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100 mg tid, in the morning, evening and before bed.
Contraindications
Lactation.
Special Precautions
Pregnancy, elderly and children.
Adverse Drug Reactions
Rash, pruritus, constipation, diarrhoea, nausea.
Mechanism of Action
Rebamipide is a mucosal protective agent and is postulated to increase gastric blood flow, prostaglandin biosynthesis and decrease free oxygen radicals.
MIMS Class
Antacids, Antireflux Agents & Antiulcerants

Rebamipide, a gastroprotective drug, is a compound selected from over 500 amino acid analogs of 2(1H)-quinolinone tested for gastroprotective action and for
efficacy to heal experimental gastric ulcers. This drug stimulates prostaglandin generation in gastric mucosa and improves not only the speed but also the quality of
ulcer healing. In addition, it protects the gastric mucosa against acute injury caused by various noxious and ulcerogenic factors. Based on these experimental results,
rebamipide had been subsequently tested in several clinical trials and approved in Japan for therapeutic use in patients with gastric ulcers and patients with acute
gastritis. The main purpose of developing this type of drug was to improve the quality of ulcer healing, especially in that antisecretory drugs lack this advantage. In a
preliminary clinical study, rebamipide improved the quality of gastric ulcer healing and reduced future ulcer recurrence. A number of basic research studies have
been performed to clarify the mechanisms of rebamipide's action. These studies demonstrated unique properties of rebamipide and convincingly showed that it
increases gastric mucus glycoprotein components, stimulates migration and proliferation of wounded epithelial cell monolayers, increases expression of epidermal
growth factor and its receptor in normal and ulcerated gastric mucosa, and scavenges active oxygen radicals. The drug also attenuates the activity of neutrophils and
the production of inflammatory cytokines stimulated by NSAIDs and/or H. pylori. Therefore, rebamipide can contribute to the management of patients who are
taking NSAIDs or are infected with H. pylori. The inhibition of immunoinflammatory responses by rebamipide in H. pylori-infected patients may prevent development
of gastritis, peptic ulcer disease, its recurrence, and possibly gastric cancer. Moreover, rebamipide may enhance eradication of H. pylori-infection using standard
eradication therapy. Further studies are needed to clarify these possible advantages of rebamipide.

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Inhibits the enzyme responsible for the conversion of purines to uric acid, thus reducing the production of uric acid with a decrease in serum and
sometimes in urinary uric acid levels, relieving the signs and symptoms of gout
Indications:
- Management of the signs and symptoms of primary and secondary gout- Management of patients with malignancies that result in elevations of
serum and urinary uric acid- Management of patients with recurrent calcium oxalate calculi whose daily uric acid excretion exceeds 800 mg/day
(males) or 750 mg/day (females)- Orphan drug use: Treatment of Chagas' disease; cutaneous and visceral leishmaniasis- Unlabeled uses:
Amelioration of granulocyte suppression with fluorouracil; as a
CNS:
Headache, drowsiness,
peripheral neuropathy, neuritis, paresthesias
Dermatologic: RashesͶmaculopapular, scaly or exfoliativeͶsometimes fatalGI:
Nausea, vomiting, diarrhea,
abdominal pain, gastritis, hepatomegaly, hyperbilirubinemia, cholestatic jaundice
GU:
Exacerbation of gout and renal calculi, renal failure
Hematologic:
Anemia, leukopenia, agranulocytosis, thrombocytopenia, aplastic anemia, bone marrow depression
Reduce uric acid synthesis
-Assess for pain-Monitor uric acid levels q2 wk-Monitor CBC, AST, BUN, creatinine before starting treatment-Monitor nutritional status: discourage
organ meat, sardines, salmon, legumes (high purine), gravies,alcohol
Precautions:
-Pregnancy C, lactation, renal disease, hepatic disease, children

Unlabeled uses: Amelioration of granulocyte suppression with fluorouracil; as a mouthwash to prevent fluorouracil-induced stomatitis
Contraindications-
allergy to allopurinol, blood dyscrasias, hypersensitivity
  c 
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×




 

 
Person with StevensʹJohnson syndrome
  c (SJS) and toxic epidermal necrolysis (TEN)[1] are two forms of a life-threatening condition affecting the
skin in which cell death causes the epidermis to separate from the dermis. The syndrome is thought to be a hypersensitivity complex
affecting the skin and the mucous membranes. Although the majority of cases are idiopathic, the main class of known causes is
medications, followed by infections and (rarely) cancers.
? 11 References
ü  
There is agreement in the medical literature that StevensʹJohnson syndrome (SJS) can be considered a milder form of toxic
epidermal necrolysis (TEN). These conditions were first recognised in 1922.[2]
Both diseases can be mistaken for erythema multiforme. Erythema multiforme is sometimes caused by a reaction to a medication
but is more often a type IV hypersensitivity reaction to an infection (caused most often by Herpes simplex) and is relatively benign.
Although both SJS and TEN can also be caused by infections, they are most often adverse effects of medications. Their consequences
are potentially more dangerous than those of erythema multiforme.
ü 

