Clindamycin

Clindamycin belongs to the lincosamide family. It binds reversibly to the 50S subunit of the bacterial ribosome, specifically at the 23S ribosomal RNA. There it prevents the formation of the peptide bond, the step that assembles amino acids into proteins. Deprived of this machinery, the bacterium no longer produces its proteins and stops growing.

Its action is mainly bacteriostatic: it blocks the multiplication of bacteria rather than destroying them, although high concentrations can be slowly bactericidal against susceptible strains. This binding site is the same as that of macrolides such as erythromycin and of streptogramin B. This shared target explains so-called MLSB cross-resistance, where a bacterium resistant to one of these antibiotics may also be resistant to clindamycin.

Clindamycin treats serious bacterial infections caused by susceptible organisms: staphylococci, whether or not they produce penicillinase, streptococci, pneumococci and anaerobic bacteria. It is described in bone and joint, intra-abdominal and gynaecological infections, in lower respiratory infections, and in skin and soft tissue infections. The choice rests with the physician, according to the organism involved.

Taken by mouth, clindamycin is absorbed rapidly and almost completely, with a bioavailability of about 90 per cent and a serum peak reached around 60 minutes. Its plasma half-life is roughly 2 to 3 hours in adults. This half-life can lengthen in the very preterm infant and in severe renal impairment, two situations in which elimination of the drug is slower.

Oral clindamycin is most often taken three to four times a day, at regular intervals through the day. The capsule is swallowed whole, without opening or crushing it, with a large glass of water of about 180 to 240 mL. It is best taken at least 30 minutes before lying down: a capsule that lingers in the oesophagus can irritate it and even cause an ulcer there.

Taking food does not appreciably change the amount of drug absorbed: a meal may only slow the rate of absorption. Clindamycin is therefore taken with or without food, and the patient keeps their usual diet unless the physician advises otherwise. The antibiotic is continued until the end point set by the physician, without stopping it on one’s own initiative even when symptoms improve.

The most common side effects are digestive. Diarrhoea and abdominal pain occur in at least 1 person in 100 and fewer than 1 in 10. Nausea and vomiting are uncommon, between 1 case in 1,000 and 1 in 100. These disturbances often accompany the passage of the antibiotic through the digestive tract.

More rarely, between 1 case in 10,000 and 1 in 1,000, oesophagitis or an oesophageal ulcer appears. A maculopapular rash or urticaria may also occur. The risk of oesophageal injury justifies the instruction to swallow the capsule with plenty of water and to remain sitting or standing for a while after taking it. A rash that spreads or comes with other signs should lead to a consultation.

Like any antibiotic, clindamycin does not reach only the targeted bacterium: it also affects part of the flora of the large intestine. This imbalance can let dangerous bacteria proliferate, in particular Clostridioides difficile, and cause diarrhoea that can go as far as life-threatening colitis. This colitis can occur during treatment, but also up to about two months after it is stopped.

Clindamycin is among the antibiotics most associated with this risk, alongside penicillins, cephalosporins and fluoroquinolones. Copious, watery or bloody diarrhoea, during or after treatment, warrants prompt medical advice. The gut flora renders other services to the body: its bacteria produce vitamin K2, one of the two forms of vitamin K, with vitamin K1 coming mainly from leafy green vegetables.

Clindamycin is metabolised mainly by the enzyme CYP3A4, and to a lesser extent by CYP3A5. Drugs that inhibit these enzymes raise its concentrations in the blood, while inducers such as rifampicin lower them. It also has neuromuscular blocking properties that can strengthen the action of curare-type agents, which calls for caution and monitoring when they are combined.

In patients treated at the same time with a vitamin K antagonist, such as warfarin, acenocoumarol or fluindione, increases in coagulation tests (PT and INR) and bleeding have been reported. These tests must therefore be monitored frequently during the combination. Medical follow-up accompanies the treatment from beginning to end, from the choice of dose to vigilance over digestive signs.