Adverse drug reactions (ADRs) are a major public health concern, particularly in hospitalized patients, and among these, cutaneous drug reactions are the most frequently observed manifestations. Drug-induced skin reactions (DISRs), also referred to as cutaneous adverse drug reactions (CADRs), are defined as undesirable changes in the skin, its appendages, or mucous membranes resulting from the intake of a medication [1]. These reactions can range from mild rashes and pruritus to severe and potentially fatal conditions such as Stevens-Johnson Syndrome (SJS), Toxic Epidermal Necrolysis (TEN), and Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) [2,3].

The reported incidence of DISRs varies widely, with studies indicating that approximately 2–3% of hospitalized patients experience some form of cutaneous drug reaction, while in outpatient settings the incidence may be lower but still clinically significant [4]. In India, where self-medication, polypharmacy, and over-the-counter drug use are common, the prevalence of these reactions may be underestimated due to underreporting and lack of awareness [5].

Various factors contribute to the development of DISRs, including genetic predisposition, age, gender, immune status, and the pharmacological profile of the drug used. The pathophysiology often involves immunological mechanisms such as Type I to Type IV hypersensitivity reactions, which manifest as urticaria, fixed drug eruptions, maculopapular rashes, or more serious conditions like SJS/TEN [6]. Some non-immunologic mechanisms, such as drug interactions, metabolic imbalances, and enzyme deficiencies (e.g., slow acetylator status), can also play a role [7].

Certain classes of drugs have been consistently implicated in a majority of DISRs. Among these, antibiotics—particularly beta-lactams, sulfonamides, and fluoroquinolones—are the most common culprits. Non-steroidal anti-inflammatory drugs (NSAIDs), antiepileptics (e.g., phenytoin, carbamazepine), antitubercular agents, and allopurinol also feature prominently in causative lists [8,9]. Identification of the offending drug is often challenging, especially in patients receiving multiple medications.

Early diagnosis and immediate cessation of the suspected drug are crucial to prevent progression of the reaction. Supportive care forms the mainstay of treatment in mild to moderate cases. In more severe reactions like SJS/TEN, intensive care, systemic corticosteroids, or immunosuppressive therapy may be warranted. The prognosis generally depends on the type and severity of the reaction, the patient’s general health, and the promptness of medical intervention [10].

Despite the clinical importance of DISRs, literature from Indian populations remains relatively sparse. There is a need for regional epidemiological data to better understand the pattern, prevalence, and management outcomes of such reactions in local healthcare settings. This prospective study was conducted to evaluate the incidence, clinical spectrum, suspected drug classes, latency period, and outcomes of drug-induced skin reactions in patients attending a tertiary care hospital over a period of one year.

Study Design

 This was a prospective observational study conducted to assess the incidence and management of drug-induced skin reactions (DISRs).

Study Setting

 The study was carried out in the Dermatology and General Medicine Departments of a tertiary care hospital over a period of 1 year.

Study Population

A total of 100 patients presenting with suspected drug-induced skin reactions were enrolled consecutively after fulfilling the inclusion and exclusion criteria.

Inclusion Criteria

• Patients of all age groupsand both genders.
• Patients presenting with new-onset cutaneous lesionssuspected to be due to drug intake.
• Patients who provided written informed consent.

Exclusion Criteria

• Patients with skin lesions caused by infections, autoimmune disorders, or other systemic diseases.
• Patients with pre-existing skin diseasesunrelated to drug intake.
• Incomplete data or refusal to give consent.

Ethical Considerations

The study was approved by the Institutional Ethics Committee. Informed written consent was obtained from each participant before inclusion in the study.

Data Collection

A pre-designed structured proforma was used to collect the following information:

• Demographic details(age, gender, occupation, etc.).
• Detailed drug historyincluding the name of the drug, dose, duration, and indication for use.
• Temporal relationshipbetween drug intake and onset of symptoms.
• Clinical examinationof skin lesions by a dermatologist.
• Past historyof similar episodes or any known drug allergies.

Diagnosis

The diagnosis of drug-induced skin reaction was based on:

• Temporal relationship between drug intake and onset of symptoms.
• Clinical pattern of the lesion.
• Exclusion of other possible causes.
• When required, skin biopsy, complete blood count, liver function tests, and renal function testswere performed.

Management Protocol

• Immediate withdrawalof the suspected offending drug(s).
• Symptomatic treatmentincluding:

• Oral or injectable antihistamines,
• Corticosteroids(topical or systemic depending on severity),
• Emollientsand skin care advice.
  • Patients with severe reactionssuch as Stevens-Johnson Syndrome (SJS)/Toxic Epidermal Necrolysis (TEN) were admitted and managed in coordination with internal medicine and critical care teams.

