Fitzgerald – have been inducted into the Grammy Hall of Fame. This class of Grammys, established in 1973, honors recordings that are at least twenty-five years old and have "qualitative or historical significance." In 2001, at the centennial of his birth, New Orleans renamed its airport in his honor, the Louis Armstrong International Airport.
For additional stories on the history of music and its impact on culture, see the "Annals of Music" page, or visit the Home page for other choices. Thanks for visiting — and if you like what you find here, please make a donation to help support the research and writing at this website. Thank you. – Jack Doyle
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Date Posted: 7 November 2012
Last Update: 26 January 2020
Comments to: firstname.lastname@example.com
Article Citation:
Jack Doyle, "What A Wonderful World – Louis Armstrong:
1967-1968," PopHistoryDig.com, November 7, 2012.
Sources, Links & Additional Information
"Louis Armstrong's Music Has Been Shaping History for Almost 30 Years," New York Times, January 29, 1950.
John S. Wilson, "Home Town Hails Armstrong; 5,000 at Jazz Fete in New Orleans Cheer Trumpeter," New York Times, Monday, May 20, 1968.
John S. Wilson, "Louis Armstrong Takes to Horn In His Comeback at the Waldorf," New York Times, Sunday, March 7, 1971.
Albin Krebs, "Louis Armstrong, Jazz Trumpeter and Singer, Dies in His Home at 71," New York Times, July 7, 1971, p. 1.
"Music: Last Trumpet for the First Trumpeter," Time, Monday, July 19, 1971.
Myrna Oliver, "Bob Thiele; Record Label Owner, Producer of Top Jazz Musicians," Los Angeles Times, February 2, 1996.
Doug Ramsey, Liner Notes, The Definitive Louis Armstrong (CD Booklet), May 2000.
"Hello, Dolly! (song)," Wikipedia.org.
Cecil Van Houten, "What A Wonderful World," Family Life, September 22, 2011.
"What A Wonderful World," ArtieButler. com.
"What a Wonderful World," Wikipedia.org.
"Smashed Hits: How Political is What A Wonderful World?, BBC News Magazine, December 10, 2011.
Neil McCormick, "What Is the Happiest Song of All Time?, The Telegraph, February 1, 2012.
"Louis Armstrong," Wikiquote.org.
"David Attenborough-Wonderful World – BBC," YouTube.com.
"What a Wonderful World – Louis Arm- strong," YouTube.com, sanny6667, Dec. 23, 2010.
John Burnett, "West End Blues," National Public Radio, NPR.org, August 6, 2000.
"Louis Armstrong, Artist Page," National Public Radio, NPR.org.
"Louis Armstrong: Biography- Jazz: A Film By Ken Burns," PBS.org.
"Louis Armstrong," Wikipedia.org.
William Ruhlmann, "Louis Armstrong, Biog- raphy," AllMusic.com.
Terry Teachout, Pops: A Life of Louis Armstrong (hardcover), Boston/New York: Houghton Mifflin Harcourt, 2009, 496pp.
K. Smith, "What a Wonderful World: The Drummer's Difference," BroadStreetReview. com, September 25, 2011.
Cornell Thomas, "What a Wonderful World…," PowerofPositivity.net, January 14, 2012.
"Louis Armstrong: What A Wonderful World/Cabaret," ChartArchive.org.
Carla A. Fellers, "What a Wonderful World: The Rhetoric of the Official and Unoffical in Good Morning Vietnam,"War, Literature & The Arts, pp.232-242.


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Shop Manitoba Made YEAR ROUND at our shop at St. Vital Centre, Winnipeg, MB. (Down the hall from The Bay)
The size of this sign is approx 12" x 15"
**IMPORTANT** Each Barn Wood sign is created from authentic, reclaimed wood. Letters are laser cut from wood and attached to create a 3 Dimensional effect. Due to the nature of this reclaimed wood, every sign is unique and special in it's own way. Your sign may not look exactly like shown. Whenever possible, the sign is key holed on the back for easy hanging on a nail or hook

subset: commoncrawl


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text:
Stella and Chewy's Freeze Dried Raw Dinner Patties - Tantalizing Turkey
VENDOR: Stella and Chewy
95% turkey, nutrient-rich organs & bone
Pea-Free, Lentil-Free, and Potato-Free
Organic fruits & vegetables
Taurine Added
Fortified with added vitamins & minerals
Enhanced with probiotics & antioxidants
100% complete & balanced dinner
- No added hormones or antibiotics
- No grains or fillers
- No gluten
- No artificial preservatives or colorings
Turkey with ground bone, turkey liver, turkey gizzard, pumpkin seed, organic cranberries, organic spinach, organic broccoli, organic beets, organic carrots, organic squash, organic blueberries, fenugreek seed, potassium chloride, dried kelp, sodium phosphate, tocopherols (preservative), choline chloride, dried Pediococcus acidilactici fermentation product, dried Lactobacillus acidophilus fermentation product, dried Bifidobacterium longum fermentation product, dried Bacillus coagulans fermentation product zinc proteinate, iron proteinate, taurine, calcium carbonate, vitamin E supplement, thiamine mononitrate, copper proteinate, manganese proteinate, sodium selenite, niacin supplement, d-calcium pantothenate, riboflavin supplement, vitamin A supplement, vitamin D3 supplement, vitamin B12 supplement, pyridoxine hydrochloride, folic acid.
Guaranteed Analysis:
- Crude Protein (min.)
- 40.0%
- Crude Fat (min.)
- 36.0%
- Crude Fiber (max.)
- 5.0%
- Moisture (max.)
- 5.0%
- Rehydrated Analysis
- Crude Protein (min.)
- 15.0%
- Crude Fat (min.)
- 12.0%
- Crude Fiber (max.)
- 2.0%
- Moisture (max.)
- 70.0%
- Calorie Content
(metabolizable energy, calculated):
- 58 kcal/patty
5100 kcal/kg


text:
Sunglasses for children - 5-10 years - 100% UV protection, category 3 - Unisex, universal model - Storage pouch included in the box - The tortoise pattern is unique for each pair
D JUNIOR SUN - Sunglasses for children Tortoise
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This model complies with the international standards for sunglasses (ISO 12312-1).


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text:
LEVOXYL - levothyroxine sodium tablet
Physicians Total Care, Inc.
–LEVOXYL® (levothyroxine sodium tablets, USP) contain synthetic crystalline L-3,3',5,5'-tetraiodothyronine sodium salt [levothyroxine (T4) sodium]. Synthetic T4 is identical to that produced in the human thyroid gland. Levothyroxine (T4) sodium has an empirical formula of C15H10I4N NaO4 • H2O, molecular weight of 798.86 g/mol (anhydrous), and structural formula as shown:
Microcrystalline cellulose, croscarmellose sodium, magnesium stearate, calcium sulfate dihydrate and sodium bicarbonate. The following are the coloring additives per tablet strength:
|Strength (mcg)
|Color additive(s)
|FD&C Yellow No. 6 Aluminum Lake
|FD&C Blue No. 1 Aluminum Lake, D&C Red No. 30 Aluminum Lake
|FD&C Yellow No. 6 Aluminum Lake, FD&C Blue No. 1 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake
|FD&C Yellow No. 6 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake
|FD&C Yellow No. 6 Aluminum Lake, FD&C Red No. 40 Aluminum Lake, D&C Red No. 30 Aluminum Lake
|FD&C Red No. 40 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake
|FD&C Blue No. 1 Aluminum Lake
|FD&C Blue No. 1 Aluminum Lake, D&C Red No. 30 Aluminum Lake
|FD&C Blue No. 1 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake
|D&C Red No. 30 Aluminum Lake, D&C Yellow No. 10 Aluminum Lake
Thyroid hormone synthesis and secretion is regulated by the hypothalamic-pituitary-thyroid axis. Thyrotropin-releasing hormone (TRH) released from the hypothalamus stimulates secretion of thyroid-stimulating hormone, TSH, from the anterior pituitary. TSH, in turn, is the physiologic stimulus for the synthesis and secretion of thyroid hormones, L-thyroxine (T4) and L-triiodothyronine (T3), by the thyroid gland. Circulating serum T3 and T4 levels exert a feedback effect on both TRH and TSH secretion. When serum T3 and T4 levels increase, TRH and TSH secretion decrease. When thyroid hormone levels decrease, TRH and TSH secretion increase.
