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This article is protected by copyright. All rights reserved.

Received Date : 30-Sep-2013

Revised Date : 19-Jun-2014

Accepted Date : 04-Aug-2014

Article type : Review Article

Onychomadesis: Literature Review

J. Hardin. R.M. Haber

University of Calgary, Division of Dermatology, Richmond Road Diagnostic and Treatment

Centre, 1820 Richmond Road SW, Calgary, Alberta T2T5C7, USA

I am submitting this manuscript to the Review section of the British Journal of Dermatology. We
feel we have addressed the reviewers’ comments from our previous two submissions to
produce this draft. To our knowledge, there are no other published literature reviews on
onychomadesis and its associations. We feel our article fills a gap in the existing literature on
nail diseases and their etiology in illness.

Corresponding Author: Jori Hardin, MD

Email: jorihardin@gmail.com

Author Contributions: Drs Haber and Hardin had full access to all of the data in the study and
take responsibility for the integrity of the data and accuracy of the data analysis.
This article is protected by copyright. All rights reserved.

Study concept and design: Hardin, Haber

Acquisition of data: Hardin, Haber

Drafting of the manuscript: Hardin. Haber

Critical revision of the manuscript for important intellectual content: Hardin, Haber

Statistical analysis: Hardin, Haber

Administrative, technical or material support: Hardin, Haber

Study supervision: Haber

Funding sources: None reported

The authors have no conflict of interest to declare.

Abstract

Introduction

Onychomadesis is characterized by separation of the nail plate from the matrix with persistent

attachment to the nail bed and often but not always, eventual shedding. Onychomadesis has

been associated with infection, autoimmune disease, critical illness, and medications and to our

knowledge a literature review of all associations with onychomadesis has not been completed

previously. Most commonly, onychomadesis has been reported in association with pemphigus

vulgaris, hand-foot-mouth disease, and following chemotherapy or antiepileptic medications.

This article summarizes these key culprit associations, postulates the pathogenesis of nail matrix

arrest and summarizes the clinical outcomes.

Methods

We conducted a retrospective review of the cases of onychomadesis reported from January

1960 until March 2013. Using the pubmed database, the literature was searched using the
This article is protected by copyright. All rights reserved.

following terms: “Onychomadesis” and “Proximal Nail shedding”. As well, an OVID search was

carried out using the same terms.

Results

A total of 56 articles have been published including our previously reported series of idiopathic

onychomadesis. Articles pertaining only to Beau’s lines and not true onychomadesis were

excluded. Onychomadesis has been associated with autoimmune disease, other major medical

illness, neonatal illness, medication induced and infection.

Introduction

In 1846, Joseph Honore Simone Beau, a Parisian cardiologist, described the evolution of

transverse grooves in the nail plate in typhoid fever and other systemic disorders 2. He observed

that normal growth of the nails is affected during states of disease and suggested that the width

of the depression or furrow was proportional to the duration of the illness. These furrows, aptly

called Beau’s lines, are caused by a temporary arrest in the activity of the nail matrix.

Onychomadesis is characterized by separation of the nail plate from the matrix with persistent

attachment to the nail bed and often but not always, eventual shedding. When a Beau’s line

results in complete loss of continuity with the matrix, then it is no longer a Beau’s line but

becomes onychomadesis 35. Onychomadesis has been associated with infection, autoimmune

disease, critical illness, and medications and to our knowledge a review of all associations with

onychomadesis has not been completed previously. This article summarizes these key culprit

associations, postulates the pathogenesis of nail matrix arrest and summarizes the clinical

outcomes.
This article is protected by copyright. All rights reserved.

Autoimmune disease

Onychomadesis has been associated with alopecia areata. LaRow published a case report of a 2
23
year old with alopecia areata universalis and Tosti et al. did a retrospective review of 272

children with alopecia areata, of which 126 had nail abnormalities 43. Three of the 126 patients

had onychomadesis of all 20 nails during the acute onset of alopecia areata universalis, with two

developing severe nail pitting as well.

A more well recognized autoimmune association with onychomadesis is pemphigus vulgaris

(PV). There are several review articles of nail abnormalities associated with PV and after

paronychia, onychomadesis is the most common nail abnormality seen in PV.

Habibi et al. found that 25/79 PV patients had nail changes with 8 having paronychia and 6

having onychomadesis 16. Schlesinger et al. did a case-controlled retrospective study of 64

patients with PV (matched to 64 patients with other skin dermatoses) and found that nail

changes were present in 30/64 PV patients; with 14 having biopsy proven PV of the nail, 6 with

paronychia, 6 with discoloration, 5 with onychomadesis, 5 with subungual hemorrhage and

38
others with onycholysis . It is generally accepted that more severe cutaneous and mucous

membrane involvement in cases of PV is a determinant of nail findings and prognosis of PV is

worse if nails are affected.

