HS develops after puberty, usually in the second or third decade. In a personal series of 164 patients mean age at onset was 22.8 years with extremes of 10 and 57 years (see Fig. 3.21). This finding was similar to those of other series [4, 12]. Genetic factors may affect the onset of disease. Patients with a familial history of HS tend to experience an earlier onset (mean age 20 versus 23 years), although positive bias through over-reporting may occur in families where HS is a communal rather than a personal problem.
The age at onset and age distribution of the cases appear to suggest co-occurrence with hormonal factors, see Chap. 12. Prepubertal cases are rare. In general they are not linked to an
Fig. 3.22. Sequelae of severe HS
severe disease as evaluated by the Sartorius' index .
The development of new lesions generally tends to slow down after 50 years, with less inflammation and suppuration but sometimes with severe sequelae with extensive fibrosis and tissue destruction (see Fig. 3.22). It may be speculated that low-grade disease resolves with age, while more severe disease persists or progresses.
early menarche, although cases have been published in which the two co-occur. Similarly, there is a tendency for the disease to burn out after menopause in women. Patients with continuously active disease after the age of 50 (mostly men), however, regularly appear, and for some the disease may even have started at that age.
For most patients the worst years are the first 10 or 15 years after onset . The chance of cure after localized excisions also appears to increase with increasing age of the patient, suggesting that the underlying pathogenic mechanisms abate at an older age . In one series older patients (>40 years) and a patient with a tardy diagnosis however had significantly more
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