Types of Psoriasis – GUTTATE PSORIASIS (GP)


Guttate means “drop” in Latin (also known as Teardrop Psoriasis, Raindrop Psoriasis or Psoriasis Exanthematic), and is the second most common type of psoriasis. Guttate psoriasis (GP), is an important clinical variant which occurs more commonly in adolescents and young adults. It is characterized by the sudden onset of widely dispersed small red scaly plaques – 0.2 – 2.0 cm’s in diameter, mainly over the trunk and proximal limbs. The symptoms of GP are numerous small, bright red or salmon coloured, drop-like spots which cover a large portion of the skin. Spots have an abundant fine scaling. The lesions are usually located on the trunk, arms, legs and scalp and spares the face, palms and soles.1

GP represents approximately 2% of psoriasis patients and 30% of guttate patients have a first degree family member with psoriasis 2. Among patients with acute guttate psoriasis, 56–98% experienced a streptococcal infection (e.g. tonsillitis, viral respiratory infections, laryngitis etc.) within a 2-3 weeks period prior to the eruption and, it is theorized that psoriasis may be induced in susceptible individuals by streptococcal superantigens. In children perianal streptococcal infections (or chronic pruritus of the anus) have also been associated with GP 3.

Because some cases of GP in childhood may be triggered or exacerbated by streptococcal pharyngeal infections, the role of tonsillectomy as a treatment option in severe refractory GP has been studied. However, the results remain controversial and at best non conclusive. In a Cochrane review the conclusion that tonsillectomy may be a successful treatment modality in selected patients with recalcitrant GP is suspect due to the fact that many of the studies were not of a high enough standard for the conclusions to be definitive.5 A study in 2012 which was a blind study found that patients with chronic GP and a history of disease exacerbation in association with sore throat, generally improved after a tonsillectomy.6

Many other infectious agents have also been implicated, although the exact frequency of GP associated with these infections/diseases is unknown.

They include the following:

  • Bacteria – other than Staphylococcus aureus – Enterococcus faecalis, Escherichia coli, Pseudomonas and Proteus species, or the bacterium implicated in duodenal ulceration, Helicobacter pylori.5
  • Fungi – Malassezia, Candida
  • Viruses – Flu, Human papillomavirus (HPV), varicella-zoster virus, human endogenous retroviruses (HERVs) e.g. cytomegalovirus and vaccinations 7.
  • Drugs (including biologic agents) sometimes cause a guttate-type flare.

The most commonly implicated drugs in association with either the initiation or exacerbation of GP include lithium, beta-blockers, antimalarial, and non steroidal anti-inflammatories. 

Immunomodulatory drugs such as infliximab, etanercept, imatinib, and adalimumab have also been reported to initiate GP. The Koebner Phenomenon e.g. tattoos, insect bites scratches etc. can trigger GP.

Approximately 70% of patients with GP will go on to develop chronic plaque psoriasis within a 10 year time frame.


Guttate with fine scale                        Guttate with no scale

Figure 1. Scattered drop like lesions                                Figure 2. Reddish – scattered drop like lesions

ranging from 0.5 to 2.0 cm, with slight scale.                   ranging from 0.2 to 1.0 cm with no scale.

Coalesing Guttate 4                     Coalesing Guttate 3

Figure 3. Note the fine scale and the                              Figure 4. Note the fine scale and the complete

coalescing (merging) of the lesions.                               merging of the lesions.

Coalesing Guttate                      Coalesing Guttate 2

Figure 5. Reddish lesions – where the                                      Figure 6. Salmon pink lesions – where the             

majority of the lesions have merged.                                       majority of the lesions have merged.


  • Zangeneh F.Z., Shooshtary F.S.; Psoriasis — Types, Causes and Medication – Chapter 1; http://cdn.intechopen.com/pdfs-wm/44173.pdf
  • Mallbris et al.: Psoriasis Phenotype at Disease Onset: Clinical Characterization of 400 Adult Cases; Journal of Investigative Dermatology; Volume 124, Issue 3, March 2005, Pages 499–504
  • Honig J.; Guttate psoriasis associated with perianal streptococcal disease; Clinical and laboratory observations The Journal of Pediatrics December 1988
  • Telfer NR,Chalmers RJ, Whale K, Colman G. The role of streptococcal infection in the initiation of guttate psoriasis. Archives of Dermatology 1992;128(1):39-42.
  • Antistreptococcal interventions for guttate and chronic plaque psoriasis (Review) 8 Copyright © 2016 The Cochrane Collaboration. http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD001976/epdf
  • Thorleifsdottir R.H. et al.; Improvement of Psoriasis after Tonsillectomy Is Associated with a Decrease in the Frequency of Circulating T Cells That Recognize Streptococcal Determinants and Homologous Skin Determinants; The Journal of Immunology; April 9, 2012, doi:10.4049/jimmunol.1102834
  • Moon Seub Shin et al; New Onset Guttate Psoriasis Following Pandemic H1N1 Influenza Vaccination; Ann Dermatol. 2013 November; 25(4): 489–492.