Conjunctivitis (inflammation of eye and eyelid) in SJS

SJS usually begins with fever, sore throat, and fatigue, which is misdiagnosed and usually treated with antibiotics. Ulcers and other
lesions begin to appear in the mucous membranes, almost always in the mouth and lips but also in the genital and anal regions.
Those in the mouth are usually extremely painful and reduce the patient's ability to eat or drink. Conjunctivitis of the eyes occurs in
about 30% of children who develop SJS. A rash of round lesions about an inch across arises on the face, trunk, arms and legs, and
[3]
soles of the feet, but usually not the scalp.
ü 
 
SJS is thought to arise from a disorder of the immune system.[3]
ü  
It can be caused by infections (usually following infections such as herpes simplex virus, influenza, mumps, cat-scratch fever,
histoplasmosis, Epstein-Barr virus, mycoplasma pneumoniae or similar).
ü   c

[4]
It can be caused by adverse effects of drugs (allopurinol, diclofenac, etravirine, Isotretinoin, aka Accutane, fluconazole, valdecoxib,
sitagliptin, oseltamivir, penicillins, barbiturates, sulfonamides, phenytoin, azithromycin, oxcarbazepine, zonisamide, modafinil,[5]
[6] [7][8]
lamotrigine, nevirapine, pyrimethamine, ibuprofen, ethosuximide, carbamazepine, nystatin, and gout medications).
Although StevensʹJohnson Syndrome can be caused by viral infections, malignancies or severe allergic reactions to medication, the
leading cause appears to be the use of antibiotics and sulfa drugs.
Medications that have traditionally been known to lead to SJS, erythema multiforme and toxic epidermal necrolysis include
sulfonamides (antibiotics), penicillins (antibiotics), barbiturates (sedatives), lamotrigine and phenytoin (e.g. Dilantin)
(anticonvulsants). Combining lamotrigine with sodium valproate increases the risk of SJS.
Non-steroidal anti-inflammatory drugs are a rare cause of SJS in adults; the risk is higher for older patients, women and those
initiating treatment.[2] Typically, the symptoms of drug-induced SJS arise within a week of starting the medication. People with
systemic lupus erythematosus or HIV infections are more susceptible to drug-induced SJS.[3]
SJS has also been consistently reported as an uncommon side effect of herbal supplements containing ginseng. SJS may also be
caused by cocaine usage.[9]
ü    
In some East Asian populations studied (Han Chinese and Thai), carbamazepine- and phenytoin-induced SJS is strongly associated
with HLA-B*1502 (HLA-B75), an HLA-B serotype of the broader serotype HLA-B15.[10][11][12] A study in Europe suggested that the gene
marker is only relevant for East Asians.[13][14] Based on the Asian findings, similar studies were performed in Europe which showed
61% of allopurinol-induced SJS/TEN patients carried the HLA-B58 (B*5801 allele - phenotype frequency in Europeans is typically 3%).
One study concluded "even when HLA-B alleles behave as strong risk factors, as for allopurinol, they are neither sufficient nor
[15]
necessary to explain the disease."
ü !c  
SJS constitutes a dermatological emergency. All medications should be discontinued, particularly those known to cause SJS
[3]
reactions. Patients with documented mycoplasma infections can be treated with oral macrolide or oral doxycycline.
Initially, treatment is similar to that for patients with thermal burns, and continued care can only be supportive (e.g. intravenous
fluids and nasogastric or parenteral feeding) and symptomatic (e.g. analgesic mouth rinse for mouth ulcer). Dermatologists and
surgeons tend to disagree about whether the skin should be debrided.[3]
Beyond this kind of supportive care, there is no accepted treatment for SJS. Treatment with corticosteroids is controversial. Early
retrospective studies suggested that corticosteroids increased hospital stays and complication rates. There are no randomized trials
[3]
of corticosteroids for SJS, and it can be managed successfully without them.
Other agents have been used, including cyclophosphamide and cyclosporine, but none have exhibited much therapeutic success.
Intravenous immunoglobulin (IVIG) treatment has shown some promise in reducing the length of the reaction and improving
symptoms. Other common supportive measures include the use of topical pain anesthetics and antiseptics, maintaining a warm
environment, and intravenous analgesics. An ophthalmologist should be consulted immediately, as SJS frequently causes the
formation of scar tissue inside the eyelids, leading to corneal vascularization, impaired vision and a host of other ocular problems.
Also, an extensive physical therapy program ensues after the patient is discharged from the hospital.
ü "c
SJS proper (with less than 10% of body surface area involved) has a mortality rate of around 5%. The risk for death can be estimated
[9]
using the SCORTEN scale, which takes a number of prognostic indicators into account. Other outcomes include organ
damage/failure, cornea scratching and blindness.
ü " 
[3] [2]
Stevens-Johnson syndrome is a rare condition, with a reported incidence of around 2.6 to 6.1 cases per million people per year.
In the United States, there are about 300 new diagnoses per year. The condition is more common in adults than in children. Women
[2]
are affected more often than men, with cases occurring at a three to two six ratio.
ü #c
Stevens-Johnson Syndrome is named for Albert Mason Stevens and Frank Chambliss Johnson, American pediatricians who in 1922
jointly published a description of the disorder in the Ú  







