Nausea metformin

Primary side effects associated with metformin therapy are gastrointestinal in nature, including decreased appetite, nausea, and diarrhea. These side effects can be minimized through slow titration of the dose and often subside within 2 weeks. Discontinuation because of side effects occurs in only 3% to 5% of patients. 

Metformin 1500-2000 mg by mouth daily in 2-3 divided doses15 Anorexia, nausea, vomiting, diarrhea, flatulence, lactic acidosis... 

Metformin, a biguanide derivative, can lower excessive blood glucose levels, provided that insulin is present Metformin does not stimulate insulin release. Glucose release from the liver is decreased, while peripheral uptake is enhanced. The danger of hypoglycemia apparently is not increased. Frequent adverse effects include anorexia, nausea, and diarrhea Overproduction of lactic acid (lactate acidosis, lethality 50%) is a rare, potentially fatal reactioa Metformin is used in combination with sulfony-lureas or by itself. It is contraindicated in renal insufficiency and should therefore be avoided in elderly patients. 

Metformin ER (1% to 5%) - Abdominal distention, abdominal pain, constipation, diarrhea, dizziness, dyspepsia/heartburn, flatulence, headache, nausea/vomiting, taste disturbance, upper respiratory tract infection. 

Sitagliptin is a selective dipeptidylpeptidase 4 (DPP-4) inhibitor which increases the active form of GLP-1 (glucagon-like-peptide-1) and GIP (glucose-dependent insulinotropic peptide). This enzyme-inhibiting drug is to be used either alone or in combination with metformin or a thiazolidinedione for control of type 2 diabetes mellitus. Adverse effects were as common with sitagliptin (whether used alone or with metformin or pioglitazone) as they were with placebo, except for nausea and common cold-like symptoms. 

Adverse gastrointestinal symptoms (nausea, vomiting, anorexia, metallic taste, abdominal discomfort, and diarrhea) occur in up to 20% of individuals taking metformin this can be minimized by starting at a low dose and slowly titrating the dose upward with food. Like phenformin, metformin can cause lactic acidosis, but its occurrence is rare except when renal failure, hypoxemia, or severe congestive heart failure is present or when coadministered with alcohol. Metformin is also contraindicated in persons with hepatic dysfunction, but it appears to be safe for use in the hepatic steatosis that often occurs with fatty infiltration of the liver in poorly controlled type II diabetics. 

The most common toxic effects of metformin are gastrointestinal (anorexia, nausea, vomiting, abdominal discomfort, and diarrhea), which occur in up to 20% of patients. They are dose-related, tend to occur at the onset of therapy, and are often transient. However, metformin may have to be discontinued in 3-5% of patients because of persistent diarrhea. Absorption of vitamin B12 appears to be reduced during long-term metformin therapy, and annual screening of serum vitamin B12 levels and red blood cell parameters has been encouraged by the manufacturer to determine the need for vitamin B12 injections. In the absence of hypoxia or renal or hepatic insufficiency, lactic acidosis is less common with metformin therapy than with phenformin therapy. 

In 82 children aged 10-16 years with type 2 diabetes, metformin lowered HbAic and fasting blood glucose compared with placebo (12). More patients who took placebo had to drop out because more medication was necessary. Most of the adverse events (abdominal pain, diarrhea, nausea, vomiting) occurred during metformin treatment. 

In a prospective, randomized, double-blind, placebo-con-trolled study for 24 weeks, 701 patients took nateglinide 120 mg before the three main meals, or metformin 500 mg tds, or the combination of the two, or placebo (20). The most frequent adverse effect was hypoglycemia, and it was most common in the combination group. There were no differences between those who took nateglinide only or metformin only and there were no episodes of serious hypoglycemia. Diarrhea was more frequent in those taking metformin or the combination, but infection, nausea, headache, and abdominal pain were comparable in the two groups. 

A 42-year-old man developed nausea and vomiting and felt suicidal. He had type 2 diabetes and was taking metformin (56). His blood lactate concentration was 8.9 mmol/1, bicarbonate 16 mmol/1, and pH 7.2. Severe hypotension required intensive care. The lactate concentration rose to 22 mmol/1 and the bicarbonate fell to 6.7 mmol/1 and the pH to 6.89. The metformin concentration was high at 191 mg/1. He survived, having been treated with intermittent hemodialysis. 