The mechanisms by which thyroid hormones exert their physiologic actions are not completely understood, but it is thought that their principal effects are exerted through control of DNA transcription and protein synthesis. T3 and T4 diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins.
Thyroid hormones regulate multiple metabolic processes and play an essential role in normal growth and development, and normal maturation of the central nervous system and bone. The metabolic actions of thyroid hormones include augmentation of cellular respiration and thermogenesis, as well as metabolism of proteins, carbohydrates and lipids. The protein anabolic effects of thyroid hormones are essential to normal growth and development.
The physiologic actions of thyroid hormones are produced predominately by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues.
Levothyroxine, at doses individualized according to patient response, is effective as replacement or supplemental therapy in hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis.
Levothyroxine is also effective in the suppression of pituitary TSH secretion in the treatment or prevention of various types of euthyroid goiters, including thyroid nodules, Hashimoto's thyroiditis, multinodular goiter and, as adjunctive therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer (see INDICATIONS AND USAGE , PRECAUTIONS , DOSAGE AND ADMINISTRATION ).
Absorption of orally administered T4 from the gastrointestinal (GI) tract ranges from 40% to 80%. The majority of the levothyroxine dose is absorbed from the jejunum and upper ileum. The relative bioavailability of LEVOXYL tablets, compared to an equal nominal dose of oral levothyroxine sodium solution, is approximately 98%. T4 absorption is increased by fasting, and decreased in malabsorption syndromes and by certain foods such as soybean infant formula. Dietary fiber decreases bioavailability of T4. Absorption may also decrease with age. In addition, many drugs and foods affect T4 absorption (see PRECAUTIONS , Drug Interactions and Drug-Food Interactions ).
Circulating thyroid hormones are greater than 99% bound to plasma proteins, including thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA), and albumin (TBA), whose capacities and affinities vary for each hormone. The higher affinity of both TBG and TBPA for T4 partially explains the higher serum levels, slower metabolic clearance, and longer half-life of T4 compared to T3. Protein-bound thyroid hormones exist in reverse equilibrium with small amounts of free hormone. Only unbound hormone is metabolically active. Many drugs and physiologic conditions affect the binding of thyroid hormones to serum proteins (see PRECAUTIONS ,Drug Interactions and Drug-Laboratory Test Interactions). Thyroid hormones do not readily cross the placental barrier (see PRECAUTIONS , Pregnancy).
T4 is slowly eliminated (see TABLE 1). The major pathway of thyroid hormone metabolism is through sequential deiodination. Approximately eighty-percent of circulating T3 is derived from peripheral T4 by monodeiodination. The liver is the major site of degradation for both T4 and T3, with T4 deiodination also occurring at a number of additional sites, including the kidney and other tissues. Approximately 80% of the daily dose of T4 is deiodinated to yield equal amounts of T3 and reverse T3 (rT3). T3 and rT3 are further deiodinated to diiodothyronine. Thyroid hormones are also metabolized via conjugation with glucuronides and sulfates and excreted directly into the bile and gut where they undergo enterohepatic recirculation.
Thyroid hormones are primarily eliminated by the kidneys. A portion of the conjugated hormone reaches the colon unchanged and is eliminated in the feces. Approximately 20% of T4 is eliminated in the stool. Urinary excretion of T4 decreases with age.
|Ratio in Thyroglobulin
|Biologic Potency
|Protein Binding (%)*
|Levothyroxine (T4)
|Liothyronine (T3)
|≤ 2
Levothyroxine sodium is used for the following indications:
As replacement or supplemental therapy in congenital or acquired hypothyroidism of any etiology, except transient hypothyroidism during the recovery phase of subacute thyroiditis. Specific indications include: primary (thyroidal), secondary (pituitary), and tertiary (hypothalamic) hypothyroidism and subclinical hypothyroidism. Primary hypothyroidism may result from functional deficiency, primary atrophy, partial or total congenital absence of the thyroid gland, or from the effects of surgery, radiation, or drugs, with or without the presence of goiter.
In the treatment or prevention of various types of euthyroid goiters (see WARNINGS and PRECAUTIONS ), including thyroid nodules (see WARNINGS and PRECAUTIONS ), subacute or chronic lymphocytic thyroiditis (Hashimoto's thyroiditis), multinodular goiter (see WARNINGS and PRECAUTIONS ) and, as an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer.
Levothyroxine is contraindicated in patients with untreated subclinical (suppressed serum TSH level with normal T3 and T4 levels) or overt thyrotoxicosis of any etiology and in patients with acute myocardial infarction. Levothyroxine is contraindicated in patients with uncorrected adrenal insufficiency since thyroid hormones may precipitate an acute adrenal crisis by increasing the metabolic clearance of glucocorticoids (see PRECAUTIONS ). LEVOXYL is contraindicated in patients with hypersensitivity to any of the inactive ingredients in LEVOXYL tablets (see DESCRIPTION , Inactive Ingredients ).
Thyroid hormones, including LEVOXYL, either alone or with other therapeutic agents, should not be used for the treatment of obesity or for weight loss. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects.
Levothyroxine sodium should not be used in the treatment of male or female infertility unless this condition is associated with hypothyroidism.
In patients with nontoxic diffuse goiter or nodular thyroid disease, particularly the elderly or those with underlying cardiovascular disease, levothyroxine sodium therapy is contraindicated if the serum TSH level is already suppressed due to the risk of precipitating overt thyrotoxicosis (see CONTRAINDICATIONS ). If the serum TSH level is not suppressed, LEVOXYL should be used with caution in conjunction with careful monitoring of thyroid function for evidence of hyperthyroidism and clinical monitoring for potential associated adverse cardiovascular signs and symptoms of hyperthyroidism.
Levothyroxine has a narrow therapeutic index. Regardless of the indication for use, careful dosage titration is necessary to avoid the consequences of over- or under-treatment. These consequences include, among others, effects on growth and development, cardiovascular function, bone metabolism, reproductive function, cognitive function, emotional state, gastrointestinal function, and on glucose and lipid metabolism. Many drugs interact with levothyroxine sodium necessitating adjustments in dosing to maintain therapeutic response (see Drug Interactions ).
In women, long-term levothyroxine sodium therapy has been associated with decreased bone mineral density, especially in postmenopausal women on greater than replacement doses or in women who are receiving suppressive doses of levothyroxine sodium. Therefore, it is recommended that patients receiving levothyroxine sodium be given the minimum dose necessary to achieve the desired clinical and biochemical response.
Exercise caution when administering levothyroxine to patients with cardiovascular disorders and to the elderly in whom there is an increased risk of occult cardiac disease. In these patients, levothyroxine therapy should be initiated at lower doses than those recommended in younger individuals or in patients without cardiac disease (see WARNINGS ; PRECAUTIONS , Geriatric Use ; and DOSAGE AND ADMINISTRATION ). If cardiac symptoms develop or worsen, the levothyroxine dose should be reduced or withheld for one week and then cautiously restarted at a lower dose. Overtreatment with levothyroxine sodium may have adverse cardiovascular effects such as an increase in heart rate, cardiac wall thickness, and cardiac contractility and may precipitate angina or arrhythmias. Patients with coronary artery disease who are receiving levothyroxine therapy should be monitored closely during surgical procedures, since the possibility of precipitating cardiac arrhythmias may be greater in those treated with levothyroxine. Concomitant administration of levothyroxine and sympathomimetic agents to patients with coronary artery disease may precipitate coronary insufficiency.
Exercise caution when administering levothyroxine to patients with nontoxic diffuse goiter or nodular thyroid disease in order to prevent precipitation of thyrotoxicosis (see WARNINGS ). If the serum TSH is already suppressed, levothyroxine sodium should not be administered (see CONTRAINDICATIONS ).
