Clinical Review

Management of Acute and Chronic Pain Associated With Hidradenitis Suppurativa: A Comprehensive Review of Pharmacologic and Therapeutic Considerations in Clinical Practice

Author and Disclosure Information

Hidradenitis suppurativa (HS), a chronic, inflammatory, recurrent cutaneous disorder of the hair follicles, is debilitating and has substantial morbidity. Hidradenitis suppurativa–related pain has a profound effect on patient quality of life, yet at present, there are no established pain management algorithms. This comprehensive review provides an update on current treatment of HS-associated pain, including a summary of existing literature surrounding pharmacologic treatments of acute, perioperative, and chronic pain. Additionally, the epidemiology, pathophysiology, and clinical features of the disease are summarized.

Practice Points

  • First-line therapies may not provide adequate pain control in many patients with hidradenitis suppurativa.
  • Pain caused by inflamed abscesses and nodules can be treated with either intralesional corticosteroids or incision and drainage. Tissue-sparing surgical techniques may lead to shorter healing times and less postoperative pain.
  • Long-term management involves lifestyle modifications and pharmacologic agents.
  • The most effective pain remedies developed thus far are limited to surgery and tumor necrosis factor α inhibitors.


 

References

Hidradenitis suppurativa (HS) is a chronic inflammatory, androgen gland disorder characterized by recurrent rupture of the hair follicles with a vigorous inflammatory response. This response results in abscess formation and development of draining sinus tracts and hypertrophic fibrous scars.1,2 Pain, discomfort, and odorous discharge from the recalcitrant lesions have a profound impact on patient quality of life.3,4

The morbidity and disease burden associated with HS are particularly underestimated, as patients frequently report debilitating pain that often is overlooked.5,6 Additionally, the quality and intensity of perceived pain are compounded by frequently associated depression and anxiety.7-9 Pain has been reported by patients with HS to be the highest cause of morbidity, despite the disfiguring nature of the disease and its associated psychosocial distress.7,10 Nonetheless, HS lacks an accepted pain management algorithm similar to those that have been developed for the treatment of other acute or chronic pain disorders, such as back pain and sickle cell disease.4,11-13

Given the lack of formal studies regarding pain management in patients with HS, clinicians are limited to general pain guidelines, expert opinion, small trials, and patient preference.3 Furthermore, effective pain management in HS necessitates the treatment of both chronic pain affecting daily function and acute pain present during disease flares, surgical interventions, and dressing changes.3 The result is a wide array of strategies used for HS-associated pain.3,4

Epidemiology and Pathophysiology

Hidradenitis suppurativa historically has been an overlooked and underdiagnosed disease, which limits epidemiology data.5 Current estimates are that HS affects approximately 1% of the general population; however, prevalence rates range from 0.03% to 4.1%.14-16

The exact etiology of HS remains unclear, but it is thought that genetic factors, immune dysregulation, and environmental/behavioral influences all contribute to its pathophysiology.1,17 Up to 40% of patients with HS report a positive family history of the disease.18-20 Hidradenitis suppurativa has been associated with other inflammatory disease states, such as inflammatory bowel disease, spondyloarthropathies, and pyoderma gangrenosum.16,21,22

It is thought that HS is the result of some defect in keratin clearance that leads to follicular hyperkeratinization and occlusion.1 Resultant rupture of pilosebaceous units and spillage of contents (including keratin and bacteria) into the surrounding dermis triggers a vigorous inflammatory response. Sinus tracts and fistulas become the targets of bacterial colonization, biofilm formation, and secondary infection. The result is suppuration and extension of the lesions as well as sustained chronic inflammation.23,24

Although the etiology of HS is complex, several modifiable risk factors for the disease have been identified, most prominently cigarette smoking and obesity. Approximately 70% of patients with HS smoke cigarettes.2,15,25,26 Obesity has a well-known association with HS, and it is possible that weight reduction lowers disease severity.27-30

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