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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 7  |  Issue : 1  |  Page : 36-39

Lichenoid drug eruption due to isoniazid presenting as generalized exfoliative dermatitis in an immunocompromised patient


Department of Dermatology and Pathology, Armed Forces Medical College, Pune, Maharashtra, India

Date of Submission15-Apr-2020
Date of Decision20-Nov-2020
Date of Acceptance11-Jan-2021
Date of Web Publication25-Jun-2021

Correspondence Address:
Preema Sinha
Department of Dermatology and Pathology, Armed Forces Medical College, Pune - 411 040, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijdd.ijdd_22_20

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  Abstract 


Lichenoid drug eruption is characterized by multiple discrete violaceous shiny papules often becoming confluent. It is a common benign adverse drug reaction and has been extensively described in the literature with various drugs. Here, we report an unusual presentation of lichenoid drug eruption in the form of generalized exfoliative dermatitis with hair loss in a patient of human immunodeficiency virus infection due to isoniazid.

Keywords: Exfoliative dermatitis, isoniazid, lichenoid drug eruption


How to cite this article:
Sinha P, Bhatt S, Kinra P, Radhakrishnan S, Awasthi S. Lichenoid drug eruption due to isoniazid presenting as generalized exfoliative dermatitis in an immunocompromised patient. Indian J Drugs Dermatol 2021;7:36-9

How to cite this URL:
Sinha P, Bhatt S, Kinra P, Radhakrishnan S, Awasthi S. Lichenoid drug eruption due to isoniazid presenting as generalized exfoliative dermatitis in an immunocompromised patient. Indian J Drugs Dermatol [serial online] 2021 [cited 2021 Dec 2];7:36-9. Available from: https://www.ijdd.in/text.asp?2021/7/1/36/319350




  Introduction Top


Patients with human immunodeficiency virus (HIV) infections are at an increased risk of adverse drug reactions (ADRs) as compared to the normal population; however, due to polypharmacy in HIV patients, it is often difficult to pinpoint the exact offending agent. The diagnosis becomes even more challenging for ADR like lichenoid drug eruption which inherently has the variable latency of onset from the starting of the offending drug ranging from weeks to years.[1] Because of such confusion, the treating physician often ends up stopping many of the prescribed drugs all at once endangering the patients to other grave implications such as treatment failure and drug resistance.

Lichenoid drug eruption is a common benign ADR associated with various drugs such as antimalarials, nonsteroidal anti-inflammatory drugs, thiazide diuretics, penicillamine, and mercury amalgams.[1] However, lichenoid drug eruptions leading to generalized exfoliative dermatitis have been infrequently described making its diagnosis difficult.[2],[3],[4],[5],[6] Herein, we report the case of an HIV-positive female who developed drug-induced lichenoid drug reaction manifesting as generalized exfoliative dermatitis 5 months after the initiation of isoniazid prophylactic therapy (IPT) for latent tuberculosis.


  Case Report Top


A 32-year-old female a known case of HIV infection on antiretroviral therapy (zidovudine, lamivudine, and efavirenz) for the past 2 years was started on tablet isoniazid (INH) for latent tuberculosis 6 months back. Five months after the initiation of the drug, she started developing scaly lesions over her trunk and arms which later progressed to involve the entire body (90%) in the form of diffuse scaling associated with itching, severe enough to disturb her sleep. She also complained of flaking and diffuse hair loss from the scalp leading to about a 50% reduction in the hair density.

Examination revealed generalized involvement of the entire body in the form of diffuse scaling with relative sparing of the face and flexures. Diffuse scaling of the scalp along with diffuse alopecia was present [Figure 1] and [Figure 2]. No involvement of nails, palms, and soles or oral mucosa was noted. No significant lymphadenopathy or hepatosplenomegaly was present.
Figure 1: (a) Generalized scaling involving the neck and back. (b) Diffuse scaling along with the loss of hair seen over the scalp

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Figure 2: (a) Diffuse scaling noted over both upper limbs with relative sparing of the flexures and palms. (b) Diffuse scaling with hyperpigmentation noted over both forearms

