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Pain and Itch Control
Introduction
Pain is the most burdensome symptom of hidradenitis suppurativa (HS), accounting for greater impairment in HS-related quality of life (QoL) than even disease severity. Although it has received relatively less attention, pruritus is also common in HS and contributes to disability and poor health-related QoL among those living with HS. This chapter summarizes what is currently known about the epidemiology, clinical characteristics, and pathophysiology of HS-related pain and itch and synthesizes these data to suggest rational approaches to clinical management of these symptoms.
Pain in Hidradenitis Suppurativa
Epidemiology of Pain in Hidradenitis Suppurativa
Prevalence and Severity of Pain in Hidradenitis Suppurativa
Nearly all individuals living with HS experience lesion-associated pain during the disease course, and a large proportion report pain that occurs on a weekly basis (77% to 91%). In a cross-sectional study of 294 patients, the mean number of days with pain in the past month was 9.51 ± 9.67. A prospective international study of 1299 HS patients found that the majority of patients (61.4%) rate their pain severity as ≥ 5 on a numeric rating scale (NRS) of 0 to 10 and that 4.5% rate their pain as the “worst possible” or 10/10. When evaluating pain severity, other studies’ findings have been comparable, with average weekly NRS pain scores ranging from 3.6 to 5.0. Compared to other painful dermatologic conditions such as blistering diseases, leg ulcers, atopic dermatitis, lichen sclerosis, and skin tumors, those with HS had more frequent and severe pain. Individuals with HS are at increased risk for chronic opioid use as well as other substance misuse when compared to non-HS controls. Poorly controlled pain may contribute to this phenomenon, increasing the importance of recognizing and managing pain in patients with HS.
Risk Factors
Risk factors for HS pain include severe HS disease activity and a higher number of anatomic regions involved. Psychiatric comorbidities such as anxiety and depression further compound pain perception. Physical factors such as friction and tight-fitting clothing have also been reported to exacerbate HS pain.
Impact of Pain on Quality of Life
HS is highly debilitating, with worse patient-reported QoL than almost any other skin disease. Pain has been identified as the major contributor to reduced QoL and disability in HS, even more so than HS severity. Painful HS lesions directly impact physical function and daily activities. Individuals living with HS commonly report that HS lesional pain impacts mobility, participation in exercise and sports, work productivity, and sexual health. HS pain is also associated with insomnia and poor sleep quality. HS pain impacts psychological well-being, resulting in increased risks for depression, anxiety, and suicide among those living with HS. The HS pain experience and the uncertainty of its course contribute to a sense of powerlessness and worsened emotional function. Further, HS patients report feeling isolated and invalidated when others fail to understand and empathize with the severity of their pain.
Clinical Characteristics of Hidradenitis Suppurativa Pain
The quality of HS pain may vary between patients and may also vary over time within the same individual. The timing of HS pain may be acute with associated flare or worsening inflammatory activity, or chronic in nature. HS pain has been described by patients as nociceptive and neuropathic in character. Nociceptive pain results from a noxious stimulus that has potential for tissue damage, and is often described as “aching,” “gnawing,” or “throbbing.” 8 In HS, nociceptive pain may result from direct inflammatory tissue damage (see Pathophysiology of Pain in HS). Neuropathic pain arises from damage to the somatosensory nervous system. Neuropathic pain is classically described as “burning,” “stinging,” or “stabbing,” and these descriptors are common among HS patients experiencing pain. In a study of 92 HS patients, 31.5% of patients reported symptoms suspicious for neuropathic pain, 41.3% had no neuropathic symptoms, and 27.2% had unclear results. Those with neuropathic pain were more likely to experience moderate to severe pain and to report psychiatric comorbidities.
Pathophysiology of Pain in Hidradenitis Suppurativa
Overview of Pain Response
The physiologic response to pain resulting from tissue injury is an important evolutionary strategy in withdrawal from and avoidance of harmful stimuli. This response, which is not specific to HS, involves four major components: (1) transduction, (2) transmission, (3) modulation or transformation, and (4) perception. Transduction is the process by which primary afferent neurons or nociceptors convert noxious stimuli including chemical, mechanical, heat, and cold into nociceptive electrical signals. Pain, in addition to itch and temperature, are transmitted mainly by unmyelinated c-fibers and thinly myelinated Aδ fibers. If this electrical signal reaches the threshold for activation potential, transmission occurs, sending a nociceptive signal from peripheral nerve fibers to the central nervous system (CNS). Modulation or transformation modifies these signals at the level of the CNS. Perception is the final stage of the nociceptive process that integrates cognitive and affective responses, resulting in the subjective pain experience ( Fig. 19.1 ) . The sections that follow incorporate current knowledge of HS pathophysiology with clinical descriptions of HS pain to suggest mechanisms which may contribute to the pain response in HS.
Nociceptors, Signal Transduction, and Transmission in Hidradenitis Suppurativa
Inflammatory tissue damage likely plays a substantial role in generating the nociceptive signals that are the first step in the HS pain response pathway. HS is associated with a mixed inflammatory infiltrate including neutrophils, T-cells, B-cells, plasma cells, NK cells, mast cells, macrophages, and dendritic cells. These cells produce a variety of cytokines, chemokines, and growth factors which serve as stimuli to nociceptors. The role of inflammatory cells in causing HS pain is supported by the finding that antiinflammatory therapies can produce an analgesic effect in HS. Lifestyle factors and comorbid conditions, such as obesity, nicotine use, and metabolic syndrome, likely contribute to the stress response and enhance recruitment of inflammatory cells. Additionally, inflammatory cells recruitment results in damage to peripheral tissue, inducing keratinocytes to release pro-inflammatory factors such as prostaglandins, substance P, and calcitonin gene-related peptide (CGRP). These mediators subsequently bind to nociceptors, resulting in a series of electrical impulses at the afferent nerve terminal.
Of particular note, tumour necrosis factor-α (TNF-α) is a pro-inflammatory cytokine that has been found in lesional skin and serum of individuals with HS. Pharmacologic neutralization of TNF-α was shown to block nociceptive activity in the thalamus, somatosensory cortex, and limbic system within the first 24 hours and prior to any anti-inflammatory effect in peripheral tissues, suggesting that this cytokine may play a role in nociception, both peripherally and centrally.
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