In patients with secondary or tertiary hypothyroidism, additional hypothalamic/pituitary hormone deficiencies should be considered, and, if diagnosed, treated (see PRECAUTIONS ,Autoimmune polyglandular syndrome ) for adrenal insufficiency.
Occasionally, chronic autoimmune thyroiditis may occur in association with other autoimmune disorders such as adrenal insufficiency, pernicious anemia, and insulin-dependent diabetes mellitus. Patients with concomitant adrenal insufficiency should be treated with replacement glucocorticoids prior to initiation of treatment with levothyroxine sodium. Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated, due to increased metabolic clearance of glucocorticoids by thyroid hormone. Patients with diabetes mellitus may require upward adjustments of their antidiabetic therapeutic regimens when treated with levothyroxine (see PRECAUTIONS , Drug Interactions ).
Infants with congenital hypothyroidism appear to be at increased risk for other congenital anomalies, with cardiovascular anomalies (pulmonary stenosis, atrial septal defect, and ventricular septal defect,) being the most common association.
Patients should be informed of the following information to aid in the safe and effective use of LEVOXYL:
The diagnosis of hypothyroidism is confirmed by measuring TSH levels using a sensitive assay (second generation assay sensitivity ≤0.1 mIU/L or third generation assay sensitivity ≤0.01 mIU/L) and measurement of free-T4.
The adequacy of therapy is determined by periodic assessment of appropriate laboratory tests and clinical evaluation. The choice of laboratory tests depends on various factors including the etiology of the underlying thyroid disease, the presence of concomitant medical conditions, including pregnancy, and the use of concomitant medications (see PRECAUTIONS , Drug Interactions and Drug-Laboratory Test Interactions). Persistent clinical and laboratory evidence of hypothyroidism despite an apparent adequate replacement dose of LEVOXYL may be evidence of inadequate absorption, poor compliance, drug interactions, or decreased T4 potency of the drug product.
In adult patients with primary (thyroidal) hypothyroidism, serum TSH levels (using a sensitive assay) alone may be used to monitor therapy. The frequency of TSH monitoring during levothyroxine dose titration depends on the clinical situation but it is generally recommended at 6—8 week intervals until normalization. For patients who have recently initiated levothyroxine therapy and whose serum TSH has normalized or in patients who have had their dosage or brand of levothyroxine changed, the serum TSH concentration should be measured after 8—12 weeks. When the optimum replacement dose has been attained, clinical (physical examination) and biochemical monitoring may be performed every 6—12 months, depending on the clinical situation, and whenever there is a change in the patient's status. It is recommended that a physical examination and a serum TSH measurement be performed at least annually in patients receiving LEVOXYL (see WARNINGS , PRECAUTIONS , and DOSAGE AND ADMINISTRATION ).
In patients with congenital hypothyroidism, the adequacy of replacement therapy should be assessed by measuring both serum TSH (using a sensitive assay) and total- or free- T4. During the first three years of life, the serum total- or free- T4 should be maintained at all times in the upper half of the normal range. While the aim of therapy is to also normalize the serum TSH level, this is not always possible in a small percentage of patients, particularly in the first few months of therapy. TSH may not normalize due to a resetting of the pituitary-thyroid feedback threshold as a result of in utero hypothyroidism. Failure of the serum T4 to increase into the upper half of the normal range within 2 weeks of initiation of LEVOXYL therapy and/or of the serum TSH to decrease below 20 mU/L within 4 weeks should alert the physician to the possibility that the child is not receiving adequate therapy. Careful inquiry should then be made regarding compliance, dose of medication administered, and method of administration prior to raising the dose of LEVOXYL.
The recommended frequency of monitoring of TSH and total or free T4 in children is as follows: at 2 and 4 weeks after the initiation of treatment; every 1—2 months during the first year of life; every 2—3 months between 1 and 3 years of age; and every 3 to 12 months thereafter until growth is completed. More frequent intervals of monitoring may be necessary if poor compliance is suspected or abnormal values are obtained. It is recommended that TSH and T4 levels, and a physical examination, if indicated, be performed 2 weeks after any change in LEVOXYL dosage. Routine clinical examination, including assessment of mental and physical growth and development, and bone maturation, should be performed at regular intervals (see PRECAUTIONS , Pediatric Use and DOSAGE AND ADMINISTRATION ).
Many drugs affect thyroid hormone pharmacokinetics and metabolism (e.g., absorption, synthesis, secretion, catabolism, protein binding, and target tissue response) and may alter the therapeutic response to LEVOXYL. In addition, thyroid hormones and thyroid status have varied effects on the pharmacokinetics and action of other drugs. A listing of drug-thyroidal axis interactions is contained in Table 2.
The list of drug-thyroidal axis interactions in Table 2 may not be comprehensive due to the introduction of new drugs that interact with the thyroidal axis or the discovery of previously unknown interactions. The prescriber should be aware of this fact and should consult appropriate reference sources. (e.g., package inserts of newly approved drugs, medical literature) for additional information if a drug-drug interaction with levothyroxine is suspected.
|Drug or Drug Class
|Drugs that may reduce TSH secretion -the reduction is not sustained; therefore, hypothyroidism does not occur
|Dopamine / Dopamine
Agonists Glucocorticoids
|Use of these agents may result in a transient reduction in TSH secretion when administered at the following doses: Dopamine (≥1 mcg/kg/min); Glucocorticoids (hydrocortisone ≥100 mg/day or equivalent); Octreotide (>100 mcg/day).
|Drugs that alter thyroid hormone secretion
|Drugs that may decrease thyroid hormone secretion, which may result in hypothyroidism
Iodide (including iodine-containing Radiographic contrast agents)
Propylthiouracil (PTU)
|Long-term lithium therapy can result in goiter in up to 50% of patients, and either subclinical or overt hypothyroidism, each in up to 20% of patients. The fetus, neonate, elderly and euthyroid patients with underlying thyroid disease (e.g., Hashimoto's thyroiditis or with Grave's disease previously treated with radioiodine or surgery) are among those individuals who are particularly susceptible to iodine-induced hypothyroidism. Oral cholecystographic agents and amiodarone are slowly excreted, producing more prolonged hypothyroidism than parenterally administered iodinated contrast agents. Long-term aminoglutethimide therapy may minimally decrease T4 and T3 levels and increase TSH, although all values remain within normal limits in most patients.
|Drugs that may increase thyroid hormone secretion, which may result in hyperthyroidism
Iodide (including iodine-containing Radiographic contrast agents)
|Iodide and drugs that contain pharmacologic amounts of iodide may cause hyperthyroidism in euthyroid patients with Grave's disease previously treated with antithyroid drugs or in euthyroid patients with thyroid autonomy (e.g., multinodular goiter or hyperfunctioning thyroid adenoma). Hyperthyroidism may develop over several weeks and may persist for several months after therapy discontinuation. Amiodarone may induce hyperthyroidism by causing thyroiditis.
|Drugs that may decrease T4 absorption, which may result in hypothyroidism
- Aluminum & Magnesium Hydroxides
- Simethicone
Bile Acid Sequestrants
- Cholestyramine
- Colestipol
Calcium Carbonate
Cation Exchange Resins
- Kayexalate
Ferrous Sulfate
|Concurrent use may reduce the efficacy of levothyroxine by binding and delaying or preventing absorption, potentially resulting in hypothyroidism. Calcium carbonate may form an insoluble chelate with levothyroxine, and ferrous sulfate likely forms a ferric-thyroxine complex. Administer levothyroxine at least 4 hours apart from these agents. Patients treated concomitantly with orlistat and levothyroxine should be monitored for changes in thyroid function.