A 61-year-old woman developed a bradydysrhythmia after a cardiac arrest (57). Her lactate concentration was 18 mmol/1, pH 6.60, blood glucose 19 mmol/1, and creatinine 1136 pmol/1. She had a 5-year history of type 2 diabetes treated with glimepiride 3 mg/day and metformin 850 mg tds, and 4 months before admission had had a serum creatinine concentration of 1.1 mg/dl. In the few days before admission she had had abdominal pain, nausea, and a speech disorder. She was treated with hemodialysis, and 6 weeks later the creatinine was 0.54 mg/dl. Further information about events leading to the acute renal insufficiency was not given, but a diagnosis of metformin-associated lactic acidosis was made. 

In 43 patients with poorly controlled type 2 diabetes using insulin, the addition of metformin improved HbAic and reduced the dose of insulin (97). Seven patients in the metformin group and four in the placebo group had nausea nine versus four had diarrhea. 

The use of metformin in polycystic ovarian syndrome, which is often accompanied by insulin resistance or other aspects of the metabolic syndrome, has been systematically reviewed (101). Metformin was therapeutically less effective than weight loss. Adverse effects were nausea, vomiting, and gastrointestinal disturbances. 

A 79-year-old woman was admitted to hospital stupor-ose and unresponsive (143). She had taken metformin 850 mg bd for 14 days, during which time she complained of loss of appetite and consumed little starch. On that morning she had had nausea and dizziness. Her blood glucose was 2.0 mmol/1 and her serum potassium 3.3 mmol/1. A CT scan of the head was normal. 

A 52-year-old man with advanced HIV infection taking many medicines took metformin 500 mg bd for 6 days (146). He became increasingly unwell, with nausea, vomiting, abdominal pain, lethargy, and jaundice. His pH was 7.28 and lactic acid 15 mmol/1. Antiviral drugs and metformin were withdrawn, but he died after 30 hours. 

Exenatide (synthetic exendin-4, from the saliva from a lizard), which has a 53% overlap with glucagon-like peptide-1 and which also binds to the glucagon-like peptide-1 receptor, has been investigated in a placebo-controlled study for 28 days in 116 patients with type 2 diabetes in addition to a sulfonylurea or metformin (1). The most common adverse effects were nausea (mostly only in the first week) and mild to moderate hypoglycemia, for which no treatment was needed. 

Of 210 patients with type 2 diabetes, 179 completed a randomized study of the effects of five different doses (0.045, 0.225, 0.45, 0.6, and 0.75 mg) or metformin 100 mg bd for 12 weeks after a 4-week metformin run-in phase. The numbers of people who reported nausea and vomiting were small (4%) and comparable to the incidence with metformin (6%) (15). Careful upwards titration allows higher doses (2 mg/day) to be tolerated (2). 

In 336 patients with type 2 diabetes who took metformin, 36% of those who were randomized to exenatide 5 micrograms bd and 45% of those who took 10 micrograms bd had nausea compared with 23% of those who took placebo (6). The frequency of nausea fell during the study in all groups. 

If metformin alone does not control the HbAlc, then metformin and a sulfonylurea should be given. A thiazolidinedione can be substituted for either agent if unacceptable side effects occur, such as nausea or hypoglycaemia. A rapid-acting insulin secretagogue may be added for people with erratic lifestyles, as it can be given once daily. 

Abdominal discomfort is frequent with metformin (15-25%), and nausea, vomiting, and diarrhea occur even in the absence of lactic acidosis. Other effects include flatulence, abdominal bloating, anorexia, and a metallic taste. Anorexia and weight loss are often seen at the beginning of treatment. Phenformin can cause hemorrhagic gastritis (65). 

Metformin can cause adverse gastrointestinal effects with anorexia, nausea and vomiting. Patients may experience a metallic taste and there may be weight loss, which in some diabetics could be an advantage. Hypoglycaemia is less of a problem with metformin than with sulphonylureas. 

Acute side effects of metformin, which occur in up to 20% of patients, include diarrhea, abdominal discomfort, nausea, metallic taste, and anorexia. These usually can be minimized by increasing the dosage of the drug slowly and taking it with meals. Intestinal absorption of vitamin B12 and folate often is decreased during chronic metformin therapy, and calcium supplements reverse the effect of metformin on vitamin B12 absorption. 

Acute side effects of metformin occur in up to 20% ofpcdients and include diarrhea, abdominal discomfort, nausea, metallic taste, and anorexia. These usually can be minimized by increasing... 

Biguanides. Metformin acts peripherally to increase glucose uptake by an unknown mechanism.. As it does not increase insulin release, it rarely cau-scs hypoglycaemia. Adverse effects include nausea, vomiting, diarrhoea and. very (Kcasionally, fatal lactic acidosis. 

---