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We report 3 patients, without bleeding disorders, presenting with onychomadesis and focal haemorrhages at multiple proximal nail folds or in the nail tissue. In one of our patients it was possible to check the appearance of a drop of blood on each side, beneath the proximal nail fold when he pressed the pulp of the fingers of his previously fractured forearm on a hard surface. All patients had major peripheral or major peripheral and central neurological deficits, prior to the nail bleeding. Peripheral vascular dilatation produced by paralysis of the vasoconstrictors in the nail area slows the venous return in the dilated vessels, mainly in the proximal nail fold.

Dear Editor: Hand-foot-mouth disease (HFMD) is a common illness of children, characterized by fever and vesicular eruptions on the hands, feet, and mouth. Variable strains of viruses are known to be related, such as coxsackievirus A5, A6, A7, A9, A10, A16 (most common), B1, B2, B3, B5; echoviruses E3, E4, E9; and enterovirus 711,2. Onychomadesis is defined as proximal nail plate separation from the nail matrix and nail bed caused by a temporary arrest in nail matrix activity, and may present as a Beau's line. We report on four Korean children who developed onychomadesis about 4 weeks after HFMD. The children presented with transverse Beau's line or onychomadesis on the fingernails or toenails (Fig. 1). They all had HFMD about a month ago, and their information is briefly summarized in Table 1. All patients had no history of trauma and periungual dermatitis, and the affected nails were not of the fingers involved in HFMD. Some were given antibiotic ointment, whereas spontaneous regression was expected in others. The affected nails eventually shed completely without deformity in the new nails. Conditions that can cause onychomadesis include severe systemic diseases, nutritional deficiencies, trauma, periungual dermatitis, chemotherapy, fever, drug ingestion, and infection1. Nail matrix arrest with fever, infection, systemic disease, or drug exposure can be explained by inflammation in the periungual and matrix regions, inhibition of cellular proliferation, alteration in the quality of manufactured nail plate, and nerve injury or dysfunction2. The mechanism of onychomadesis after HFMD is not fully understood. However, viral infection is responsible for onychomadesis, as a temporal latency exists between HFMD and onychomadesis. Bettoli et al.3 reported that inflammation secondary to viral infection around the nail matrix may be induced directly by viruses or indirectly by virus-specific immunocomplexes and consequent distal embolism, and Cabrerizo et al.4 suggested that virus replication directly damage the nail matrix, based on the presence of coxsackievirus 6 in shed nails. Because fingernails with onychomadesis are not always of the fingers affected by HFMD, as in our cases, an indirect effect of viral infection on the nail matrix is more plausible. Onychomadesis can also occur on toenails; however, it is less frequent even when vesicles were present on the feet previously. Whether this is due to less frequent detection or a different mechanism is not known. As previously mentioned, many different types of viruses are known to be associated. Furthermore, more than one viral strain may be involved in nail matrix arrest1. In reality, onychomadesis cases after HFMD are underestimated because onychomadesis spontaneously regresses, and the interval between HFMD and onychomadesis is about a month. In all cases, the onset of onychomadesis was about a month or two later than the peak prevalence of HFMD (May-August 2013)5. By reporting these cases for the first time in Korea, we emphasize the importance of recognizing the association between HFMD and onychomadesis especially when children with onychomadesis present a month after an HFMD outbreak, to avoid unnecessary overtreatment and to reassure the patient's parents. Fig. 1 (A) Three-year-old boy with onychomadesis on the left middle, right index, and right ring fingernails. (B) Four-year-old girl with prominent Beau's lines on the left index and middle fingernails. (C) Third patient with onychomadesis on the left index ... Table 1 Characteristics of cases of onychomadesis after hand-foot-mouth disease

The records of six dogs in which a diagnosis of symmetrical lupoid onychodystrophy (SLO) had been made were examined retrospectively. The age at onset ranged from six months to eight years. All the dogs had been presented with onycholysis, onychomadesis, onychalgia and onychodystrophy. The diagnosis of SLO was confirmed in all cases by histological examination. Histological features were similar in all cases and included hydropic degeneration of the basal cell layer, pigmentary incontinence and a cell-rich interface dermatitis. Response (defined as good, partial or failure) to various therapies was compared. Treatments (as initial therapy or following previous treatment failure) included essential fatty acids (EFA) (three cases), a combination of tetracycline and nicotinamide (four cases) and azathioprine and/or prednisolone (one case each). EFA therapy resulted in one good response, one partial and one failure, tetracycline and nicotinamide in two good responses, one partial and one failure, and azathioprine and/or prednisolone in one good and one partial response. Although all treatments were successful in some cases, none was universally effective.