|Drugs that may alter T4 and T3 serum transport — but FT4 concentration remains normal; and, therefore, the patient remains euthyroid
|Drugs that may increase serum TBG concentration
|Drugs that may decrease serum TBG concentration
Estrogen-containing oral contraceptives
Estrogens (oral)
Heroin / Methadone
|Androgens / Anabolic Steroids
Slow-Release Nicotinic Acid
|Drugs that may cause protein-binding site displacement
|Furosemide ( > 80 mg IV)
Non Steroidal Anti-Inflammatory Drugs
- Fenamates
- Phenylbutazone
Salicylates ( > 2 g/day)
|Administration of these agents with levothyroxine results in an initial transient increase in FT4. Continued administration results in a decrease in serum T4 and normal FT4 and TSH concentrations and, therefore, patients are clinically euthyroid. Salicylates inhibit binding of T4 and T3 to TBG and transthyretin. An initial increase in serum FT4 is followed by return of FT4 to normal levels with sustained therapeutic serum salicylate concentrations, although total-T4 levels may decrease by as much as 30%.
|Drugs that may alter T4 and T3 metabolism
|Drugs that may increase hepatic metabolism, which may result in hypothyroidism
|Stimulation of hepatic microsomal drug-metabolizing enzyme activity may cause increased hepatic degradation of levothyroxine, resulting in increased levothyroxine requirements. Phenytoin and carbamazepine reduce serum protein binding of levothyroxine, and total- and free-T4 may be reduced by 20% to 40%, but most patients have normal serum TSH levels and are clinically euthyroid.
|Drugs that may decrease T4 5'-deiodinase activity
Beta-adrenergic antagonists
- (e.g., Propranolol > 160 mg/day)
- (e.g., Dexamethasone > 4 mg/day)
Propylthiouracil (PTU)
|Administration of these enzyme inhibitors decreases the peripheral conversion of T4 to T3, leading to decreased T3 levels. However, serum T4 levels are usually normal but may occasionally be slightly increased. In patients treated with large doses of propranolol (>160 mg/day), T3 and T4 levels change slightly, TSH levels remain normal, and patients are clinically euthyroid. It should be noted that actions of particular beta-adrenergic antagonists may be impaired when the hypothyroid patient is converted to the euthyroid state. Short-term administration of large doses of glucocorticoids may decrease serum T3 concentrations by 30% with minimal change in serum T4 levels. However, long-term glucocorticoid therapy may result in slightly decreased T3 and T4 levels due to decreased TBG production (see above).
|Anticoagulants (oral)
- Coumarin Derivatives
- Indandione Derivatives
|Thyroid hormones appear to increase the catabolism of vitamin K-dependent clotting factors, thereby increasing the anticoagulant activity of oral anticoagulants. Concomitant use of these agents impairs the compensatory increases in clotting factor synthesis. Prothrombin time should be carefully monitored in patients taking levothyroxine and oral anticoagulants and the dose of anticoagulant therapy adjusted accordingly.
- Tricyclics (e.g., Amitriptyline)
- Tetracyclics (e.g., Maprotiline)
- Selective Serotonin Reuptake Inhibitors (SSRIs; e.g., Sertraline)
|Concurrent use of tri/tetracyclic antidepressants and levothyroxine may increase the therapeutic and toxic effects of both drugs, possibly due to increased receptor sensitivity to catecholamines. Toxic effects may include increased risk of cardiac arrhythmias and CNS stimulation; onset of action of tricyclics may be accelerated. Administration of sertraline in patients stabilized on levothyroxine may result in increased levothyroxine requirements.
|Antidiabetic Agents
- Biguanides
- Meglitinides
- Sulfonylureas
- Thiazolidediones
- Insulin
|Addition of levothyroxine to antidiabetic or insulin therapy may result in increased antidiabetic agent or insulin requirements. Careful monitoring of diabetic control is recommended, especially when thyroid therapy is started, changed, or discontinued.
|Cardiac Glycosides
|Serum digitalis glycoside levels may be reduced in hyperthyroidism or when the hypothyroid patient is converted to the euthyroid state. Therapeutic effect of digitalis glycosides may be reduced.
- Interferon-α
- Interleukin-2
|Therapy with interferon-α has been associated with the development of antithyroid microsomal antibodies in 20% of patients and some have transient hypothyroidism, hyperthyroidism, or both. Patients who have antithyroid antibodies before treatment are at higher risk for thyroid dysfunction during treatment. Interleukin-2 has been associated with transient painless thyroiditis in 20% of patients. Interferon-β and -γ have not been reported to cause thyroid dysfunction.
|Growth Hormones
- Somatrem
- Somatropin
|Excessive use of thyroid hormones with growth hormones may accelerate epiphyseal closure. However, untreated hypothyroidism may interfere with growth response to growth hormone.
|Concurrent use may produce marked hypertension and tachycardia; cautious administration to patients receiving thyroid hormone therapy is recommended.
|Methylxanthine Bronchodilators
- (e.g., Theophylline)
|Decreased theophylline clearance may occur in hypothyroid patients; clearance returns to normal when the euthyroid state is achieved.
|Radiographic Agents
|Thyroid hormones may reduce the uptake of 123I, 131I, and 99mTc.
|Concurrent use may increase the effects of sympathomimetics or thyroid hormone. Thyroid hormones may increase the risk of coronary insufficiency when sympathomimetic agents are administered to patients with coronary artery disease.
|Chloral Hydrate
Para-aminosalicylate sodium
Resorcinol (excessive topical use)
Thiazide Diuretics
|These agents have been associated with thyroid hormone and / or TSH level alterations by various mechanisms.
Levothyroxine increases the response to oral anticoagulant therapy. Therefore, a decrease in the dose of anticoagulant may be warranted with correction of the hypothyroid state or when the LEVOXYL dose is increased. Prothrombin time should be closely monitored to permit appropriate and timely dosage adjustments (see Table 2).
The therapeutic effects of digitalis glycosides may be reduced by levothyroxine. Serum digitalis glycoside levels may be decreased when a hypothyroid patient becomes euthyroid, necessitating an increase in the dose of digitalis glycosides (see Table 2).
Consumption of certain foods may affect levothyroxine absorption thereby necessitating adjustments in dosing. Soybean flour (infant formula), cotton seed meal, walnuts, and dietary fiber may bind and decrease the absorption of levothyroxine sodium from the GI tract.
Changes in TBG concentration must be considered when interpreting T4 and T3 values, which necessitates measurement and evaluation of unbound (free) hormone and/or determination of the free T4 index (FT4I). Pregnancy, infectious hepatitis, estrogens, estrogen-containing oral contraceptives, and acute intermittent porphyria increase TBG concentrations. Decreases in TBG concentrations are observed in nephrosis, severe hypoproteinemia, severe liver disease, acromegaly, and after androgen or corticosteroid therapy (see also Table 2). Familial hyper- or hypo-thyroxine binding globulinemias have been described, with the incidence of TBG deficiency approximating 1 in 9000.
Animal studies have not been performed to evaluate the carcinogenic potential, mutagenic potential or effects on fertility of levothyroxine. The synthetic T4 in LEVOXYL is identical to that produced naturally by the human thyroid gland. Although there has been a reported association between prolonged thyroid hormone therapy and breast cancer, this has not been confirmed. Patients receiving LEVOXYL for appropriate clinical indications should be titrated to the lowest effective replacement dose.
Studies in women taking levothyroxine sodium during pregnancy have not shown an increased risk of congenital abnormalities. Therefore, the possibility of fetal harm appears remote. LEVOXYL should not be discontinued during pregnancy and hypothyroidism diagnosed during pregnancy should be promptly treated.
Hypothyroidism during pregnancy is associated with a higher rate of complications, including spontaneous abortion, pre-eclampsia, stillbirth and premature delivery. Maternal hypothyroidism may have an adverse effect on fetal and childhood growth and development. During pregnancy, serum T4 levels may decrease and serum TSH levels increase to values outside the normal range. Since elevations in serum TSH may occur as early as 4 weeks gestation, pregnant women taking LEVOXYL should have their TSH measured during each trimester. An elevated serum TSH level should be corrected by an increase in the dose of LEVOXYL. Since postpartum TSH levels are similar to preconception values, the LEVOXYL dosage should return to the pre-pregnancy dose immediately after delivery. A serum TSH level should be obtained 6—8 weeks postpartum.
