{'fraction_non_alphanumeric': 0.030440024110910187, 'fraction_numerical': 0.006027727546714889, 'mean_word_length': 5.297912713472486, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Successful use of infliximab in a patient with recalcitrant folliculitis decalvans

Folliculitis decalvans (FD) is a rare disease belonging to the group of disorders of primary cicatricial alopecia [1]. The clinical appearance consists of severe follicular pustules and perifollicular erythema affecting the scalp [2]. The inflammatory lesions heal with centrifugal scarring [3]. A secondary “tufted” appearance is sometimes seen [4] in which several hair shafts protrude from a single enlarged ostium. Staphylococcus aureus is detectable in culture. FD is extremely resistant to therapy. Commonly used treatments are systemic antibiotics [5], topical and oral corticosteroids [6], and dapsone [7]. Zinc substitution and diverse anti-inflammatory topical agents have also been used. Because the disease is so rare, treatment methods are based on isolated reports and smaller studies. We report on a 45-year-old man who had progressive FD for several years. The lesions oozed at night and were covered with crusts. The patient, who worked as a teacher, was under a considerable psychological burden as a result of having the disease. Clinical inspection revealed severe cicatricial alopecia with perifollicular pustules as well as tufted hair. Biopsy showed an inflammatory infiltrate, located primarily around the follicles, which was made up of lymphohistiocytic cells and abundant neutrophilic granulocytes. Initial treatment attempts failed to achieve long-term improvement. These included topical treatments, several months of systemic isotretinoin (20 mg/daily), oral corticosteroids (methylprednisolone 8 mg/daily), and various systemic antibiotics against staphylococcal infection. Dapsone therapy had to be discontinued due to hot flashes and fatigue along with a significant loss of concentration. Oral zinc substitution was ineffective. After thoroughly informing the patient about possible risks and side effects, we initiated treatment with the TNFalpha-Blocker infliximab. The dosage of 5 mg/kg of body weight, as well as the treatment intervals, corresponded to those used in psoriasis patients. After only three infusions there was rapid remission of the inflammatory lesions (Figure 1a, b). We continued treatment, and after a 12-month-long follow-up observation period there was still no recurrence. There were no clinical side effects, nor were any detected on laboratory chemical tests. Yet, why would a TNF-alpha blocker be useful? In FD there is an apparent discrepancy between the local pathogens and the extent of the inflammation [8]. Also, the susceptibility to inflammation may be genetically determined [9]. In our view, this raises the question as to whether FD might be considered a disease of the congenital autoinflammatory syndrome. Certain diseases belonging to this group of disorders, such as pyoderma gangrenosum, have also been successfully treated with TNF-alpha blockade [10]. Our results show that patients with FD can benefit from therapy with TNF-alpha blocking substances. These agents could thus broaden the narrow range of available therapies for this highly chronic disease. TNF-alpha inhibitors should be restricted to use in highly recalcitrant disease, however, given their cost and the need for off-label use. Further reports and systematic studies are clearly needed.