diarrhea, weight loss, and abdominal pain for 4 months. Noticeable signs of nail dystrophy (onychomadesis of all nails) were present (●" Fig. 1a) along with alopecia and cutaneous foci of hyperpigmentation (●" Fig. 1b). Upper-gastrointestinal endoscopy revealed a large number of strawberry-like polyps of different size in the stomach (●" Fig. 2). Colonoscopy revealed polyposis of the whole colon, including the rectum. The majority of the polyps had a strawberrylike, adenomatous, and hyperplastic appearance (●" Fig. 3). Histologically, the majority of the polyps were juvenile-like with cystic dilatations of the glands and a benign mucinous epithelium. The glands were filled with a large amount of mucin (●" Fig. 4). Some adenomatous polyps with lowgrade dysplasia in the colon were also detected. A subsequent enteroscopy did not find polyps; however, edema and small indentation of the jejunum were present. Immunohistochemistry showed total alactasia and a strong positivity for tumor necrosis factor (TNF) in the macrophages and lymphocytes. Based on both the clinical and endoscopic picture, a diagnosis of Cronkhite-Canada syndrome was established. Despite complex treatment, the clinical course was unfavourable. Since the clinical state of the patient did not improve, anti-TNF-α treatment was considered. TNF-α activity was examined in the small-intestinal mucosa, and the results showed a strong intracellular expression of TNF-α. Unfortunately, an experimental anti-TNF-α treatment could not be introduced, because of the rapid progression of the disease. The patient died 4 months after the diagnosis of Cronkhite-Canada syndrome was established. A fulminant course of Cronkhite-Canada syndrome

Nail involvement in pemphigus vulgaris is relatively rare. We describe a case of severe pemphigus involving both the skin and oral mucosa in which an acute exacerbation was preceded by the onset of nail involvement of all 4 extremities. Nail involvement occurred in the form of hemorrhagic paronychia of multiple digits. Oral, cutaneous, and nail manifestations of the disease were all well controlled by systemic therapy. A review of the literature on nail involvement in pemphigus reveals that this involvement may be manifested in multiple ways, with chronic paronychia and onychomadesis being the most common. Involvement of the nail occurs most frequently either as part of the initial presentation, or just before or concurrent with a flare of pre-existing disease. Nail involvement, when it occurs, is usually present when the disease is severe. Topical therapy is insufficient, and systemic therapy is warranted. In the majority of cases, nail recovery is complete, with no residual damage. (J Am Acad Dermatol 2000;43:529–35.)

Onychomadesis is defined as spontaneous separation of the nail plate from the nail bed, beginning at its proximal end and resulting in the shedding of the nail. It has been associated with a variety of clinical settings, including systemic illnesses, generalized skin diseases, and drug therapies. There have been a small number of reports in the older literature of idiopathic onychomadesis occurring in a familial pattern. We report the case of a healthy 12-year-old girl and her mother, both of whom have experienced recurrent onychomadesis affecting multiple digits, and in the absence of any causal disease or medication.

Valproic acid (VPA) is frequently used as an antiepileptic drug. Several side effects are known. We report on a child with onychomadesis as a possible side-effect of treatment with VPA. Normal nail growth was observed after stopping VPA. The pathomechanism of onychomadesis due to VPA treatment remains unclear.

