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Clindamycin induced Cutaneous Drug Reaction – A Case Report

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Clindamycin induced Cutaneous Drug Reaction A Case Report
Kirti Vishwakarma1, Imtiyaz Ahmad Shah1
1Department of Pharmacology, Teerthanker Mahaveer Medical college and Research Centre, Moradabad, India.
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Case Report
International Archives of BioMedical and Clinical Research | Jan-Mar 2016 | Vol 2 | Issue 1
INTRODUCTION ______________________________________________________
Antibiotics are one of the most commonly used agents to
treat various kind of infections. Adverse drug reactions
(ADRs) caused by these agents is one of the major concern.
Among all ADRs 75-80% are classified into type-A
(predictable) whereas 20-25% as type-B (unpredictable).
Unpredictable ADRs may be of immediate or delayed type
that occur in susceptible individuals. Immediate reactions are
usually IgE-mediated whereas delayed reactions are usually
non-IgE or T-cell mediated.[1,2] Clinically these ADRs could
be cutaneous (e.g., maculopapular rashes, erythroderma,
exfoliative dermatitis and fixed drug reactions), organ-
specific (e.g., blood dyscracias, hepatitis, interstitial
nephritis), systemic (e.g., anaphylaxis, drug induced
hypersensitivity syndrome) or various combinations of these.
Severe cutaneous ADRs such as Stevens Johnson Syndrome
(SJS), Toxic Epidermal Necrolysis (TEN) and Acute
Generalized Exanthematous Pustulosis (AGEP) could be life-
threatening.[1,3] Beta-lactam antibiotics were found to be the
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Received: 10.03.16 | Revised: 14.03.16 | Accepted: 15.03.16
*Correspondence to: Dr. Kirti vishwakarma
Assistant Professor, Department of Pharmacology,
Teerthanker Mahaveer Medical college and Research
Centre, Moradabad, India
E-mail: drkirtivishwakarma@gmail.com
ABSTRACT
Adverse drug reactions (ADRs) due to antibiotics is one of the major concern. Hypersensitivity reactions
with clindamycin may be immediate or delayed type, but their frequency and severity are relatively rare.
We here report a case of a 32-year-old male patient with road traffic accident, who later developed
osteomyelitis of occipital bone. After two weeks of therapy and debridement, the patient was on
maintenance therapy receiving clindamycin 300 mg q8h, ciprofloxacin 500 mg q12 h and rifampicin 450mg
fasting. After six days, he developed erythematous maculopapular rashes, initially on the trunk followed
by neck and arm of both upper limbs with limitation of movement, fever, chills and night sweats. The
reaction subsided after withdrawal of clindamycin and administering i.v. hydrocortisone 100mg stat
followed by tablet promethazine 25mg 12hourly for 3 days. The causality assessment was done as per
WHO-UMC scale and it was “probable” in this case. Although the incidence of clindamycin induced drug
reaction is rare, the clinicians should be aware of such reactions before prescribing it.
Keywords: Clindamycin, Cutaneous Drug Reaction, Adverse Drug Reactions.
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Vishwakarma K, et al.: Clindamycin induced Cutaneous Drug Reaction
International Archives of BioMedical and Clinical Research | Jan-Mar 2016 | Vol 2 | Issue 1
commonest cause of these ADRs. A special committee on
drug allergy of the world allergy organization (WAO)
presented the most relevant information about the
hypersensitivity reactions due to other antibiotics also and it
was found that they are relatively frequent.
Hypersensitivity reactions with clindamycin may be
immediate or delayed type, but their frequency and severity
are relatively rare. Clindamycin was mostly found to cause
exanthematous eruptions, however other reactions that has
been reported are anaphylactic shock; urticarial; angioedema;
fixed drug eruptions; bullous eruptions; Acute Generalised
Exanthematous Pustulosis (AGEP); Sweet’s Syndrome;
Stevens Johnsons Syndrome (SJS); Drug-induced
Hypersensitivity Syndrome (DIHS)/Drug Rash with
Eosinophilia and Systemic Symptoms (DRESS) and TEN. We
report here a case of Cutaneous Drug reaction caused by
Clindamycin.