Thyroid hormones do not readily cross the placental barrier; however, some transfer does occur as evidenced by levels in cord blood of athyreotic fetuses being approximately one-third maternal levels. Transfer of thyroid hormone from the mother to the fetus, however, may not be adequate to prevent in utero hypothyroidism.
Although thyroid hormones are excreted only minimally in human milk, caution should be exercised when LEVOXYL is administered to a nursing woman. However, adequate replacement doses of levothyroxine are generally needed to maintain normal lactation.
The goal of treatment in pediatric patients with hypothyroidism is to achieve and maintain normal intellectual and physical growth and development.
The initial dose of levothyroxine varies with age and body weight (see DOSAGE AND ADMINISTRATION , Table 3). Dosing adjustments are based on an assessment of the individual patient's clinical and laboratory parameters (see PRECAUTIONS , Laboratory Tests ).
In children in whom a diagnosis of permanent hypothyroidism has not been established, it is recommended that levothyroxine administration be discontinued for a 30-day trial period, but only after the child is at least 3 years of age. Serum T4 and TSH levels should then be obtained. If the T4 is low and the TSH high, the diagnosis of permanent hypothyroidism is established, and levothyroxine therapy should be reinstituted. If the T4 and TSH levels are normal, euthyroidism may be assumed and, therefore, the hypothyroidism can be considered to have been transient. In this instance, however, the physician should carefully monitor the child and repeat the thyroid function tests if any signs or symptoms of hypothyroidism develop. In this setting, the clinician should have a high index of suspicion of relapse. If the results of the levothyroxine withdrawal test are inconclusive, careful follow-up and subsequent testing will be necessary.
Since some more severely affected children may become clinically hypothyroid when treatment is discontinued for 30 days, an alternate approach is to reduce the replacement dose of levothyroxine by half during the 30-day trial period. If, after 30 days, the serum TSH is elevated above 20 mU/L, the diagnosis of permanent hypothyroidism is confirmed, and full replacement therapy should be resumed. However, if the serum TSH has not risen to greater than 20mU/L, levothyroxine treatment should be discontinued for another 30-day trial period followed by repeat serum T4 and TSH.
The presence of concomitant medical conditions should be considered in certain clinical circumstances and, if present, appropriately treated (see PRECAUTIONS ).
(see PRECAUTIONS , Laboratory Tests and DOSAGE AND ADMINISTRATION )
Rapid restoration of normal serum T4 concentrations is essential for preventing the adverse effects of congenital hypothyroidism on intellectual development as well as on overall physical growth and maturation. Therefore, LEVOXYL therapy should be initiated immediately upon diagnosis and is generally continued for life.
During the first 2 weeks of LEVOXYL therapy, infants should be closely monitored for cardiac overload, arrhythmias, and aspiration from avid suckling.
The patient should be monitored closely to avoid undertreatment or overtreatment. Undertreatment may have deleterious effects on intellectual development and linear growth. Overtreatment has been associated with craniosynostosis in infants, and may adversely affect the tempo of brain maturation and accelerate the bone age with resultant premature closure of the epiphyses and compromised adult stature.
The patient should be monitored closely to avoid undertreatment and overtreatment. Undertreatment may result in poor school performance due to impaired concentration and slowed mentation and in reduced adult height. Overtreatment may accelerate the bone age and result in premature epiphyseal closure and compromised adult stature.
Treated children may manifest a period of catch-up growth, which may be adequate in some cases to normalize adult height. In children with severe or prolonged hypothyroidism, catch-up growth may not be adequate to normalize adult height.
Because of the increased prevalence of cardiovascular disease among the elderly, levothyroxine therapy should not be initiated at the full replacement dose (see WARNINGS , PRECAUTIONS , and DOSAGE AND ADMINISTRATION ).
Adverse reactions associated with levothyroxine therapy are primarily those of hyperthyroidism due to therapeutic overdosage. They include the following:
General: fatigue, increased appetite, weight loss, heat intolerance, fever, excessive sweating;
Central nervous system: headache, hyperactivity, nervousness, anxiety, irritability, emotional lability, insomnia;
Musculoskeletal: tremors, muscle weakness;
Cardiac: palpitations, tachycardia, arrhythmias, increased pulse and blood pressure, heart failure, angina, myocardial infarction, cardiac arrest;
Pulmonary: dyspnea;
GI: diarrhea, vomiting, abdominal cramps;
Dermatologic: hair loss, flushing;
Reproductive: menstrual irregularities, impaired fertility.
Pseudotumor cerebri and slipped capital femoral epiphysis have been reported in children receiving levothyroxine therapy. Overtreatment may result in craniosynostosis in infants and premature closure of the epiphyses in children with resultant compromised adult height.
Seizures have been reported rarely with the institution of levothyroxine therapy.
Inadequate levothyroxine dosage will produce or fail to ameliorate the signs and symptoms of hypothyroidism.
Hypersensitivity reactions to inactive ingredients have occurred in patients treated with thyroid hormone products. These include urticaria, pruritus, skin rash, flushing, angioedema, various GI symptoms (abdominal pain, nausea, vomiting and diarrhea), fever, arthralgia, serum sickness and wheezing. Hypersensitivity to levothyroxine itself is not known to occur.
In addition to the above events, the following have been reported, predominately when Levoxyl tablets were not taken with water: choking, gagging, tablet stuck in throat and dysphagia (see Information for Patients ).
The signs and symptoms of overdosage are those of hyperthyroidism (see PRECAUTIONS and ADVERSE REACTIONS ). In addition, confusion and disorientation may occur. Cerebral embolism, shock, coma, and death have been reported. Seizures have occurred in a child ingesting approximately 20 mg of levothyroxine. Symptoms may not necessarily be evident or may not appear until several days after ingestion of levothyroxine sodium.
Levothyroxine sodium should be reduced in dose or temporarily discontinued if signs or symptoms of overdosage occur.
The goal of replacement therapy is to achieve and maintain a clinical and biochemical euthyroid state. The goal of suppressive therapy is to inhibit growth and/or function of abnormal thyroid tissue. The dose of LEVOXYL that is adequate to achieve these goals depends on a variety of factors including the patient's age, body weight, cardiovascular status, concomitant medical conditions, including pregnancy, concomitant medications, and the specific nature of the condition being treated (see WARNINGS and PRECAUTIONS ). Hence, the following recommendations serve only as dosing guidelines. Dosing must be individualized and adjustments made based on periodic assessment of the patient's clinical response and laboratory parameters (see PRECAUTIONS , Laboratory Tests ).
The LEVOXYL should be taken in the morning on an empty stomach, at least one-half hour before any food is eaten. LEVOXYL should be taken at least 4 hours apart from drugs that are known to interfere with its absorption (see PRECAUTIONS , Drug Interactions ).
LEVOXYL should be taken with water (see Information for Patients and ADVERSE REACTIONS ).
Due to the long half-life of levothyroxine, the peak therapeutic effect at a given dose of levothyroxine sodium may not be attained for 4—6 weeks.
Caution should be exercised when administering LEVOXYL to patients with underlying cardiovascular disease, to the elderly, and to those with concomitant adrenal insufficiency (see PRECAUTIONS ).
(see WARNINGS and PRECAUTIONS ,Laboratory Tests )
Therapy may begin at full replacement doses in otherwise healthy individuals less than 50 years old and in those older than 50 years who have been recently treated for hyperthyroidism or who have been hypothyroid for only a short time (such as a few months). The average full replacement dose of levothyroxine sodium is approximately 1.7 mcg/kg/day (e.g., 100—125 mcg/day for a 70 kg adult). Older patients may require less than 1 mcg/kg/day. Levothyroxine sodium doses greater than 200 mcg/day are seldom required. An inadequate response to daily doses ≥300 mcg/day is rare and may indicate poor compliance, malabsorption, and/or drug interactions.