×
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pg=1815&pos=121">>/script>
Sodium bicarbonate is an antacid that neutralizes stomach acid.
Sodium bicarbonate is used to relieve heartburn and indigestion. Sodium bicarbonate is also used to make the blood and urine less acidic in certain
conditions
Sodium bicarbonate may also be used for purposes other than those listed in this medication guide.
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Do not take sodium bicarbonate or any antacids without first talking to your doctor if you take any other medications.
Sodium bicarbonate contains a large amount of sodium. If you are on a sodium restricted diet or have high blood pressure talk to your health care
professional before taking sodium bicarbonate.


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Do not take sodium bicarbonate or any antacids without first talking to your doctor if you have:
? an intestinal problem or appendicitis;
? heart problems;
? high blood pressure;
? swelling of the arms or legs;
? kidney disease;
? liver disease; or
? problems urinating;
Talk to your doctor before taking sodium bicarbonate if you are pregnant. Talk to your doctor before taking sodium bicarbonate if you are breast-
feeding.

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Take sodium bicarbonate exactly as directed by your doctor or follow the directions on the package. If you do not understand these directions, ask
your pharmacist, nurse, or doctor to explain them to you.
Take the sodium bicarbonate tablets with a full glass of water. Store sodium bicarbonate at room temperature away from moisture and heat.
 ' Sodium bicarbonate dosage in more detail
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Take the missed dose as soon as you remember. However, if it is almost time for the next dose, skip the missed dose and take only the next
regularly scheduled dose. Do not take a double dose of this medicine unless your doctor directs otherwise.
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Seek emergency medical attention if an overdose is suspected.

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If you take other medicines, do not take sodium bicarbonate without first talking to your doctor.


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Stop taking sodium bicarbonate and seek emergency medical attention if you experience a rare allergic reaction (difficulty breathing; closing of the
throat; swelling of the lips, tongue, or face; or hives).
Stop taking sodium bicarbonate and notify your doctor if you experience
? nausea or vomiting;
? headache;
? sever mood changes;
? muscle pain;
? swelling of feet, ankles or legs
? decreased appetite;
? unusual tiredness;
? constipation;
? dry mouth or increased thirst; or
? increased urination.
Side effects other than those listed here may also occur. Talk to your doctor about any side effect that seems unusual or that is especially
bothersome. You may report side effects to FDA at 1-800-FDA-1088.

Read more: http://www.drugs.com/mtm/sodium-bicarbonate.html#ixzz0w2vZ56rX

Indication
Listed in Dosage.
Dosage
Ú
 "m  c % Up to 10 g/day in divided doses w/ sufficient fluid intake. c  
   ш4.8 g/day as needed.
  1-5 g when needed. ¦   c  
   By slow inj of a hypertonic soln ч8.4% or by continuous infusion of a weaker soln,
usually 1.26% .
Click to view Dosage by Indications
Administration
Should be taken on an empty stomach (i.e. At least one hour before food or two hours after food).
Contraindications
Metabolic or respiratory alkalosis; hypernatraemia, severe pulmonary oedema; hypocalcaemia, hypochlorhydria.
Special Precautions
Epilepsy, CHF, renal impairment, liver cirrhosis, hypertension, oedema, eclampsia, aldosteronism. Monitor serum electrolyte concentrations and
acid-base status regularly during treatment of acidosis. Pregnancy; lactation.
Adverse Drug Reactions
Metabolic alkalosis; mood changes, tiredness, shortness of breath, muscle weakness, irregular heartbeat; muscle hypertonicity, twitching, tetany;
hypernatraemia, hyperosmolality, hypocalcaemia, hypokalaemia; stomach cramps, flatulence. Tissue necrosis at inj site.
Drug Interactions
Increases toxicity of amphetamines, ephedrine, pseudoephedrine, flecainide, quinidine and quinine. Decreases effects of lithium, chlorpropamide
and salicylates due to increased clearance. May affect the absorption of certain drugs due to raised intra-gastric pH.
Click to view more Drug Interactions
Pregnancy Category (US FDA)

 c: Either studies in animals have revealed adverse effects on the foetus (teratogenic or embryocidal or other) and there are no controlled
studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk
to the foetus.
Mechanism of Action
For details of the mechanism of action, pharmacology and pharmacokinetics and toxicology ... click to view
MIMS Class
Antacids, Antireflux Agents & Antiulcerants / Other Drugs Acting on the Genito-Urinary System / Electrolytes
ATC Classification
B05CB04 - sodium bicarbonate; Belongs to the class of salt solutions used as irrigating solutions.
B05XA02 - sodium bicarbonate; Belongs to the class of electrolyte solutions used in I.V. solutions.