A 65-year-old man presented with a 2-year history of progressive hair loss involving the scalp, the eyebrows and the upper trunk, and recent onset of small papules and blisters on the dorsal hands as well as longitudinal ridging and fissuring of the fingernails. Clinical examination showed diffuse alopecia most pronounced on the androgen dependent scalp; the skin was slightly indurated on palpation []. There were focal petechiae. The lateral sides of both eyebrows and most of the hair on the chest were absent too. The axillary, pubic, and limb hair was preserved.\nTrichoscopic examination of the scalp showed prominent salmon colored halos (0.3-1 mm in diameter) surrounding the follicular ostia []. These halos were seen around empty follicles as well as around follicles containing terminal and vellus hairs, black dots, and/or broken hairs. This trichoscopic finding was present over the entire scalp.\nA 4 mm punch biopsy from the alopecic scalp was obtained and bisected in horizontal sections. There was overall preserved follicular architecture with intact sebaceous glands []. There were no terminal anagen follicles, one terminal telogen follicles, two vellus anagen follicles and 10 atrophic follicular structures reminiscent of telogen germinal units (secondary germs). All follicular structures were surrounded by amorphous eosinophilic material, which formed either a compact- or loosely- folded fibrillar cast []. The same material was deposited in all fibrous streamers, which appeared eosinophilic, homogenized and avascular. Congo red stain evaluated under polarized light highlighted the apple green stain of the amyloid [].\nSerum electrophoresis and bone marrow biopsy established the diagnosis of multiple myeloma.
A 74-year-old otherwise healthy woman presented with diffuse alopecia of the scalp. Two biopsies were taken for investigation of suspected telogen effluvium or diffuse alopecia areata. No clinical features of amyloidosis, such as macroglossia, purpura, infiltrative skin lesions or nail changes, were observed.\nThe skin biopsies showed no inflammation or evidence of a scarring alopecia. A large proportion of follicles were shifted into catagen and telogen phase in both biopsies. The residual fibrous stelae within the deep dermis and subcutis showed a remarkable appearance, with an empty center and a peripheral zone containing eosinophilic periodic acid Schiff (PAS)-positive and diastase-resistant ( and ), Congo-red-positive (), apple-green-birefringent material characteristic of amyloid. Similar amyloid deposits were also evident to a lesser extent surrounding follicular epithelium within the mid-dermis. There was no discernible amyloid deposition within dermal blood vessels, surrounding sweat apparati or adipocytes, or within the dermal interstitium.\nFurther special staining was carried out on one of the biopsies, with PAS with diastase (PASD) staining showing no fungal organisms or dermoepidermal basement-membrane-zone thickening. Alcian blue staining showed no dermal mucin accumulation and was negative within the amyloid deposits. Verhoeff staining showed no scarring that might suggest a scarring alopecia.\nWithin one biopsy, 14 of 37 (38%) hairs were vellus or vellus-like. Of the non-miniaturized hairs, 16 of 23 (70%) were in catagen or telogen phase. The other biopsy was more irregularly shaped and subsequently obliquely sectioned, allowing visualization of only 14 hairs, 5 of which (36%) were vellus or vellus-like; of the 9 remaining hairs, 2 were in catagen or telogen phase (22%).\nAs such, the biopsies were assessed to show a shift toward catagen and telogen hair follicles, consistent with the early phase of telogen effluvium. There was also moderate hair miniaturization consistent with pre-existing senile alopecia or androgenetic hair loss.\nPerifollicular deposition of amyloid prompted further workup of the patient for systemic forms of amyloidosis. Plasma protein electrophoresis and immunofixation showed a 1.4 g/L monoclonal band in the mid-to-late gamma region. Additional minor bands were noted in the beta-gamma region of both the alpha heavy chain and lambda light-chain classes and migrated with slightly different mobility, suggesting that they were not the same paraprotein. Urine protein electrophoresis showed moderate proteinuria in a glomerular pattern, without excretion of the monoclonal protein in the urine.\nBased on these findings, the patient was diagnosed with lambda AL amyloidosis. A bone-marrow biopsy performed 6 months after presentation showed a plasma-cell dyscrasia with lambda light-chain restriction and 8% plasma cells in the bone marrow. She subsequently received treatment with melphalan, and her disease is stable. At time of publication, she has no known involvement of the lymph nodes, oropharynx, liver, spleen, and cardiovascular system, and only mild renal impairment and proteinuria.