For most patients older than 50 years or for patients under 50 years of age with underlying cardiac disease, an initial starting dose of 25—50 mcg/day of levothyroxine sodium is recommended, with gradual increments in dose at 6—8 week intervals, as needed. The recommended starting dose of levothyroxine sodium in elderly patients with cardiac disease is 12.5—25 mcg/day, with gradual dose increments at 4—6 week intervals. The levothyroxine sodium dose is generally adjusted in 12.5—25 mcg increments until the patient with primary hypothyroidism is clinically euthyroid and the serum TSH has normalized.
In patients with severe hypothyroidism, the recommended initial levothyroxine sodium dose is 12.5—25 mcg/day with increases of 25 mcg/day every 2—4 weeks, accompanied by clinical and laboratory assessment, until the TSH level is normalized.
In patients with secondary (pituitary) or tertiary (hypothalamic) hypothyroidism, the levothyroxine sodium dose should be titrated until the patient is clinically euthyroid and the serum free-T4 level is restored to the upper half of the normal range.
(see PRECAUTIONS , Laboratory Tests )
In general, levothyroxine therapy should be instituted at full replacement doses as soon as possible. Delays in diagnosis and institution of therapy may have deleterious effects on the child's intellectual and physical growth and development.
Undertreatment and overtreatment should be avoided (see PRECAUTIONS ,Pediatric Use ).
LEVOXYL may be administered to infants and children who cannot swallow intact tablets by crushing the tablet and suspending the freshly crushed tablet in a small amount (5—10 mL or 1—2 teaspoons) of water. This suspension can be administered by spoon or dropper. DO NOT STORE THE SUSPENSION. Foods that decrease absorption of levothyroxine, such as soybean infant formula, should not be used for administering levothyroxine sodium tablets. (see PRECAUTIONS , Drug-Food Interactions ).
The recommended starting dose of levothyroxine sodium in newborn infants is 10—15 mcg/kg/day. A lower starting dose (e.g., 25 mcg/day) should be considered in infants at risk for cardiac failure, and the dose should be increased in 4—6 weeks as needed based on clinical and laboratory response to treatment. In infants with very low (< 5 mcg/dL) or undetectable serum T4 concentrations, the recommended initial starting dose is 50 mcg/day of levothyroxine sodium.
Levothyroxine therapy is usually initiated at full replacement doses, with the recommended dose per body weight decreasing with age (see TABLE 3). However, in children with chronic or severe hypothyroidism, an initial dose of 25 mcg/day of levothyroxine sodium is recommended with increments of 25 mcg every 2—4 weeks until the desired effect is achieved.
Hyperactivity in an older child can be minimized if the starting dose is one-fourth of the recommended full replacement dose, and the dose is then increased on a weekly basis by an amount equal to one-fourth the full recommended replacement dose until the full recommended replacement dose is reached.
|Daily Dose Per Kg Body Weight *
|0—3 months
|10—15 mcg/kg/day
|3—6 months
|8—10 mcg/kg/day
|6—12 months
|6—8 mcg/kg/day
|1—5 years
|5—6 mcg/kg/day
|6—12 years
|4—5 mcg/kg/day
|>12 years
|2—3 mcg/kg/day
|Growth and puberty complete
|1.7 mcg/kg/day
Pregnancy may increase levothyroxine requirements (see PREGNANCY).
If this condition is treated, a lower levothyroxine sodium dose (e.g., 1 mcg/kg/day) than that used for full replacement may be adequate to normalize the serum TSH level. Patients who are not treated should be monitored yearly for changes in clinical status and thyroid laboratory parameters.
The target level for TSH suppression in these conditions has not been established with controlled studies. In addition, the efficacy of TSH suppression for benign nodular disease is controversial. Therefore, the dose of LEVOXYL used for TSH suppression should be individualized based on the specific disease and the patient being treated.
In the treatment of well differentiated (papillary and follicular) thyroid cancer, levothyroxine is used as an adjunct to surgery and radioiodine therapy. Generally, TSH is suppressed to <0.1 mU/L, and this usually requires a levothyroxine sodium dose of greater than 2 mcg/kg/day. However, in patients with high-risk tumors, the target level for TSH suppression may be <0.01 mU/L.
In the treatment of benign nodules and nontoxic multinodular goiter, TSH is generally suppressed to a higher target (e.g., 0.1—0.5 mU/L for nodules and 0.5—1.0 mU/L for multinodular goiter) than that used for the treatment of thyroid cancer. Levothyroxine sodium is contraindicated if the serum TSH is already suppressed due to the risk of precipitating overt thyrotoxicosis (see CONTRAINDICATIONS , WARNINGS and PRECAUTIONS ).
Myxedema coma is a life-threatening emergency characterized by poor circulation and hypometabolism, and may result in unpredictable absorption of levothyroxine sodium from the gastrointestinal tract. Therefore, oral thyroid hormone drug products are not recommended to treat this condition. Thyroid hormone products formulated for intravenous administration should be administered.
– LEVOXYL(levothyroxine sodium tablets, USP) are supplied as oval, color-coded, potency marked tablets in 11 strengths:
|Strength (mcg)
|NDC # for bottles
|30's NDC 54868-4087-1
|30's NDC 54868-4092-2
90's NDC 54868-4092-1
|30's NDC 54868-4534-1
90's NDC 54868-4534-2
|30's NDC 54868-4177-1
90's NDC 54868-4177-2
|30's NDC 54868-4176-1
90's NDC 54868-4176-2
|30's NDC 54868-3849-1
|20's NDC 54868-4536-2
30's NDC 54868-4536-1
100's NDC 54868-4536-0
|30's NDC 54868-4535-1
Rx ONLY
Manufactured and Distributed by:
King Pharmaceuticals, Inc.
Bristol, TN 37620
Prescribing Information as of August 2008
Distributed by:
Physicians Total Care, Inc.
Tuisa, OK 74146
(levothyroxine sodium tablets, USP)
25 mcg
Rx only
(levothyroxine sodium tablets, USP)
50 mcg
Rx only
(levothyroxine sodium tablets, USP)
75 mcg
Rx only
(levothyroxine sodium tablets, USP)
88 mcg
Rx only
(levothyroxine sodium tablets, USP)
100 mcg
Rx only
(levothyroxine sodium tablets, USP)
112 mcg
Rx only
(levothyroxine sodium tablets, USP)
125 mcg
Rx only
levothyroxine sodium tablet
levothyroxine sodium tablet
levothyroxine sodium tablet
levothyroxine sodium tablet
levothyroxine sodium tablet
levothyroxine sodium tablet
levothyroxine sodium tablet
levothyroxine sodium tablet
|Labeler - Physicians Total Care, Inc. (194123980)
|Business Operations
|Physicians Total Care, Inc.
|relabel(54868-4087, 54868-4092, 54868-4534, 54868-4177, 54868-4176, 54868-3849, 54868-4536, 54868-4535) , repack(54868-4087, 54868-4092, 54868-4534, 54868-4177, 54868-4176, 54868-3849, 54868-4536, 54868-4535)


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text:
acetaminophen tablet
Acetaminophen has been associated with cases of acute liver failure, at times resulting in liver transplant and death. Most of the cases of liver injury are associated with the use of acetaminophen at doses that exceed 4000 milligrams per day, and often involve more than one acetaminophen-containing product.
Acetaminophen and codeine phosphate is supplied in tablet form for oral administration.
Acetaminophen, 4'-hydroxyacetanilide, a slightly bitter, white, odorless, crystalline powder, is a non-opiate, non-salicylate analgesic and antipyretic. It has the following structural formula:
Codeine phosphate, 7,8-didehydro-4,5α-epoxy-3-methoxy-17-methylmorphinan-6α-ol phosphate (1:1) (salt) hemihydrate, a white crystalline powder, is a narcotic analgesic and antitussive. It has the following structural formula:
Each Acetaminophen and Codeine Phosphate Tablet USP (300 mg/15 mg) contains:
Each Acetaminophen and Codeine Phosphate Tablet USP (300 mg/30 mg) contains:
Each Acetaminophen and Codeine Phosphate Tablet USP (300 mg/60 mg) contains:
In addition, each Acetaminophen and Codeine Phosphate Tablet USP contains the following inactive ingredients: crospovidone, magnesium stearate, microcrystalline cellulose, povidone, pregelatinized starch, stearic acid.