CASE REPORT
One month back, a 32-year-old male patient was admitted
confronting with a road traffic accident soon followed by
transient loss of consciousness, occipital headache, and
dizziness with lacerated wound on left side of back of skull.
Depressed fracture of occipital bone of left side of skull was
treated surgically with open drainage and received oral
antibiotic therapy with cefpodoxime 200mg 12hourly and
linezolid 600mg 12hourly. 15 days after the surgery, he
developed wound infection and received antibiotic and
surgical debridement. Due to the persistent wound discharge,
infectious disease specialist consultation was requested and
osteomyelitis of occipital bone was suggested. A CT scan of
his brain showed depressed bone fracture with underlying
haemorrhagic contusion of left occipital lobe. Past medical
and drug history was negative. Other findings were
normochromic-normocytic anaemia, negative CRP, increased
WBC count and an elevated ESR equal to 50 mm/h. In wound
culture, the methicillin-sensitive Staphylococcus aureus was
grown.
Considering all clinical and paraclinical evidences compatible
with osteomyelitis, intravenous (IV) 1 g of ceftriaxone 12
hourly plus 500 mg of oral ciprofloxacin 12 hourly daily and
rifampicin 450mg fasting begun and the patient was
transferred to the infectious ward. The debridement of
infected soft tissues and bone was performed through a
neurosurgeon. After two weeks of intravenous antibiotic
therapy, wound discharge was stopped and the patient was
released from the hospital with the maintenance, oral
antibiotic therapy including clindamycin 300 mg q8h,
ciprofloxacin 500 mg q12 h and rifampicin 450mg fasting.
After six days, the patient developed erythema,
maculopapular rashes, initially on the trunk followed by neck
and arm of both upper limbs with limitation of movement,
fever, chills, night sweats. Physical examination were normal.
The laboratory findings were as following: ESR: 31 mm/h,
CRP: +1, Wright and Coombs Wright tests, rheumatoid factor
and anti CCP were negative and uric acid was 4.5. BUN, Cr
and U/A were normal. Patient was immediately given
intravenous hydrocortisone 100mg stat followed by tablet
promethazine 25mg 12hourly for 3 days.
After discontinuing treatment with clindamycin rashes
improved and a triple therapy with ciprofloxacin 500mg BD,
linezolid 600mg BD and rifampicin 450mg TDS was given
for 3 weeks. In follow-up visits, the wound was normal and
the patient had no problem after 3 months.
However, on the 4th post-operative day, the patient became
drowsy and developed weakness of the left side of the body.
Figure 1. Maculopapular rashes on the trunk.
Figure 2. Maculopapular rashes on arm of both upper
limbs.
DISCUSSION
Clindamycin is a lincosamide antibiotic that inhibits
bacterial protein synthesis. It is approved for the treatment
of anaerobic, streptococcal and staphylococcal infections. It
was found that clindamycin shows prompt clinical and
bacteriologic response. It has excellent tissue as well as bone
penetration. Thus, there is increasing use of clindamycin in
clinical practice to treat infections. In spite of the increased
use of this antibiotic, the adverse reactions are minor. Rash
is the only cutaneous adverse reaction that has been reported
so far with an incidence of <1%.[5] Recently, a rare adverse
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Vishwakarma K, et al.: Clindamycin induced Cutaneous Drug Reaction
International Archives of BioMedical and Clinical Research | Jan-Mar 2016 | Vol 2 | Issue 1
reaction of wrist monoarthritis occurred due to
clindamycin.[6]
In our case, we found erythematous maculopapular rash
associated with fever and chills causing hospitalization of
the patient six days after initiating clindamycin therapy. The
patient had no previous history of any kind of allergy or drug
reactions. The most common presentation for clindamycin
allergy is a delayed maculopapular exanthema which usually
occurs after 7-10 days of initiation of drug therapy.[2] In our
case the patient presented with rash initially on the trunk
followed by neck and arm of both upper limbs with
limitation of movement, fever, chills, night sweats. A similar
case was seen where the patient presented with rash on
antecubital fossa, neck, abdomen, thighs, legs and face after
10 days of clindamycin therapy along with methyl-
prednisolone and was diagnosed with DRESS syndrome.[7]
Our case did not have DRESS syndrome as his general
physical examinations were normal, there was no systemic
involvement and his laboratory values were within normal
limits. The administration of systemic corticosteroids is the
standard therapy for this condition, but it may be susceptible
to cause infections.
