Onychomadesis can be attributed to a wide variety of causes, including allergic contact dermatitis, paronychia, pustular psoriasis, and trauma, and most cases are considered to be idiopathic. Onychomadesis at the same level involving several nails suggests a systemic cause, such as fever, erythroderma, use of drugs such as anti-tumoral chemotherapeutics, carbamazepine, lithium salts, retinoids and, at the infantile age, viral infections such as Kawasaki disease, and hand, foot, and mouth disease (HFMD).[1-10]
In September 2011, in the arc of a few days, three adults came to our specialized nail outpatient clinic for a suspicion of “onychomycosis”. Upon physical exam, we observed onychomadesis, while mycological exam excluded the presence of fungi. Clinical history and work-up allowed us, in all three cases, to link this nail alteration to HFMD experienced by these patients in the late springtime.
A 27-year-old female babysitter, who lived in Florence, came to our ambulatory care clinic because of the presence of nail alterations. She was otherwise in excellent health. Upon physical exam, onychomadesis was present on six nails of her hands (Fig. 1). The detachment was at the same level in all nails, and a regrowth of the lamina of approximately 0.8 cm was visible. No alterations were found on the periungueal tissue. The other fingernails and all toenails were normal. According to the patient, onychomadesis appeared at the same time in all fingernails in the first days of July. There was no history of any drug intake. The patient stated that in May she developed HFMD, which was contracted from the child that she was taking care of. This diagnosis was confirmed by an isolation of coxsackievirus A6 taken from laryngeal and fecal samples. She affirmed that the infection spared the fingers and the periungueal tissue in particular. During this period, she took solely anti-inflammatory medications and antipyretics for three days. The body temperature never reached above 38 °C. Complete blood count (CBC) with differential and a complete metabolic panel were unremarkable. IgG antibodies vs coxsackievirus and enteroviruses demonstrated a high titer for coxsackievirus A6. No therapy was prescribed, and a clinical follow-up was performed after six weeks, during which the lesions had completely disappeared.
Cases 2 and 3
Two brothers, residents of Florence, 25 and 30 years old, respectively, were referred to our dermatological clinic due to a clinical presentation similar to that of Case 1 but with involvement of all fingernails. As in the preceding case, the periungueal tissue of nails was not altered. Clinical history was positive for a slight afebrile HFMD presented in May, which was confirmed by pharyngeal swab and isolation of the coxsackievirus A6. The patient had not taken any prescription drugs during and after having this disease. As in the preceding case, the vesicles were not seen on periungueal tissue. Onychomadesis on all nails was seen after 40 days (Fig. 2). CBC with differential and a complete metabolic panel were within normal range. A positive IgG titer for coxsackievirus A6 was found. After eight weeks, the onychomadesis completely resolved.
In all three patients, the temporal onset of onychomadesis was 40 days after the viral infection. The absence of drug intake and of trauma, or other skin or systemic diseases, is suggestive of a causal relationship between nail shedding and HFMD. In addition, we excluded fever as a causative factor as none of our patients had a body temperature above 38 °C. The existence of an HFMD followed by nail shedding was first reported in pediatric patients in 2000 by Clementz and Mancini, and in 2001 by Bernier et al. This finding was subsequently confirmed in infectious disease literature by epidemiological studies performed in Spain and Finland.[4-7] Research studies performed in Finland by Österback et al. demonstrate that onychomadesis is associated specifically with coxsackievirus A6, as in our three patients. These data have also been confirmed in Taiwan, where nail alterations were seen in 37% of patients with a previous coxsackievirus A6 infection and only in 5% of patients with non-A6 virus infection. The mechanism by which onychomadesis develops has not yet been identified. Haneke, who did not exclude that total arrest of nail growth was caused by the virus, hypothesized that nail shedding may be the consequence of vesicles localized in the periungueal tissue. This hypothesis is not supported by our case series, as none of the three patients had lesions on the fingers. In this sense, Österback et al. detected CA6 in shedding nail fragments of a patient who had onychomadesis following an HFMD episode by using reverse transcriptase-polymerase chain reaction and suggested that CA6 virus replication could damage the nail matrix, resulting in onychomadesis.
To our knowledge, there are few reports in the current dermatological literature describing onychomadesis from HFMD in adults. This suggests that the occurrence may be exceptional; however, we support the notion that it is most probably underreported. HFMD generally affects children younger than 10 years old and in adults has minor manifestations and thereby easily goes unrecognized. We maintain that among the diverse causes of onychomadesis in adults, HFMD should be taken into consideration even if considered rare in this age group.