Follow-Up

Patients were followed up regularly until complete resolution of skin lesions or as required for complications.

Data Analysis

Collected data were entered into Microsoft Excel and analyzed using appropriate statistical tools. Results were expressed in terms of percentages, means, and standard deviations. Categorical data were compared using the Chi-square test. A p-value of <0.05 was considered statistically significant.

The present study included 100 patients with drug-induced skin reactions over a period of one year. The data were analyzed for demographic distribution, clinical pattern, suspected drugs, latency period, and outcome.

Table 1: Age and Gender Distribution of Patients

Mean Age: 38.6 ± 14.7 years

Sex Ratio (M:F): 1:1

Table 2: Clinical Patterns of Drug-Induced Skin Reactions

Table 3: Suspected Drug Classes Causing Reactions

Table 4: Latency Between Drug Intake and Skin Reaction

Table 5: Outcome Following Treatment

Drug-induced skin reactions (DISRs) are among the most frequently reported adverse drug reactions and present a significant clinical burden due to their varied manifestations, potential severity, and impact on patient quality of life and healthcare resources. In this prospective observational study involving 100 patients over a 1-year period, we attempted to evaluate the incidence, clinical spectrum, common culprit drugs, latency period, and outcomes associated with DISRs in a tertiary care center.

The overall incidence of cutaneous drug reactions in our hospital’s dermatology and medicine departments during the study period was notable, especially in patients receiving multiple drug therapies. This highlights the growing concern of polypharmacy, which is increasingly prevalent due to the rise in chronic diseases, especially in elderly patients. It also emphasizes the importance of rational drug prescription practices, careful drug histories, and heightened awareness among clinicians [1,2].

In our cohort, antibiotics were the most common causative group, with beta-lactams, fluoroquinolones, and sulfonamides being particularly prominent. This finding is in line with previous Indian and international studies, which consistently implicate antibiotics—especially penicillin and its derivatives—as leading agents in the etiology of DISRs [3,4]. The widespread and sometimes irrational use of antibiotics in clinical practice contributes to this trend. In rural and urban Indian settings alike, over-the-counter availability and self-medication further exacerbate this issue [5].

Nonsteroidal anti-inflammatory drugs (NSAIDs) were the second most frequently implicated class in our study. Drugs such as diclofenac, ibuprofen, and paracetamol were associated with urticarial reactions, fixed drug eruptions (FDEs), and maculopapular rashes. Similar observations were made by Nayak and Acharjya [6], who reported NSAIDs as a significant contributor to drug-induced skin reactions due to their widespread availability and use in managing fever, pain, and inflammation.

Another notable category was anticonvulsants, especially phenytoin, carbamazepine, and phenobarbital. These drugs were predominantly associated with DRESS syndrome and erythema multiforme-like lesions. These drugs are known for causing delayed hypersensitivity reactions, often involving Type IV immune mechanisms, and may also involve metabolic idiosyncrasies such as defects in the epoxide hydrolase enzyme pathway [7,8]. The latency period for these reactions was longer (1–3 weeks), supporting the theory of immune sensitization rather than direct toxicity.

Antitubercular therapy (ATT) was also observed to cause a considerable number of reactions, particularly isoniazid, rifampicin, and pyrazinamide. In India, where tuberculosis remains endemic and long-term ATT is common, this finding is clinically significant. The prolonged exposure and combination of multiple hepatotoxic and immunologically active agents in ATT regimens predispose patients to hypersensitivity and skin manifestations [9].

The most commonly observed clinical patterns in our study were maculopapular rashes (36%), followed by urticaria (22%), FDE (18%), erythema multiforme (8%), DRESS (6%), and SJS/TEN (6%). These findings are consistent with the general trend reported in literature, where morbilliform eruptions dominate the spectrum of DISRs [10]. Although SJS and TEN were relatively less frequent, they were associated with significant morbidity, prolonged hospital stay, and intensive management, underscoring the need for early recognition and prompt withdrawal of the offending drug [11].

The latency period observed in our study ranged from a few hours in cases of urticaria and anaphylaxis to several weeks in SCARs like DRESS and SJS/TEN. A significant observation was that early identification and withdrawal of the offending drug led to resolution in the majority of cases within 1–2 weeks, especially in non-severe presentations. In contrast, delayed diagnosis, polypharmacy, or continuation of the suspected drug contributed to worsening symptoms and longer recovery durations, reaffirming the need for pharmacovigilance and prompt clinical decision-making [12].

