Rashes clindamycin

Nausea vomiting diarrhea (clindamycin 3.4% to 30%) pseudomembranous colitis (clindamycin 0.01% to 10% 3 to 4 times more frequent with oral administration) neutropenia (sometimes transient) leukopenia agranulocytosis thrombocytopenic purpura skin rashes, urticaria, erythema multiforme anaphylaxis jaundice liver function test abnormalities (serum transaminase elevations). 

Clindamycin can be administered orally with a high bioavailability. Also formulations for intravenous administration exist. Protein binding is about 90%. It is distributed throughout the body except the CNS. It shows excellent penetration in bone and in empyema and abscesses. It is metabolized in the liver and excreted in the bile. The elimination half-life is about 3 h. Adverse effects include gastrointestinal distress, skin rashes and decreased liver function. Pseudomembranous colitis is relatively frequently seen due to resistance of Clostridium difficile. 

Common adverse effects are diarrhea, nausea, and skin rashes. Impaired liver function (with or without jaundice) and neutropenia sometimes occur. Severe diarrhea and enterocolitis have followed clindamycin administration. Administration of clindamycin is a risk factor for diarrhea and colitis due to Clostridium difficile. 

A 5-year-old child with diabetes, Pierre Robin syndrome, cleft palate, allergic rhinitis, recurrent sinusitis, and obstructive sleep apnea, who had previously had skin rashes after penicillin, sulfonamides, and clindamycin, was given soluble and isophane human insulins (131). Three years later she developed local reactions, 2-5 cm areas, 30-120 minutes after injection. Skin-prick tests were negative for the diluent, isophane, and soluble insulin, but intradermal testing was positive with both insulins. Cetirizine and dexamethasone added to the insulin gave temporary relief. She was... 

Common adverse effects are diarrhea, nausea, and skin rashes. Impaired liver function (with or without jaundice) and neutropenia sometimes occur. Severe diarrhea and enterocolitis have followed clindamycin administration. Antibiotic-associated colitis that has followed administration of clindamycin and other drugs is caused by toxigenic C difficile. This potentially fatal complication must be recognized promptly and treated with metronidazole, 500 mg orally or intravenously three times a day (the preferred therapy), or vancomycin, 125 mg orally four times a day (less desirable given the increasing prevalence of vancomycin-resistant enterococci). Relapse may occur. 

A 44-year-old HIV-1 infected woman from the Ivory Coast, who was taking stavudine, lamivudine, efavirenz, and pyrimethamine plus sulfadiazine for Toxoplasma encephalitis, developed a maculopapular rash on both arms. The sulfadiazine was withdrawn and clindamycin was added. Ten days later her condition had worsened. Her temperature was 40 C, pulse rate 137/minute, and respiratory rate 26/minute. She had a generalized maculopapular rash without mucosal involvement, moderate abdominal tenderness, hepatomegaly, jaundice, and bilateral crackles. Her white cell count was 16 x 10 /1 with 9% eosinophils and 51% lymphocytes. A chest X-ray showed moderate bilateral interstitial pneumonitis. All drugs were withdrawn and she was given intravenous methylprednisolone. The skin rash and aU systemic manifestations resolved within 1 week and HIV treatment was restarted uneventfully with lamivudine, stavudine, and nehinavir. 

In a multicenter, double-blind, randomized trial in 87 patients, clindamycin + primaquine was compared with co-trimoxazole as therapy for AIDS-related Pneumocystis jiroveci pneumonia efficacy was similar. In patients with a Pa02 under 70 mmHg, clindamycin + primaquine was associated with fewer adverse events and less glucocorticoid use, but more rashes (2). 

A 57-year-old Caucasian woman with a history of ocular toxoplasmosis, treated with intravitreal clindamycin (1 mg/0.1 ml) and dexamethasone (0.4 mg/0.1 ml), developed a generalized eiythematous macular rash over the scalp, face, arms, thighs, and trunk 2 days after the start of treatment (37). 

Successful desensitization has been described in a 35-year-old woman who developed a generalized rash after taking clindamycin (600 mg 6-hourly) and pyrimethamine for 12 days for AIDS-associated cerebral toxoplasmosis the rash resolved after withdrawal of clindamycin (44). Subsequent oral rechallenge was performed (without pretreatment with glucocorticoids or antihistamines), starting with three doses of 20 mg on day 1, 40 mg on day 2, 80 mg on day 3, and so on, until a dose of 600 mg qds was reached on day 7. A transient rash lasting 5 hours developed after the second dose of... 