This product combines the analgesic effects of a centrally acting analgesic, codeine, with a peripherally acting analgesic, acetaminophen.
The behavior of the individual components is described below.
Codeine – Codeine is readily absorbed from the gastrointestinal tract. It is rapidly distributed from the intravascular spaces to the various body tissues, with preferential uptake by parenchymatous organs such as the liver, spleen and kidney. Codeine crosses the blood-brain barrier, and is found in fetal tissue and breast milk. The plasma concentration does not correlate with brain concentration or relief of pain; however, codeine is not bound to plasma proteins and does not accumulate in body tissues.
The plasma half-life is about 2.9 hours. The elimination of codeine is primarily via the kidneys, and about 90% of an oral dose is excreted by the kidneys within 24 hours of dosing. The urinary secretion products consist of free and glucuronide conjugated codeine (about 70%), free and conjugated norcodeine (about 10%), free and conjugated morphine (about 10%), normorphine (4%), and hydrocodone (1%). The remainder of the dose is excreted in the feces.
At therapeutic doses, the analgesic effect reaches a peak within 2 hours and persists between 4 and 6 hours.
See OVERDOSAGE for toxicity information.
Acetaminophen – Acetaminophen is rapidly absorbed from the gastrointestinal tract and is distributed throughout most body tissues. The plasma half-life is 1.25 to 3 hours, but may be increased by liver damage and following overdosage. Elimination of acetaminophen is principally by liver metabolism (conjugation) and subsequent renal excretion of metabolites. Approximately 85% of an oral dose appears in the urine within 24 hours of administration, most as the glucuronide conjugate, with small amounts of other conjugates and unchanged drug.
See OVERDOSAGE for toxicity information.
Acetaminophen and codeine phosphate tablets are indicated for the relief of mild to moderately severe pain.
This product should not be administered to patients who have previously exhibited hypersensitivity to codeine or acetaminophen.
Acetaminophen has been associated with cases of acute liver failure, at times resulting in liver transplant and death. Most of the cases of liver injury are associated with the use of acetaminophen at doses that exceed 4000 milligrams per day, and often involve more than one acetaminophen-containing product. The excessive intake of acetaminophen may be intentional to cause self-harm or unintentional as patients attempt to obtain more pain relief or unknowingly take other acetaminophen-containing products.
The risk of acute liver failure is higher in individuals with underlying liver disease and in individuals who ingest alcohol while taking acetaminophen.
Instruct patients to look for acetaminophen or APAP on package labels and not to use more than one product that contains acetaminophen. Instruct patients to seek medical attention immediately upon ingestion of more than 4000 milligrams of acetaminophen per day, even if they feel well.
There have been post-marketing reports of hypersensitivity and anaphylaxis associated with use of acetaminophen. Clinical signs included swelling of the face, mouth, and throat, respiratory distress, urticaria, rash, pruritus, and vomiting. There were infrequent reports of life-threatening anaphylaxis requiring emergency medical attention. Instruct patients to discontinue acetaminophen and codeine phosphate tablets USP immediately and seek medical care if they experience these symptoms. Do not prescribe acetaminophen and codeine phosphate tablets USP for patients with acetaminophen allergy.
In the presence of head injury or other intracranial lesions, the respiratory depressant effects of codeine and other narcotics may be markedly enhanced, as well as their capacity for elevating cerebrospinal fluid pressure. Narcotics also produce other CNS depressant effects, such as drowsiness, that may further obscure the clinical course of the patients with head injuries.
Codeine or other narcotics may obscure signs on which to judge the diagnosis or clinical course of patients with acute abdominal conditions.
Codeine is habit-forming and potentially abusable. Consequently, the extended use of this product is not recommended.
Acetaminophen and codeine phosphate tablets should be prescribed with caution in certain special risk patients, such as the elderly or debilitated, and those with severe impairment of renal or hepatic function, head injuries, elevated intracranial pressure, acute abdominal conditions, hypothyroidism, urethral stricture, Addison's disease, or prostatic hypertrophy.
Ultra-rapid Metabolizers of Codeine - Some individuals may be ultra-rapid metabolizers due to a specific CYP2D6*2x2 genotype. These individuals convert codeine into its active metabolite, morphine, more rapidly and completely than other people. This rapid conversion results in higher than expected serum morphine levels. Even at labeled dosage regiments, individuals who are ultra-rapid metabolizers may experience overdose symptoms such as extreme sleepiness, confusion or shallow breathing.
The prevalence of this CYP2D6 phenotype varies widely and has been estimated at 0.5 to 1% in Chinese and Japanese, 0.5 to 1% in Hispanics, 1 to 10% in Caucasians, 3% in African Americans, and 16 to 28% in North Africans, Ethiopians and Arabs. Data is not available for other ethnic groups.
When physicians prescribe codeine-containing drugs, they should choose the lowest effective dose for the shortest period of time and should inform their patients about these risks and the signs of morphine overdose (see PRECAUTIONS, Nursing Mothers).
Codeine may impair mental and/or physical abilities required for the performance of potentially hazardous tasks such as driving a car or operating machinery. Such tasks should be avoided while taking this product.
Alcohol and other CNS depressants may produce an additive CNS depression when taken with this combination product, and should be avoided.
Codeine is habit-forming. Patients should take the drug only for as long as it is prescribed, in the amounts prescribed, and no more frequently than prescribed.
Caution patients that some people have a variation in a liver enzyme and change codeine into morphine more rapidly and completely than other people. These people are ultra-rapid metabolizers and are more likely to have higher-than-normal levels of morphine in their blood after taking codeine which can result in overdose symptoms such as extreme sleepiness, confusion, or shallow breathing. In most cases, it is unknown if someone is an ultra-rapid codeine metabolizer.
Nursing mothers taking codeine can also have higher morphine levels in their breast milk if they are ultra-rapid metabolizers. These higher levels of morphine in breast milk may lead to life-threatening or fatal side effects in nursing babies. Instruct nursing mothers to watch for signs of morphine toxicity in their infants including increased sleepiness (more than usual), difficulty breastfeeding, breathing difficulties, or limpness. Instruct nursing mothers to talk to the baby's doctor immediately if they notice these signs and, if they cannot reach the doctor right away, to take the baby to an emergency room or call 911 (or local emergency services).
In patients with severe hepatic or renal disease, effects of therapy should be monitored with serial liver and/or renal function tests.
This drug may enhance the effects of other narcotic analgesics, alcohol, general anesthetics, tranquilizers such as chlordiazepoxide, sedative-hypnotics, or other CNS depressants, causing increased CNS depression.
Codeine may increase serum amylase levels.
Acetaminophen may produce false positive test results for urinary 5-hydroxyindoleacetic acid.
No adequate studies have been conducted in animals to determine whether acetaminophen and codeine have a potential for carcinogenesis or mutagenesis. No adequate studies have been conducted in animals to determine whether acetaminophen has a potential for impairment of fertility.
Acetaminophen and codeine have been found to have no mutagenic potential using the Ames Salmonella-Microsomal Activation test, the Basc test on Drosophila germ cells, and the Micronucleus test on mouse bone marrow.
Codeine – A study in rats and rabbits reported no teratogenic effect of codeine administered during the period of organogenesis in doses ranging from 5 to 120 mg/kg. In the rat, doses at the 120 mg/kg level, in the toxic range for the adult animal, were associated with an increase in embryo resorption at the time of implantation. In another study a single 100 mg/kg dose of codeine administered to pregnant mice reportedly resulted in delayed ossification in the offspring.
There are no adequate and well-controlled studies in pregnant women. Acetaminophen and codeine phosphate should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
Dependence has been reported in newborns whose mothers took opiates regularly during pregnancy. Withdrawal signs include irritability, excessive crying, tremors, hyperreflexia, fever, vomiting, and diarrhea. These signs usually appear during the first few days of life.
