fig10

Figure 10. Challenging hair mass index (HMI) abacus in male pattern hair loss (MPHL) during fluctuating hair productivity associated with drug treatment. All graphs display the time points on the x-axis (time in months). Baseline [from month -12 (m-12) to month -1 and month 0 (m-1 and m0)] was followed by the monitoring of drug-induced effects according to study protocol at selected time points [1, 2, 3, 6, 12 and 24 months (m)]. The scales (y-axis) on the main graph represent fluctuations of hair productivity measured in one male subject with MPHL [compound Index for hair growth per cent of controls (CIHG%)]. Inserts (a-c) show the top of the head viewed one year and one month before and at m0, i.e., at entry into the drug trial (a, green outline; m-12, m-1 and m0). Global views were documented at monthly intervals along with the combined oral and topical drug treatment (b, blue outline; m1, m2 and m3). This was followed by the last three visits starting three months after arrest of topical lotion, i.e., during the oral drug only (c, red outline; m6, m12 and m24). All measured hair variables recorded during these three successive timeslots are shown using the same colour codes, i.e., baseline in green, combined drugs in blue and oral finasteride only in red. On the y-axis, besides productivity (CIHG% of controls), the two smaller inserts (d, e) show the TTCC (days) and SCS (per cent of maximum). In the latter, each dot is the average of triplicate scoring viewed one at a time from three series of randomised source images. The baseline (green dot) shows average SCS on images recorded during the one year before inclusion, while blue dots are SCS on combined drugs and red dots on oral drug only. It is understood that a decreased TTCC means improved hair follicle performance. The values dropped below 30 days on their way to normalisation of time to complete coverage, i.e., 19.62 days. Maximum improvement was observed at m3, the time-point where topical minoxidil applications were about to be interrupted according to protocol. All data points perfectly match with one another except for time-points m2 and m6: (1) SCS significantly drops at m2 [blue dot at m2 in (e)] while analytical measures document improved hair growth. Shifted SCS highlights the transient effects of intervention of the hairdresser {one month later impact on SCS almost vanished [m3 in (e)]}. (2) SCS slightly improves at m6 as compared with m3 when the actual indicators of growth worsened. This reflects a delay of perception of hair cycling by the clinician and most probably a delayed hair cut with more efficient coverage due to cumulative effect. During the first three months, the combined drug regimen almost normalised hair growth but subsequent transition of anagen into catagen-telogen occurred, albeit an apparently stable mass of hair. After completion of telogen and shedding of exogen, i.e., after m6, there was a decrease of SCS at m12 and partial recovery at m24, which reflects maintenance of hair regrowth with long-term oral drug intake. Hence, SCS and hair productivity fluctuate with an immediate correlation when cycling improves and with a trimester delay when cycling arrests; this is consistent and is in line with follicle pharmacodynamics. SCS: scalp coverage scoring; TTCC: Time To Complete Coverage; CIHG: compound index of hair growth.