Several tests are there to confirm the causative agent. These
are skin prick test, intradermal test, patch test or oral
rechallenge test. Of these, skin prick test, intradermal test,
have not found to be effective for the diagnosis of
clindamycin induced drug reaction. Patch test with
clindamycin showed maximum result.[4] However, we could
not perform any of these tests to confirm the causative agent.
In our case the patient recovered after withdrawing of
clindamycin from the therapy and causality assessment as
per WHO-UMC, scale was “probable” in this case.
CONCLUSION
Although the incidence of clindamycin induced drug reaction
is rare, but it has the propensity to cause serious life
threatening conditions. Thus, the clinicians should be aware
of such reactions before prescribing Clindamycin.
REFERENCES
1. Bernard Yu-Hor Thong. Update on the Management of
Antibiotic Allergy. Allergy Asthma Immunol Res. 2010
April;2(2):77-86.
2.Johansson SG, Bieber T, Dahl R, Friedmann PS, Lanier
BQ, Lockey RF, Motala C, Ortega Martell JA, Platts-
Mills TA, Ring J, Thien F, Van Cauwenberge P, Williams
HC. Revised nomenclature for allergy for global use:
Report of the Nomenclature Review Committee of the
World Allergy Organization, October 2003. J Allergy
Clin Immunol 2004;113:832-6.
3. Nayak S, Acharjya B. Adverse Cutaneous Drug Reaction.
Indian J Dermatol. 2008 Jan-Mar; 53(1): 2-8.
4. Sanchez-Borges et al.; Hypersensitivity reactions to non
beta-lactam antimicrobial agents, a statement of the WAO
special committee on drug allergy. World Allergy
organization Journal 2013, 6:18.
5. Thanusubramanian H, Chogtu B, Magazine R. Adverse
reaction due to Clindamycin. Asian J Pharm Clin Res, Vol
9, Issue 2, 2016, 8-9.
6. Alikhania A and Salehifarb E. Unreported Clindamycin
Adverse Reaction: Wrist Monoarthritis. Iranian Journal of
Pharmaceutical Research (2012), 11 (3): 959-62.
7. 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.
How to cite this article: Vishwakarma K, Shah IA.
Clindamycin induced Cutaneous Drug Reaction – A Case
Report. Int Arch BioMed Clin Res. 2016 Mar;2(1):40-42
Source of Support: Nil, Conflict of Interest: None declared
What this study adds
1. What is known about this subject?
Hypersensitivity reactions with clindamycin may
be immediate or delayed type, but their frequency
and severity are relatively rare. Among them
exanthematous eruptions are the mostly commonly
found reaction due to clindamycin.
2. What new information is offered in this
study?
Adverse drug reactions (ADRs) due to antibiotics
is one of the major concern. Although the
incidence is rare, but the clinicians should be aware
of such reactions before prescribing Clindamycin.
... 6 Outside of the setting of IM, there have also been reports of clindamycin-induced AISEs in the setting of osteomyelitis and erysipelas. 7,8 There have been rare reports of Stevens-Johnson's syndrome and acute generalized exanthematous pustulosis caused by clindamycin. 3 ...
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Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization
  • S G Johansson
  • T Bieber
  • R Dahl
  • P S Friedmann
  • B Q Lanier
  • R F Lockey
  • C Motala
  • Ortega Martell
  • J A Plattsmills
  • T A Ring
  • J Thien
  • F Van Cauwenberge
  • P Williams
Johansson SG, Bieber T, Dahl R, Friedmann PS, Lanier BQ, Lockey RF, Motala C, Ortega Martell JA, PlattsMills TA, Ring J, Thien F, Van Cauwenberge P, Williams HC. Revised nomenclature for allergy for global use: Report of the Nomenclature Review Committee of the World Allergy Organization, October 2003. J Allergy Clin Immunol 2004;113:832-6.