Narcotic analgesics cross the placental barrier. The closer to delivery and the larger the dose used, the greater the possibility of respiratory depression in the newborn. Narcotic analgesics should be avoided during labor if delivery of a premature infant is anticipated. If the mother has received narcotic analgesics during labor, newborn infants should be observed closely for signs of respiratory depression. Resuscitation may be required (see OVERDOSAGE). The effect of codeine, if any, on the later growth, development, and functional maturation of the child is unknown.
Acetaminophen is excreted in breast milk in small amounts, but the significance of its effects on nursing infants is not known. Because of the potential for serious adverse reactions in nursing infants from acetaminophen, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.
Codeine is secreted into human milk. In women with normal codeine metabolism (normal CYP2D6 activity), the amount of codeine secreted into human milk is low and dose-dependent. Despite the common use of codeine products to manage postpartum pain, reports of adverse events in infants are rare. However, some women are ultra-rapid metabolizers of codeine. These women achieve higher-than-expected serum levels of codeine's active metabolite, morphine, leading to higher-than-expected levels of morphine in breast milk and potentially dangerously high serum morphine levels in their breastfed infants. Therefore, maternal use of codeine can potentially lead to serious adverse reactions, including death, in nursing infants.
The prevalence of this CYP2D6 phenotype varies widely and has been estimated at 0.5 to 1% in Chinese and Japanese, 0.5 to 1% in Hispanics, 1 to 10% in Caucasians, 3% in African Americans, and 16 to 28% in North Africans, Ethiopians and Arabs. Data is not available for other ethnic groups.
The risk of infant exposure to codeine and morphine through breast milk should be weighed against the benefits of breastfeeding for both the mother and baby. Caution should be exercised when codeine is administered to a nursing woman. If a codeine containing product is selected, the lowest dose should be prescribed for the shortest period of time to achieve the desired clinical effect. Mothers using codeine should be informed about when to seek immediate medical care and how to identify the signs and symptoms of neonatal toxicity, such as drowsiness or sedation, difficulty breastfeeding, breathing difficulties, and decreased tone, in their baby. Nursing mothers who are ultra-rapid metabolizers may also experience overdose symptoms such as extreme sleepiness, confusion or shallow breathing. Prescribers should closely monitor mother-infant pairs and notify treating pediatricians about the use of codeine during breastfeeding (see PRECAUTIONS, General, Ultra-rapid Metabolizers of Codeine).
The most frequently reported adverse reactions are drowsiness, lightheadedness, dizziness, sedation, shortness of breath, nausea and vomiting. These effects seem to be more prominent in ambulatory than in non-ambulatory patients, and some of these adverse reactions may be alleviated if the patient lies down. Other adverse reactions include allergic reactions, euphoria, dysphoria, constipation, abdominal pain, pruritus, rash, thrombocytopenia, agranulocytosis.
At higher doses, codeine has most of the disadvantages of morphine including respiratory depression.
Acetaminophen and codeine phosphate tablets are classified as a Schedule III controlled substance.
Codeine can produce drug dependence of the morphine type and, therefore, has the potential for being abused. Psychological dependence, physical dependence, and tolerance may develop upon repeated administration and it should be prescribed and administered with the same degree of caution appropriate to the use of other oral narcotic medications.
Following an acute overdosage, toxicity may result from codeine or acetaminophen.
Toxicity from codeine poisoning includes the opioid triad of pinpoint pupils, depression of respiration, and loss of consciousness. Convulsions may occur.
In acetaminophen overdosage, dose-dependent, potentially fatal hepatic necrosis is the most serious adverse effect. Renal tubular necrosis, hypoglycemic coma and coagulation defects may also occur. Early symptoms following a potentially hepatotoxic overdose may include nausea, vomiting, diaphoresis and general malaise. Clinical and laboratory evidence of hepatic toxicity may not be apparent until 48 to 72 hours post-ingestion.
A single or multiple drug overdose with acetaminophen and codeine is a potentially lethal polydrug overdose, and consultation with a regional poison control center is recommended. Immediate treatment includes support of cardiorespiratory function and measures to reduce drug absorption.
Oxygen, intravenous fluids, vasopressors, and other supportive measures should be employed as indicated. Assisted or controlled ventilation should also be considered. For respiratory depression due to overdosage or unusual sensitivity to codeine, parenteral naloxone is a specific and effective antagonist.
Gastric decontamination with activated charcoal should be administered just prior to N-acetylcysteine (NAC) to decrease systemic absorption if acetaminophen ingestion is known or suspected to have occurred within a few hours of presentation. Serum acetaminophen levels should be obtained immediately if the patient presents 4 hours or more after ingestion to assess potential risk of hepatotoxicity; acetaminophen levels drawn less than 4 hours post-ingestion may be misleading. To obtain the best possible outcome, NAC should be administered as soon as possible where impending or evolving liver injury is suspected. Intravenous NAC may be administered when circumstances preclude oral administration.
Vigorous supportive therapy is required in severe intoxication. Procedures to limit the continuing absorption of the drug must be readily performed since the hepatic injury is dose dependent and occurs early in the course of intoxication.
Dosage should be adjusted according to severity of pain and response of the patient.
The usual adult dosage for tablets is:
|Single Doses (Range)
|Maximum 24 Hour Dose
|Codeine Phosphate
|15 mg to 60 mg
|360 mg
|300 mg to 1000 mg
|4000 mg
The usual dose of codeine phosphate in children is 0.5 mg/kg.
Doses may be repeated up to every 4 hours.
The prescriber must determine the number of tablets per dose, and the maximum number of tablets per 24 hours based upon the above dosage guidance. This information should be conveyed in the prescription.
It should be kept in mind, however, that tolerance to codeine can develop with continued use and that the incidence of untoward effects is dose related. Adult doses of codeine higher than 60 mg fail to give commensurate relief of pain but merely prolong analgesia and are associated with an appreciably increased incidence of undesirable side effects. Equivalently high doses in children would have similar effects.
Each Acetaminophen and Codeine Phosphate Tablet USP 300 mg/15 mg tablet contains acetaminophen 300 mg and codeine phosphate 15 mg. It is available as a round, white to off-white tablet debossed with "2" on one side and an on the other side.
|Bottles of 100 . . . . . . . NDC 0406-0483-01
Each Acetaminophen and Codeine Phosphate Tablet USP 300 mg/30 mg tablet contains acetaminophen 300 mg and codeine phosphate 30 mg. It is available as a round, white to off-white tablet debossed with "3" on one side and an on the other side.
|Bottles of 20 . . . . . . . . NDC 0406-0484-20
|Bottles of 30 . . . . . . . . NDC 0406-0484-03
|Bottles of 50 . . . . . . . . NDC 0406-0484-50
|Bottles of 100 . . . . . . . NDC 0406-0484-01
|Bottles of 1000 . . . . . . NDC 0406-0484-10
|Unit Dose (10 x 10) . . NDC 0406-0484-62
Each Acetaminophen and Codeine Phosphate Tablet USP 300 mg/60 mg tablet contains acetaminophen 300 mg and codeine phosphate 60 mg. It is available as a round, white to off-white tablet debossed with "4" on one side and an on the other side.
|Bottles of 100 . . . . . . . NDC 0406-0485-01
|Bottles of 500 . . . . . . . NDC 0406-0485-05
Store at 20° to 25°C (68° to 77°F) [see USP Controlled Room Temperature].
Dispense in tight, light-resistant container as defined in the USP.
is a trademark of Mallinckrodt Inc.
Mallinckrodt Inc.
Hazelwood, MO 63042 USA
Rev 06/2011
GENERIC: acetaminophen and codeine phosphate
STRENGTH:300 mg
COLOR: white
SCORE: No score
SIZE: 11 mm
acetaminophen and codeine phosphate tablet
|Marketing Information
|Marketing Category
|Application Number or Monograph Citation
|Marketing Start Date
|Marketing End Date
|Labeler - REMEDYREPACK INC. (829572556)