Major Medical Illness

Onychomadesis has been reported in association with severe Guillain Barre syndrome 46, major
46
depressive disorder , 6 weeks after Stevens Johnson syndrome 1, Cronkhite- Canada syndrome
This article is protected by copyright. All rights reserved.

30
, peritoneal dialysis 7, immunodeficiency 36, meningitis and pneumonia complicated by

pulmonary abscess 45, and recurrent eythroderma secondary to mycosis fungoides. Two cases of
10; 28
onychomadesis have been reported following Kawasaki disease .

Medication

Although many nail disorders have been associated with drug intake, most reports are

anecdotal. Most nail changes caused by drugs are the outcome of acute toxicity to the nail

epithelia, but other mechanisms can be involved. Drug-induced nail changes usually involve

several or all 20 nails and appear in temporal correlation with drug intake. Some nail changes

are asymptomatic and cause only cosmetic problems, whereas others cause pain and discomfort

and impair manual activities or ambulation. Drug-induced nail abnormalities are usually

transitory and disappear with drug withdrawal, but they may persist over time 29. A drug should

be suspected when these signs affect all nails at the same level. A drug taken 2 to 3 weeks

before the appearance of these nail symptoms should be considered because a fingernail takes

about 40 days to emerge from the proximal nail fold, and a toenail about takes 80 days 29.

Piraccini et al. cite three factors complicating the diagnosis of medication induced nail changes.

First, the nail changes may appear several weeks after drug intake because of nail kinetics and

the slow growth rate of the nail plate. Second, nail symptoms often improve or resolve without

drug withdrawal. Lastly, re-challenge often is negative 29.

Most commonly implicated medications are chemotherapeutic agents such as capecitabine,

8; 9; 22
adriamycin with cytosine arabinoside and etoposide . Antiepileptics, specifically
12; 24; 32; 33
carbamazepine and valproic acid have also been implicated . A case report was
This article is protected by copyright. All rights reserved.

published by Shah et al in 2012 of penicillin V induced erythema multiforme and subsequent

onychomadesis in all 20 nails 39. Further cases have been published linking onychomadesis to
29
azithromycin, retinoids, lead, and lithium .

We have observed a case of chemotherapy-induced onychomadesis in a patient with

acute myelogenous leukemia in which the separated fingernails failed to detach totally

which resulted in some of the fingernails becoming perpendicular to the nail bed. The patient

had received the following conditioning chemotherapy: HDAC (Idarubicin and cytarabine A) and

Flag IDA (Idarubicin, Fludarabine and Cytarabine A) pre stem cell transplant. We have termed

this phenomenon “vertical onychomadesis”. The patient’s major concern was the inability to

grasp with her fingers.

Neonatal

20; 26; 27; 31

Four cases of neonatal onychomadesis have been reported . Two of these cases
27; 31
support an association with candida albicans . However, each report is in agreement that

the trauma of birth alone, whether vaginal or by Caesarian section, is sufficient to induce

onychomadesis.

Infection

The infection most commonly reported in association with onychomadesis is hand-foot- mouth

disease (HFMD). Hand-foot-mouth disease is a common and contagious Coxsackie virus

infection, most commonly seen in childhood. It occurs as an isolated phenomenon or in

This article is protected by copyright. All rights reserved.

epidemic form, usually in autumn or spring. Coxsackie viruses are members of the family of

Enteroviruses. Within the family of Enteroviruses, Coxsackie serotype A16 and Enterovirus 71

are most commonly associated with HFMD. HFMD is characterized by a low-grade fever, a

vesicular eruption of the hands, feet and buttocks, and ulcerations of the tongue, soft palate,

buccal mucosa, or gingiva. Vesicles are commonly present on the dorsal aspect and lateral

borders of the extremities and have a characteristic elliptical football-shaped appearance often

with a surrounding erythematous halo. Resolution is spontaneous and usually occurs by 6 days.

Complications are rare.

Reports of HFMD associated onychomadesis are well documented and have come from France

and Belgium 3, Italy 4, Spain 6; 13; 15; 34

, Finland 5; 25
, and Chicago 11
with more recent reports from
17
Japan and Taiwan . All cases occurred in children less than 7 years old and latency periods,

when reported, ranged from 4-10 weeks post-infection. Davia et in the Spanish onychomadesis

outbreak secondary to HFMD, found that onychomadesis could be seen due to several

serotypes of enteroviruses including Coxsackie A5, A6,A10, A16,B1,B3, Echoviruses 3,4,9 and

Enterovirus 71 13. However, in the Finnish and Taiwanese outbreaks, the predominant virus

subtype isolated was Coxsackie A6 which tends to cause more severe HFMD. It has been

postulated that Coxsackie A6 may be the major subtype associated with HFMD onychomadesis
5
.

The mechanism of onychomadesis in HFMD is still unknown. However, onychomadesis means

that nail matrix proliferation was temporarily inhibited. It is still debated whether the inhibition

results from direct inflammation spreading from skin lesions of HFMD around nails or

coxsackievirus-specific nail matrix involvement, or HFMD’s severe systemic impact on the

This article is protected by copyright. All rights reserved.

general condition of the small children. Reported onychomadesis without preceding skin
17
eruptions around nails suggested that it was coxsackievirus-specific nail matrix dysfunction .

