Congestive heart failure metformin

Under certain circumstances, and very rarely, the inhibition of gluconeogenesis by metformin may suppress lactic acid metabolism and precipitate a potentially fatal lactic acidosis. Impairment of renal function, liver disease, alcoholism, conditions that give rise to increased lactate production (e.g. congestive heart failure, infections) are therefore contraindications for the application of metformin. 

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. 

L A. Metformin causes lactic acidosis in patients with renal failure and severe congestive heart failure. It does not increase the risk of ketoacidosis and showed a reduction in cardiovascular comorbidities in a large study. It is contraindicated in patients with severe liver disease but does not cause hepatic necrosis. When used as monotherapy, metformin rarely causes hypoglycemia. 

Metformin Obscure Reduced hepatic and renal gluconeogenesis Decreased endogenous glucose production Type 2 diabetes Oral maximal plasma concentration in 2-3 h Toxicity Gastrointestinal symptoms, lactic acidosis (rare) cannot use if impaired renal/hepatic function congestive heart failure (CHF), hypoxic/acidotic states, alcoholism... 

Reconsideration of contraindications has also been proposed in a prospective study in patients with serum creatinine concentrations of 130-220 pmol/1 and coronary heart disease (n — 226), congestive heart failure (n = 94) and chronic obstructive pulmonary disease (n = 91). Half of the patients continued to take metformin and the other half stopped (39). Bodyweight and HbAic increased over 4 years in those who stopped taking metformin. Lactic acid concentrations were similar in the two groups. Deaths were similar in the two groups (62 and 64 respectively). The incidences of myocardial infarction, all cardiovascular events, and cardiovascular mortality were the same. Changes in additional therapy were only significant for insulin (30% versus 45% respectively) and diet (25% versus 0% respectively). 

The most important susceptibility factors are pre-existing chronic kidney disease (CKD eGFR below 60 mVmin) and chronic kidney disease associated with diabetes [15]. Other factors include age over 70 years, the presence of congestive heart failure, nephrotoxic drugs (loop diuretics, metformin, nonsteroidal anti-inflammatory agents), volume depletion, and repeated exposure within short periods of time (under 72 hours). 

Of 21 patients with lactic acidosis between 2001 and 2005,13 were taking metformin 18 had acute gastrointestinal problems and three had congestive heart failure [37 ]. None of the patients stopped taking metformin, despite having had several days of illness before... 

Urinary tract Contrast-induced nephrotoxicity has been reviewed in successive volumes of SEDA [SEDA-29, 575 SEDA-30, 535 SEDA-31, 731 SEDA-32, 846]. The EIDOS and DoTS descriptions of this reaction are shown in Figure 2. Susceptibility factors include age (over 70 years), drugs (nephrotoxic drugs, such as non-steroidal anti-inflammatory drugs metformin mannitol, and diuretics, particularly loop diuretics multiple repeat exposures to contrast media within 72 hours), and diseases (pre-existing renal insufflciency, particularly if it is associated with diabetes melli-tus, congestive heart failure, dehydration). There is also an increased risk in organ transplant recipients. 

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