Pyrimethamine 50 mg/day has been nsed in combination with clindamycin for the treatment of Toxoplasma encephalitis in AIDS. Adverse effects were common (rash, diarrhea, nansea), bnt the incidence of hematological reactions was lower than with the combination of snlfadiazine and pyrimethamine (SEDA-16, 309). 

MB is a 39-year-old man who is diagnosed with cellulitis. Since he has an allergy to penicillins (urticarial rash), he is prescribed clindamycin for 10 days. Nine days into therapy he develops diarrhea. A stool culture detects C difTidk toxin. What is the best treatment for MB s diarrhea ... 

Vancomycin hydrochloride is always administered intravenously (never intramuscularly), either by slow injection or hy continuous infusion, for the treatment of systemic infections. In shott-term therapy, the toxic side reactions arc usually slight, hut continued u.sc may lead to impaired auditory acuity, renal damage, phlebitis, and rashes. Bccau.se it is nut assorted or signilicantly degraded in the gastrointc.stinal tract, vancomycin may he administered orally fur the treatment of staphylococcal enterocolitis and for pseudomembranous colitis associated with clindamycin therapy. Some conversion to aglucovancomycin likely (Kcurs in the low pH of the stomach. The latter retains about three-fourths of the activity of vancomycin. 

Skin rashes occur in approximately 10% of patients treated with clindamycin, and may be more common in patients with HIV infection. Other reactions, which are uncommon, include exudative erythema multiforme (Stevens-Johnson syndrome), reversible elevation of aspartate aminotransferase and alanine aminotransferase, granulocytopenia, thrombocytopenia, and anaphylactic reactions. Local thrombophlebitis may follow intravenous administration of the drug. Clindamycin can inhibit neuromuscular transmission and may potentiate the effect of a neuromuscular blocking agent administered concurrently. 

The occurrence of anaphylactic shock (Lochmann et al. 1977), acute urticaria, and angioedema (Walker 1969) have been reported and postulated to be hypersensitivity reactions. In addition, other cutaneous reactions such as rashes (Geddes et al. 1970 Maulide and Villar 1974), and the Stevens-Johnson syndrome (Fulghum and Catalano 1973 Maulide and Villar 1974) have been described, but their etiology has not been defined. However, allergic contact dermatitis due to clindamycin therapy has been observed in two patients (Coskey 1978 Herstoff 1978). 

Skin A 25-year-old man developed a drug rash with eosinophilia and systemic symptoms (DRESS) associated with clindamycin the symptoms responded promptly to prednisolone [65 ]. 

The safety of continuous intravenous infusion of clindamycin has been evaluated retrospectively in 70 patients with bone and joint infections who were treated with a median daily dose of 2400 mg for a median of 40 days [67 ]. Three developed moderate adverse events an allergic rash, diarrhea not related to Clostridium difficile, and a cytolytic hepatitis, all of which resolved on drag withdrawal. Continuous intravenous infusion of clindamycin may be suitable for parenteral treatment in out-patients. 

Tian D, Mohan RJ, Stallings G. Drug rash with eosinophilia and systemic symptoms syndrome associated with clindamycin. Am J Med 2010 123(11) e7-8. 

Delayed-type cutaneous reactions to clindamycin include pruritus, exanthematous rash, generalized maculopapular exanthema, erythroderma, generalized exanthematous pustulosis, and Stevens-Johnson syndrome. 

Observational studies In a retrospective study in 70 patients with bone and joint infections, prolonged, continuous, intravenous clindamycin therapy (600 mg as a loading dose infused over 60 minutes, followed immediately by a continuous infusion of 30-40 mg/kg/day) one patient developed cytolytic hepatitis and one had an allergic rash, both resolved after clindamycin withdrawal [llO ]. 

A 47-year-old man with a history of rash to cephalexin was treated for erysipelas with clindamycin. His condition did not improve on clindamycin, so it was discontinued and he was initiated on ertapenem. After 2 days of ertapenem treatment, he developed fever, a generalised rash and neufrophilia of 28 x fi cells/L (7.1 x 10 cells/L the day before). All other laboratory values, cultures and chest X-rays were normal. He was diagnosed with acute generalised exanthematous pustulosis (AGEP). Patch tests were posihve for penicillin, cephalothin, meropenem and ertapenem at 48 h. Per the autiiors, this was the first reported cause of carbapenem-induced AGEP confirmed by patch testing [79 ]. 

A single case of DRESS S5mdrome was reported in a 63-year-old lady treated for an metiiidllin sensitive S. aureus infection with clindamycin for 4 days. This unfortunately progressed rapidly and led to death [88 ]. A 34-year-old female developed a hypersensitivity syndrome following 23 days of treatment with clindamycin (900 mg per day). The reaction consisted of a skin rash, fever, facial erythema and oedema [89 ]. 

---