Management strategies in our study were based on severity. Most mild to moderate cases were managed with antihistamines, topical corticosteroids, and emollients. Severe cases, including SJS/TEN and DRESS, required systemic corticosteroids, intravenous fluids, electrolyte management, and ICU admission. Our experience echoes current literature, where systemic immunosuppressants like steroids or cyclosporine are used cautiously and judiciously, although their use remains controversial and should be individualized [13,14].

One of the major challenges encountered was establishing causality. Since rechallenge testing is unethical in most cases involving severe or life-threatening reactions, we relied on Naranjo’s algorithm and WHO-UMC criteria to establish probable or possible associations. While not definitive, these tools are widely accepted for their standardized approach [15].

Another limitation of our study was the lack of long-term follow-up. We could not track the recurrence of reactions upon re-exposure or confirm latent sensitizations. Furthermore, genetic factors, such as HLA-B*1502 association with carbamazepine-induced SJS in Southeast Asians, were not explored due to resource limitations. This opens avenues for future research into pharmacogenomics in adverse drug reactions, especially in genetically diverse populations like India [16].

Our findings underline the need for robust drug surveillance systems, electronic medical records with allergy alerts, and educational programs for healthcare professionals. Instituting hospital-based pharmacovigilance programs can help monitor trends, identify at-risk patients, and promote safer prescribing habits.

This study highlights the significant incidence of drug-induced skin reactions (DISRs) in a tertiary care setting, with antibiotics, NSAIDs, and anticonvulsants being the most common culprits. While most cases resolved with treatment, severe reactions like Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis require prompt intervention. Early recognition, cessation of the offending drug, and supportive care are crucial for positive outcomes. The study emphasizes the need for enhanced pharmacovigilance, awareness among healthcare providers, and further research into genetic factors to improve patient safety and management of DISRs.

1. Bigby M. Rates of cutaneous reactions to drugs. Arch Dermatol. 2001;137(6):765–770.
2. Roujeau JC, Stern RS. Severe adverse cutaneous reactions to drugs. N Engl J Med. 1994;331(19):1272–1285.
3. Sushma M, Noel MV, Ritika MC, James J, Guido S. Cutaneous adverse drug reactions: A 9-year study from a South Indian hospital. Pharmacoepidemiol Drug Saf. 2005;14(8):567–570.
4. Arulmani R, Rajendran SD, Suresh B. Adverse drug reaction monitoring in a secondary care hospital in South India. Br J Clin Pharmacol. 2008;65(2):210–216.
5. Sharma VK, Sethuraman G. Adverse cutaneous drug reactions. Indian J Dermatol Venereol Leprol. 2010;76(6):603–612.
6. Pichler WJ. Drug hypersensitivity reactions: classification and relationship to T-cell activation. Curr Opin Allergy Clin Immunol. 2002;2(4):301–305.
7. Rieder MJ. Mechanisms of adverse drug reactions in children. Clin Pharmacol Ther. 2008;84(4):558–560.
8. Nayak S, Acharjya B. Adverse cutaneous drug reaction. Indian J Dermatol. 2008;53(1):2–8.
9. Padmavathi S, Rao PN, Bhat RM. A study of 100 cases of adverse cutaneous drug reactions. Indian J Dermatol. 2012;57(2):118–121.
10. Sehgal VN, Srivastava G. Management of adverse cutaneous drug reactions. Int J Dermatol. 2006;45(7):757–768.
11. Patel RM, Marfatia YS. Clinical study of cutaneous drug eruptions in 200 patients. Indian J Dermatol Venereol Leprol. 2008;74(1):80.
12. George R, Kanish B. A study of adverse cutaneous drug reactions in a tertiary care hospital. J Clin Diagn Res. 2013;7(12):2747–2750.
13. Kardaun SH, Sidoroff A, Valeyrie-Allanore L, et al. Variability in the clinical pattern of SJS/TEN across Europe: a study of the RegiSCAR group. Br J Dermatol. 2007;156(5):911–917.
14. Bastuji-Garin S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau JC. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme. Arch Dermatol. 1993;129(1):92–96.
15. Naranjo CA, Busto U, Sellers EM, et al. A method for estimating the probability of adverse drug reactions. Clin Pharmacol Ther. 1981;30(2):239–245.
16. Chen P, Lin JJ, Lu CS, et al. Carbamazepine-induced toxic effects and HLA-B*1502 screening in Taiwan. N Engl J Med. 2011;364(12):1126–1133.