We describe a case of moderate hand–foot syndrome and nail toxicity simultaneously occurred in a 69-year-old man with advanced gastric cancer (cT4-N3-M1, G3) previously treated with numerous antineoplastic agents, including PELFw (5-fluorouracil, epidoxorubicin, leucovorin, and cisplatin) and taxoids. Due to a recalcitrant course, the above therapeutic agents were discontinued for 4 weeks and he was given solely capecitabine 1250 mg twice daily for 2 weeks at 3-weekly intervals. After the third course of chemotherapy he developed a moderate hand–foot syndrome, acute paronychia, exudative hyponychial dermatitis, multiple periungual pyogenic granuloma-like lesions, onychomadesis and onycholysis (Figures 1A,B and 2A,B). Figure 1 (A,B) Exudative hyponychial dermatitis with transparent nonviscous exudative discharge; hyperkeratosis, onycholysis, onychomadesis and periungual pyogenic granuloma-like lesions Figure 2 (A,B) Subungual hyperkeratosis, onycholysis, and Beau's lines; erythema and desquamation involving the hands Clinical examination revealed subungual hyperkeratosis, onycholysis, onychomadesis, acute paronychia and transparent malodorous, nonviscous, exudative discharge from toenails, especially upon squeezing. Slightly erythematous papular and vascular lesions (granuloma-like) in the proximal nail fold region of four of his toes and Beau's lines were also observed. Hypercurvature on the transverse axis of the nail plates was present, giving a pinched shape to the free edges. No other nail changes such as leukonychia or hyponychium hyperpigmentation were observed. Microbiological examination did not reveal bacterial infections, and repeated potassium hydroxide examinations of the nails did not show fungal hyphae. Treatment was initiated with soaking the nails with 0–5% potassium permanganate solution and application of gentamicin ointment. The hyponychial dermatitis and the above-described nail changes, including periungual pyogenic granuloma-like lesions, gradually resolved after the cessation of capecitabine for 8–12 weeks. The patient lost the nail of the great toes after about 3 weeks. Naranjo algorithm evaluation obtained a score of 9, which indicates a high probability that the adverse reaction was due to the drug [1]. Several chemotherapeutic agents, including taxoids, cyclophosphamide, doxorubicin/daunorubicin, 5-fluorouracil and vincristine, and combinations have been reported to induce nail and periungual changes: alterations may involve nail matrix (e.g. Beau's lines, onychomadesis, hyperpigmentation), nail bed (e.g. onycholysis, subungual haemorrhage, haematoma), and proximal nail fold (e.g. acute paronychia, periungual pyogenic granuloma) [2]. These adverse events are mostly mild to moderate in severity, but, if not properly managed, can result in significant pain and interfere with activities of daily living. Capecitabine (Xeloda®; Roche, Basel, Switzerland) is a fluoropyrimidine carbamate with antineoplastic activity. It is an orally administered systemic prodrug of 5′-deoxy-5-fluorouridine which is converted to 5-fluorouracil and preferentially activated at the tumour site. Fluoropyrimidine carbamate is a chemotherapeutic drug currently approved by the US Food Drug Administration for use as first-line therapy in patients with metastatic colorectal cancer or metastatic breast cancer. Capecitabine has also been used, alone or in different combinations, as a treatment of advanced gastric cancer, with interesting results [3, 4]. In clinical trials, the most frequent side-effects include gastrointestinal and haematological complications, hand–foot syndrome, hyperbilirubinaemia and anorexia. Although hand–foot syndrome is observed in up to 50% of patients treated with capecitabine, other mucocutaneous side-effects such as dermatitis, stomatitis, skin/nail discoloration and alopecia have been rarely reported [3, 4]. The incidence of nail changes is probably underestimated and still ill-defined; in particular, although the effects of taxoids [5] and epidermal growth factor receptor inhibitors (anti-EGFR agents) [6] are well described, there are, to our knowledge, only few reports of nail toxicity associated with capecitabine as monotherapy [7–9]. The aetiology of chemotherapy-induced nail changes is unclear; probably, immunosuppression and consequent colonization of the nail bed, change and disruption of the nail plate, subungual oedema with loss of adhesion between nail bed and nail plate and inflammatory and erosive processes may contribute to the development of nail and periungual abnormalities [7–10]. The nail toxicity seen in our patient was unique for the simultaneous occurrence of subungual hyperkeratosis, onycholysis, onychomadesis, paronychia, hyponychial dermatitis and periungual pyogenic granuloma-like lesions. As capecitabine is being increasingly used in the treatment of advanced breast and colorectal cancers as well as other solid cancers, clinicians should be aware of the novel clinical side-effects of this medication that could lead to substantial subjective toxicity, with impairment of quality of life and discontinuation of chemotherapy.

The unusual case of a patient on peritoneal dialysis who progressively developed onychodystrophy of the hands 2 months after Acinetobacter peritonitis had been reported. The nail disease consisted of acute pseudoclubbing, elkonyxis, severe Beau's lines and onychomadesis and showed spontaneous recovery within 4 months. Although reminiscent of severe Beau's lines and reflex sympathetic dystrophy, this observation shows a peculiar nail disorder of unknown cause.