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All hematological and biochemical parameters were within the normal limits. A skin biopsy was taken from a representative lesion which showed hyperkeratosis, parakeratosis, and acanthosis in the epidermis. Dermis shows perivascular inflammatory infiltrate consisting of eosinophils, neutrophils, and lymphocytes with numerous melanophages and widespread vacuolar alteration of the basal layer of the epidermis. Few colloid bodies were noted [Figure 3] and [Figure 4].
Figure 3: ×100 (H and E) Epidermis shows hyperkeratosis, parakeratosis, and acanthosis. Dermis shows perivascular inflammatory infiltrate consisting of eosinophils, neutrophils, and lymphocytes with numerous melanophages and widespread vacuolar alteration of the basal layer of the epidermis

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Figure 4: ×400 (H and E) (a) Few colloid bodies were noted (red arrow). (b) Eosinophils are seen in the dermis (black arrows)

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Based on the clinical and histopathological findings, the patient was managed as a case of drug-induced lichenoid eruption most likely due to INH (Naranjo's score: 5). The offending drug was stopped, and she was exhibited tablet prednisolone 30 mg (0.75 mg/kg) at tapering doses along with antihistaminics and topical emollients. The patient responded favorably to the treatment in the form of complete resolution of the lesions within 3 weeks of initiation of the therapy [Figure 5].
Figure 5: Marked resolution of lesions over both forearms

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  Discussion Top


INH is widely used in the management of tuberculosis as a first-line drug in anti-tubercular therapy (ATT) and as IPT in latent tuberculosis. Various types of cutaneous drug reactions reported due to INH include urticaria, purpura, lupus erythematosus-like syndrome, photosensitive lichenoid eruptions, lichenoid drug reaction, Steven-Johnson syndrome, and rarely exfoliative dermatitis.[2]

The recent National AIDS Control Organization (NACO) guidelines recommend the administration of IPT in all freshly diagnosed individuals of HIV for 6 months based on a preliminary screening for active tuberculosis by evaluating just for the four symptoms, namely cough, night time fever, night time sweat, and weight loss.

In such a scenario, there is a huge load of freshly detected individuals of HIV who are being administered INH. Patients with HIV infection are a hundred times more susceptible than the normal population in developing ADRs as well they are subject to polypharmacy for various ailments further predisposing them to drug-related side effects.[6] ATT drugs are the most implicated group of drugs for causing ADRs in cases of HIV patients (28.3%).[7],[8] Inadvertent interruption and change in antitubercular therapy due to ADRs adversely affect the treatment leading to the development of drug resistance, treatment failure, relapse, and the increase in the transmission of disease.

Etiopathogenesis of increased ADR in HIV patients is mostly unknown, but reactivation of certain viruses, immunedysregulation in form of decreased Th1 cytokines, and increased Th2 cytokines leading to polyclonal B-cell expansion are a few proposed hypotheses. Interestingly, the role of cytotoxic CD8 T-cells in lichenoid drug reactions has been demonstrated.[1] CD8 cells >460/mm3 are an independent risk factor for the development of ADRs in HIV patients.[9] Other risk factors that have been implicated for the development of ADRs in HIV patients include polypharmacy, glutathione deficiency, slow acetylator status, latent cytomegalovirus and Epstein–Barr virus infections, and CD4+ T-cell counts of <25 cells/mm3.[1],[7],[8]

Lichenoid drug eruptions can present after a latency period of weeks, months to even years after the initiation of the offending drug. This variable and protracted latency often makes the diagnosis of the offending agent difficult, especially in cases of HIV where polypharmacy is a rule. Drug-induced erythroderma while being a distinctive entity has been characteristically described in the literature to have an acute onset, mucosal involvement, and histopathology revealing epidermal necrosis with lymphocytic infiltration.[1] Whereas, lichenoid drug eruptions normally present as purple itchy papules soon becoming confluent with continued exposure of the drug. However, progression to erythroderma has been rarely described in the literature. This makes the diagnosis of the condition in such patients difficult.

A literature review revealed a similar case by Thakur et al. in a patient with HIV who developed exfoliative dermatitis 4 months after the initiation of ATT.[2] Histopathology had revealed lichenoid morphology, and the patient was managed by stopping INH and treating with dexamethasone.