However, all previous reports describing onychomadesis were retrospectively analyzed. Shikuma

et al prospectively observed a case of HFMD, in which onychomadesis only developed in

40
fingernails and toenails following healing of severe cutaneous lesions around affected nails .

Nail dysfunction due to direct inflammation spreading from skin eruptions around affected nails

was postulated by the authors as one of the causes of onychomadesis linked to HFMD.

Onychomadesis has also been associated more recently with cases of varicella 21, candida
41 42 19
albicans outside of the neonatal period, fusarium solani , and trichophyton tonsurans .

Idiopathic

There are rare cases reported of idiopathic onychomadesis not associated with any disease or

drug therapy, which presented in a familial autosomal dominant pattern. Idiopathic cases of

onychomadesis can be classified as familial (autosomal dominant inheritance) or sporadic. The

authors previously published a report of a young, healthy female with no family history of

onychomadesis and no seasonal variation in nail shedding and proposed such unusual cases be
18
called “idiopathic sporadic onychomadesis” .

Discussion

Nail plate formation takes place at the nail matrix. The proximal matrix forms the dorsal aspect

of the nail plate and the distal matrix forms the ventral part of the nail. Longitudinal nail growth

must continue for a deformity to be manifested. Therefore, a discrepancy between dorsal and
This article is protected by copyright. All rights reserved.

ventral nail growth must be mandatory to leave a morphologic clue. Nail plate deformities range

from slight indentations of the nail plate (classic form of Beau’s lines) to separation of the nail

plate from the matrix with persistent attachment to the nail bed, a process called

onychomadesis or defluvium unguim. The characteristic early finding is symmetric proximal

onycholysis. When associated with major medical illness, temporary slowing or cessation of nail

plate production results in a transverse groove across the nail. Ultrasound is a modality that has

been used to establish the date of the original nail insult by correlating the length of the nail

plates (new and old) with the normal rate of nail growth. As a result, the timing of the injury

and therefore, the causal agent may be more accurately discerned 46.

Samman suggested nail shedding be divided into two classifications. The first is based on where

the shedding begins. Onychomadesis is proximal shedding from the nail base and onycholysis is

distal shedding, from the nail bed. The second classification is based on whether or not there is

nail loss as well as whether or not scarring occurs. He described loss without scarring as periodic

shedding and depicted autosomal dominant periodic nail shedding as a subgroup of this

category. In this clinical entity, one or more nails is repeatedly shed and replaced with nails on

various digits being shed independently so that there is seldom more than one missing at a time
37
.

The mechanism of nail matrix arrest in the setting of infection, fever, systemic disease, or drug

exposure is unknown. Inhibition of cellular proliferation may occur and would be a logical

explanation during treatment with antimitotic therapy. Another hypothesis is that the matrix

activity and growth rate of the nails remains intact, but the quality of the manufactured nail
44
plate differs, becoming thinner and dystrophic .
This article is protected by copyright. All rights reserved.

Prognosis

In all cases, the condition is described as a temporary event with eventual regrowth of the nails.

Treatment

Most often, treatment entailed management of inciting illness or withdrawal of medication

without mention of nail specific modalities. Two cases reported nail-specific treatments; (1) nails

were treated with 40% urea under occlusion 14 and (2) another case reported using topical
24
halcinonide 0.1% under occlusion for 5 days . In our case of vertical onychomadesis secondary

to chemotherapy, the affected fingernails were mechanically removed as they interfered with

the patient’s ability to grasp objects.

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Figure 1. Onychomadesis. Chemotherapy induced “vertical onychomadesis”.

Figure 2. Onychomadesis. Also note the prescence of Mee’s lines (horizontal white lines which

are concave proximally, corresponding to the shape of the lunulae).

Figure 3. Onychomadesis. Five year-old boy with onychomadesis following HFMD.

Figure 4. Onychomadesis . Thumbnail of patient with idiopathic onychomadesis.

Table 1. Summary
This article is protected by copyright. All rights reserved.

Associations

Autoimmune Alopecia areata, pemphigus vulgaris,

Major medical illness Guillain Barre, major depressive disorder, SJS,

Cronkhite Canada syndrome, peritoneal
dialysis, immunodeficiency, meningitis, MF,
Kawasaki disease

Medication induced Chemotherapeutic agents, antiepileptics,

penicillin, azithromycin, retinoids, lead, lithium

Neonatal Trauma of birth, ?candida albicans

Infection HFMD, varicella, candida albicans, fusarium

solani, T. tonsurans

Idiopathic Hereditary, idiopathic

SJS: Stevens Johnson Syndrome

MF: Mycosis Fungoides

HFMD: Hand-foot-mouth disease

This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.