PSORIASIS – the Relationship with Drugs


Cutaneous drug eruptions are one of the most common types of adverse reaction to drug therapy, with an overall incidence rate of 2–3% in hospitalized patients. Almost any medicine can induce skin reactions, and certain drug classes, such as non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics and anti-epileptics have drug eruption rates approaching 1–5%.1

Drug Relationship

Psoriasis & Drugs

Drug ingestion may result in several different responses:-

  1. a) Drugs may trigger the condition in a Patient who is genetically predisposed to psoriasis.
  2. b) Drugs may trigger the condition “de novo”, in a Patient non–predisposed.
  3. c) Drugs may exacerbate existing psoriatic lesions in a Patient.
  4. d) Drugs may trigger a psoriatic flare up in “clinically normal” skin in patients with psoriatic 2

In view of their relationship to psoriasis, therapeutic agents may be classified as follows:

(1)     Drugs with strong reported case evidence for a causal relationship to psoriasis including lithium, beta blockers, and synthetic antimalarial drugs;

(2)     Drugs with a considerable number of studies but insufficient data to support induction  or aggravation of the disease;

(3)     Drugs occasionally reported to be associated with aggravation or induction. 2.3

Drug-provoked psoriasis can be divided into two categories:-

1]       Drug-INDUCED psoriasis – where discontinuation of the causative drug stops the further progression of the disease. This form tends to occur in a “de novo” fashion in patients with no family or previous history of psoriasis. The clinical presentation of   these lesions  may often mimic the pustular variant of psoriasis, often with no nail involvement or associated arthritis. 2

2]       Drug-AGGRAVATED psoriasis – where the disease progresses even after the discontinuation of the offending drug and usually occur in patients with a history of  psoriasis or with a genetic predisposition for the disease. Patients can have exacerbation of pre-existing psoriatic lesions or develop new lesions in previously   uninvolved skin. Histological examination reveals features that are more characteristicof psoriasis vulgaris. 2

These two reactions are not to be confused with “Psoriasiform drug eruption”. This is a broad term that refers to a group of disorders that clinically and/or histologically simulate psoriasis at some point during the course of the disease. This type of eruption is usually associated with seborrheic dermatitis, pityriasis rubra pilaris, secondary syphilis, pityriasis rosea, mycosis fungoides, and some malignancies. 2

Some Drugs that Trigger or Exacerbates Psoriasis

Although a several drugs have been implicated in provoking psoriasis, the strongest evidence is for lithium, beta-blockers, anti-malarials, non-steroidal anti-inflammatory drugs and tetracyclines. In addition, angiotensin-converting enzyme inhibitors, interferons, digoxin, clonidine, carbamazepine, valproic acid, calcium-channel blockers, granulocyte-colony stimulating factor, potassium iodide, ampicillin, penicillin, progesterone, morphine and acetazolamide have been reported to exacerbate psoriasis. 4

 DRUG Mechanism of ActionComments
 Beta-blockers A delayed type hypersensitivity reaction, an immune mediated response and a decrease in intraepidermal cAMP and a consequent increase in peidermal cell turnoverBoth cardioselective and non-cardioselective drugs have been implicated but the frequency is higher with the latter.

Also with topical timolol, reported to induce psoriasis and to transform psoriasis vulgaris (Plaque) into psoriatic erythroderma.

 Lithium      Acts directly by blocking cell differentiation and leading to dysregulation of inflammatory cytokines and indirectly by decreasing cAMP levelsProvokes or induces chronic plaque psoriasis, localized or gnerealized pustular psoriasis and even psoriatic erythroderma.
 Antimalarials May trigger psoriasis by inhibiting the enzyme transglutaminaseDoes not induce psoriasis although they are known to trigger psoriasis in 18% of patients.
 NSAIDs Inhibits the cyclo-oxygenase pathway, leading to accumulation of leukotrienes and hence may exacerbate psoriasis 
 Tetracyclines May provoke psoriasis either by inhibiting cAMP or by inducing Koebner’s phenomenon due to their photosensitizing potential 

It is important for the patient to supply information to their GP or Practitioner as to all medications being used and when the lesions were first noticed, or when they noticed their existing lesions worsening. In some instances the eruption of new lesions may take several weeks or even months to occur, when this happens it may be difficult to determine the exact causal relationship between a drug and an eruption. The following chart may be of assistance in determining if one of your medications may be involved.

 Date Time Medication  Name Dose Reason for MedicationSymptoms ExperiencedWhen Symptoms

First Noticed

  e.g. 15/2 8.00am Carvedilol  25mg Blood PressureNew lesions on skin not affecting old lesions2 weeks after first taking it.
 Or e.g. 15/2 8.00am Bisoprolol 10mg CardiomyopathyWorsening of old lesionsAfter 72 hours, burning red skin, lesions rapidly spread


  • Lee A. Thomson J.; Drug-induced skin reactions; Adverse Drug Reactions, 2nd edition (ISBN: 0 85369 601 2) Pharmaceutical Press 2006; http://www.pharmpress.com/files/docs/ADRe2Ch05.pdf
  • GRACE K. KIM, DO; b JAMES Q. DEL ROSSO, DO ; Drug-Provoked Psoriasis: Is It Drug Induced or Drug Aggravated? Understanding Pathophysiology and Clinical Relevance; J Clin Aesthetic Dermatol. 2010;3(1):32–38.
  • Milavec-Pureti? V. et al.; Drug Induced Psoriasis; Acta Dermatovenerol Croat; 2011;19(1):39-42
  • Mahajan R, Handa S. Pathophysiology of psoriasis. Indian J Dermatol Venereol Leprol 2013;79, Suppl S1:1-9