Garg et al. reported a 63-year-old individual with drug-induced erythroderma along with hair loss which developed 8 weeks after the initiation of ATT. Here, the diagnosis of INH being the culprit agent was clinched by sequential rechallenge of the drugs starting with ethambutol, pyrazinamide followed by rifampicin. INH was introduced at the last and resulted in similar lesions within 48 h of the administration.[9]

Various other case reports of lichenoid erythroderma with ATT are present but in them, a single offending agent could not be pinpointed. Lehloenya et al. reported a similar case of erythroderma in a patient of HIV, three months after the initiation of classical ATT which on histopathology revealed lichenoid morphology.[3] Katare et al. and Sharma et al. also reported ATT-induced lichenoid drug eruptions.[4],[10]

INH is metabolized in the liver by acetylation to acetyl hydrazine. Polymorphism of acetylase enzyme exists in the population inherited in an autosomal recessive fashion leading to around 50% population being slow acetylators. Although slow acetylators have not specifically been implicated for lichenoid drug eruptions or erythroderma, due to the rarity of the conditions, various other skin conditions such as acneiform eruptions and pellagra are reported in slow acetylators.[11]


  Conclusion Top


INH-induced generalized exfoliative dermatitis with lichenoid histopathology has been infrequently described in the literature. Cases similar to our case have been described who also developed marked hair loss in a short span along with the rash. In the current scenario, where INH prophylaxis is being administered to almost all HIV-infected individuals for 6 months according to NACO, knowledge of such an occurrence is a must for all physicians-treating HIV cases.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ardern-Jones MR, Lee HY. Benign cutaneous adverse reactions to drugs. In: Griffiths C, Barker J, Bleiker T, Chalmers R, Creamer D, editors. Rook's Textbook of Dermatology. 9th ed. United Kingdom: John Wiley & Sons Ltd.; 2016. p. 118.1-118.17.  Back to cited text no. 1
    
2.
Thakur BK, Verma S, Mishra J. Lichenoid drug reaction to isoniazid presenting as exfoliative dermatitis in a patient with acquired immunodeficiency syndrome. Int J STD AIDS 2015;26:512-5.  Back to cited text no. 2
    
3.
Lehloenya RJ, Todd G, Mogotlane L, Gantsho N, Hlela C, Dheda K. Lichenoid drug reaction to antituberculosis drugs treated through with topical steroids and phototherapy. J Antimicrob Chemother 2012;67:2535-7.  Back to cited text no. 3
    
4.
Katare A, Arora P, Sardana K, Malhotra P. Lichenoid drug reaction due to anti-tubercular therapy presenting as erythroderma. Dermatol Ther 2020;33:e13169.  Back to cited text no. 4
    
5.
Reynolds NJ, Jones SK, Crossley J, Harman RR. Exfoliative dermatitis due to nifedipine. Br J Dermatol 1989;121:401-4.  Back to cited text no. 5
    
6.
Carr A, Cooper DA. Adverse effects of antiretroviral therapy. Lancet 2000;356:1423-30.  Back to cited text no. 6
    
7.
Jha AK, Gadgade A, Shenoy AK, Chowta MN, Ramapuram JT. Evaluation of adverse drug reactions in HIV positive patients in a tertiary care hospital. Perspect Clin Res 2015;6:34-8.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Hoosen K, Mosam A, Dlova NC, Grayson W. An update on adverse cutaneous drug reactions in HIV/AIDS. Dermatopathology (Basel) 2019;6:111-25.  Back to cited text no. 8
    
9.
Garg Y, Gore R, Jain S, Kumar A. A rare case of isoniazid-induced erythroderma. Indian J Pharmacol 2015;47:682-4.  Back to cited text no. 9
[PUBMED]  [Full text]  
10.
Sharma PK, Gautam RK, Bhardwaj M, Kar HK. Isonicotinic acid hydrazide induced anagen effluvium and associated lichenoid eruption. J Dermatol 2001;28:737-41.  Back to cited text no. 10
    
11.
Cohen LK, George W, Smith R. Isoniazid induced acne and pellagra. Occurrence in slow acetylators of isoniazid. Arch Dermatol 1974;109:377-81.  Back to cited text no. 11
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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