An epileptic teenager put on carbamazepine therapy presented with onychomadesis 6 months later. Carbamazepine was substituted with phenytoin. Affected nails were shed and healthy nails regrew in 5 months.

We describe a case of pemphigus foliaceus (PF) confined to the nails in a 3-year-old male Hungarian short-haired pointer. The dog was presented with multiple painful nails causing lameness. Various treatments (antibiotics, antiseptic lotions) were ineffective. The lesions were confined to the nails. Dermatological examination showed sub- or intraungueal pustules progressively causing onychomadesis. Examination of the inside of the nails revealed a yellowish malodorous material. Some nails exhibited onychoschizis and onychogryphosis. An erythematous perionyxis was observed around some nails. Cytology of this yellowish material showed nondegenerative neutrophils and numerous acidophilic acantholytic keratinocytes. Fungal and bacterial cultures performed from nails were negative. Histopathological examination of an entire nail revealed the presence of stratified pustules within the nails and under the nail. These pustules contained nondegenerative neutrophils, eosinophils and numerous acidophilic acantholytic keratinocytes. These lesions were compatible with pemphigus foliaceus. Prednisolone (1 mg/kg twice daily, orally) plus a dermocorticoid (clobetasol, twice daily) was prescribed for 1 month. Clinical improvement was observed. The same treatment was discontinued for another month. Then, the dosage of prednisolone was tapered to a 3-day regimen for 2 months with daily clobetasol applications. During the following 6 months, topical therapy was discontinued. Four relapses were observed within 4 years. This is the first report of a case of PF strictly confined to the nails. Funding: Self-funded.

Summary With the exception of acropustulosis, nail disease responds poorly to etretinate. When used to treat other dermatological conditions etretinate is frequently toxic to the normal nail and may affect any or all of its epidermal components. The desquamative dermatitis, induced by etretinate, may account for many of the drug's side-effects on the nail. These include chronic paronychia, onycholysis, onychomadesis, nail shedding, onychoschizia, fragility and the formation of excess granulation tissue. Some of these changes resemble those found in psoriatic paronychia and similarities are drawn between psoriasis and the retinoid dermatitis which presents with identical features in the discharge from beneath the proximal nail-fold. The desquamative reaction in patients taking etretinate always affects the lips and, in addition, may be widespread or mainly localized to the nail apparatus.

Background Treatment of symmetrical onychomadesis (symmetrical lupoid onychodystrophy) is a challenging task for dermatologists. The acute phase is characterized by sloughing of claw plates and loose claws have to be removed and secondary infections treated. The goal of long-term treatment is to allow claws to re-grow with normal quality and to achieve life-long lack of recurrence. The aim of this randomized treatment trial was to see if adding fish oil or cyclosporine to a diet rich in omega-3 could improve the treatment outcome of symmetrical onychomadesis in Gordon and English setters. All dogs were fed Eukanuba Veterinary Diets Dermatosis® exclusively during the six month treatment trial. The treatment outcome was measured as the change in number of healthy claws during treatment, as well as the long-term effect on hunting ability and recurrence of onychomadesis. The hypothesis was that cyclosporine provides a stronger and different immune modulating property than fish oil and therefore would give a better treatment outcome in dogs with symmetrical onychomadesis eating a diet rich in omega-3 fatty acids. Results Six Gordon setters and one English setter were treated with 5 mg/kg cyclosporine once daily for six months and seven Gordon setters were treated with 10 ml Dr Baddaky fish oil® once daily for six months. All dogs were evaluated every month and the numbers of healthy claws were recorded. There was a statistically significant improvement in the number of healthy claws after six months of treatment with a median increase of 13.5 claws for both groups. However, there was no statistically significant difference between the two treatment groups regarding the improvement in number of healthy claws, as assessed using the Wilcoxon rank-sum test (P = 0.15). Dogs in the cyclosporine group had a median increase of 10 healthy claws after six months of treatment while the median for the fish oil group was 14. Long-term cure was not achieved with either treatment. Conclusion Cyclosporine and fish oil appeared to be equally effective in treating symmetrical onychomadesis when the dog is fed a diet high in omega-3.

