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Scalp Pathology for the Hair Transplant Surgeon: Beware of the "Imitators" Bernard Nusbaum, M.D. Reprinted from Hair Transplant Forum International: The primary requirement in a hair transplant consultation is to make the correct diagnosis. The scalp examination usually begins by looking for a recognizable pattern. Generally recognizable patterns are seen in male or female pattern alopecia, traction alopecia, post-facelift alopecia, etc. Certainly if these patterns are not recognized, an index of suspicion should immediately arise and a more through history and physical examination are performed. Scalp diseases, however, can mimic other entities and, in those situations a cursory scalp examination may suggest one of the above patterns, when in fact, the correct diagnosis is hidden behind diagnostic clues only to be found with a more in-depth exam. Two such cases are presented. In both the initial appearance suggested a diagnosis of female pattern alopecia. Case 1A 69 year old woman presented with a 10 year history of hair loss. She denied a family history of female pattern alopecia but had several male relatives with male pattern alopecia. She also denied any history of virilization, thyroid disease, iron deficiency or collagen-vascular disease. Physical exam showed extensive alopecia of the top of the scalp with sparing of the frontal hairline and "donor fringe" suggestive of Ludwig type III female pattern alopecia (Fig 1). The donor density and caliber was excellent. Upon closer inspection, however, the alopecic area appeared smooth and devoid of pores. In addition, erythema and scaling were observed at the periphery of the alopecia (Fig. 2) and perifollicular erythema could be seen in hairs emerging from this area (Fig. 3). Scalp biopsy was performed and showed perfollicular lymphocytic inflammation at the level of the isthmus and infundibulum with perifollicular fibrosis. Diagnosis: Fibrosing Alopecia in a Pattern Distribution (FADP). Discussion: FAPD represents an entity characterized by a progressive scarring alopecia of the central scalp without the multifocal areas of involvement seen in lichen planopilaris and pseudopelade.1 Histopatholgy of the early stages shows follicle miniaturization and a lichenoid infiltrate around the upper follicle. Advanced lesion show fibrosis indistinguishable from end-stage Lichen Planopilaris or Pseudopelade. FADP may be a variant of Lichen Planopilaris or may represent a separate "overlap" entity where the immune system of these patients recognizes miniaturizing, androgenetic affected follicles as antigenic and targets them with inflammation and subsequent destruction. Since some perifollicular inflammation is seen in up to 30% of patients with classical AGA and trichograms consistent with AGA as well as histologic miniaturization were observed in patients with FADP, a better understanding of FADP patients may hold clues to decipher the etiology of AGA.2 As with any patients with scarring alopecia, initial treatment is always medical with transplantation becoming an option after the disease is inactive for one year.2 Case 2A 32 year old woman presented with an 8 year history of hair loss. Treatment consisted of 3% minoxodil for 6 months with slight improvement. Three years prior she was diagnosed with hypothyroidism and takes Euthroid with good control of her thyroid levels. Past medical history was unremarkable except for post-partum exacerbation of her alopecia. Physical exam revealed diffuse thinning most prominent on the top area of the scalp with preservation of the hairline suggestive of a Ludwig Type II female pattern alopecia. (Figs. 4&5) Close examination showed areas with more severe thinning interspersed with less affected areas with hairs in the most affected areas shorter in length than those seen in more dense areas. The hair pull test was normal. Scalp biopsy was performed which showed perifollicular lymphocytic infiltration with no evidence of scarring, diagnostic of Alopecia Areata. Diagnosis: Alopecia Areata. Diffuse type. Discussion: Diffuse alopecia of undetermined origin requires a work-up including thyroid profile, iron, ferritin, CBC and ANA. If there are signs or symptoms of virilization or polycystic ovarian disease, work-up for hyperandrogenism and hyperprolactinemia should be performed. If the hair pull test suggests Telogen Effluvium, the history should attempt to elicit a precipitating factor. When there is doubt of the diagnosis, a scalp biopsy is performed. The clinical differential diagnosis in this patient includes:
Alopecia areata is an autoimmune, inflammatory process. It classically presents as a patchy, non-scarring alopecia but can present as a diffuse type. Diagnostic clues include: "exclamation point hairs" and hair pigment changes, in that alopecia areata often spares unpigmented, white hairs and regrowth of involved areas is often initiated by white hairs. Alopecia areata is associated with autoimmune diseases including thyroid disease. To make a diagnosis clinically in this patient would be extremely difficult since the affected areas were on the top of the head and inability to grow long anagen hairs in involved areas is a feature also seen in androgenetic alopecia. The clinical photos show the thinning areas to be somewhat multifocal (Fig.4) although this change is subtle. The association with hypothyroidism is notable for alopecia areata but might be overlooked due to the common incidence of thyroid disease in the female general population. The only way to confirm the diagnosis is by scalp biopsy. The treatment of alopecia areata is medical, since the inflammatory process can result in lack of growth or subsequent loss of transplanted hair. CommentThese two cases represent why there is a general perception that is difficult to make a diagnosis in alopecia cases. Like in any medical discipline, however, the first step is developing a differential diagnosis.3 This is accomplished with a history, physical exam and, in some cases, scalp biopsy or microscopic hair examination. The first and most important aspect of the physical exam is determining whether the hair loss is 1) scarring or non-scarring and 2) diffuse or focal. In scarring alopecia the scalp appears shiny, smooth and devoid of pores. Also, there may be signs of inflammation such as erythema and scaling at the periphery of active lesions. These observations were in fact the key to recognizing case #1 as a scarring alopecia despite its overall appearance of AGA. Diffuse hair loss means that the hair loss is evenly distributed. This determination is usually recognized easily. If there is any doubt, parting the hair in different areas and comparing the part width can be helpful. This maneuver may have revealed the subtle irregularity of the severely affected areas in case #2. In both cases the scalp biopsy was diagnostic. Once the above two key determinations have been made on physical examination, one can narrow down the diagnostic possibilities into categories and make a definitive diagnosis. The additional steps required are beyond the scope of this article but are covered in detail in appropriate texts.3 Certainly, the two entities discussed are not common but if one sees enough consultations, you may encounter such patients. Some alopecias, if transplanted will surely result in failure so, keep your differential diagnosis in mind, remember the old adage: "if you don’t look, you won’t find," and BEWARE OF THE IMITATORS! Legends to Figures Fig 1: Fibrosing Alopecia in a Pattern Distribution (FADP). Note the similarity to Classical Female Pattern Alopecia. Fig 2: FADP. Erythema and scaling are present at the periphery of the alopecia. Fig 3: FADP. Close-up showing perifollicular erythema. Fig 4: Diffuse Alopecia Areata. Easily confused with Female Pattern Alopecia. Fig 5: Diffuse Alopecia Areata. Side view. References
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