Nails are underutilized as diagnostic tools, despite being involved in many dermatologic conditions. This paper explores new concepts in the treatment of median nail dystrophy (MND), onychomycosis, and the nail pathology of hand, foot, and mouth disease (HFMD). A Pubmed database literature search was conducted for MND treatment, onychomycosis treatment, and HFMD nail pathology. Only papers published after January 2008 were reviewed. The results showed that 0.1% tacrolimus ointment can be an effective treatment for MND. Early studies on laser therapy indicate that it is a safe and efficacious treatment option for onychomycosis, compared to conventional oral antifungal agents. Vicks VapoRub (The Proctor & Gamble Company, Cincinnati, OH) is effective against onychomycosis and is a reasonable option in patients who choose to forgo conventional treatments. Lastly, there is evidence to support a correlation between HFMD and onychomadesis.

Nail changes are observed in 25% ofpatients with SLE; these include pitting, ridging, onychomadesis, splinter hemorrhages, clubbing, onycholysis, and leukonychia that may be total, striate, punctate, longitudinal, or variegate in nature." According to Urowitz et al.,10 these nail changes represent nonspecific defects in keratinization caused by traumas or the underlying systemic disease. PWSO caused by T. rubrum should be added to the list of nail changes in SLE and should be differentiated from leukonychia caused by trauma and systemic or congenital diseases. 11

To the Editor.— A patient with pemphigus vulgaris who had onychomadesis was seen by us for the first time recently. We believe that many clinicians familiar with cases of pemphigus vulgaris would not have seen this unusual feature. Report of a Case.— A 28-year-old man was admitted to our hospital with blisters on his skin and ulcerations in his oral cavity of two months' duration. The clinical diagnosis of pemphigus

In most disorders of the nail in which the aromatic retinoid etretinate has been used, the results have been generally disappointing. The exception is its success in acropustulosis. In other dermatological conditions, the same therapeutic regime may induce a variety of unwanted effects on the nail apparatus, including chronic paronychia, onycholysis, onychomadesis, nail shedding, onychoschizia, fragility and periungual granulation tissue. Many of these changes resemble those found in psoriasis, particularly psoriatic paronychia. In this presentation, parallels will be drawn between psoriatic pathology and retinoid desquamative dermatitis which resembles it in producing similar discharge from beneath the proximal nail fold. This may be the basis for the nail signs induced by etretinate.

A case of allergic contact dermatitis to a new nail hardening formula put out by a well-known cosmetic firm is reported. This caused a subacute paronychia, onycholysis, and onychomadesis. Regrowth of the nails occurred normally after a topical steroid ointment was applied. Patch tests with the preparation confirmed the diagnosis.

Examination of the hands and feet for small punctate keratoderma will sometimes provide an explanation for nail deformities or changes, such as longitudinal fissures, onychomadesis, and onychogryphosis.

In spite of much literature, the nails remain one of the subjects about which there is very little knowledge. Histopathologic studies are manifestly difficult, and the etiology of many lesions remains as obscure now as it ever has been. It is known, of course, that fungi may attack the nails and cause lesions of various forms, that some of the generalized dermatoses are accompanied by changes in the nails, and that there are a number of congenital anomalies of the finger-nails and toe-nails. Beyond this very little is known. Among the lesions most infrequently seen is the group that presents a partial or total loss of the nails without any previous inflammatory process to which this loss may be ascribed. Various causes have been suggested for this condition, but there is no unanimity of opinion on the subject. The cases described in the literature can be divided into two

Background In 2010, we observed children with atypical presentations of hand-foot-mouth disease (HFMD), such as rashes on earlobes and faces, or bullae on trunks and bilateral limbs. Hyperpigmentation later developed as the bullous lesions crusted. Thus, we intended to study the etiology of the illness and the phylogeny of the pathogens. Method Patients were prospectively enrolled in a tertiary medical center in Taipei, Taiwan. The definition of atypical HFMD includes symptoms of acute viral infection with either of the following presentations: (1) maculopapular rashes presenting on the trunks, buttocks or facial areas, or (2) large vesicles or bullae on any sites of the body. Patients were classified into two groups according to vesicle sizes by two pediatricians at different points in time. The large vesicle group was defined as having vesciculobullous lesions ≥ 1 cm in diameter; the small rashes group had maculopapular rashes < 1cm in diameter. Two throat swabs were collected from each patient for virus isolation and reverse transcription polymerase chain reactions. Results We enrolled 101 patients between March and December 2010. The mean age of the participants was 3.3 ± 3.0 years (median age: 2.5 years, range: 21 days-13.5 years). The ratio of males to females was 1.8 to 1. All samples were enterovirus-positive, including coxsackievirus A6 (80%), coxsackievirus A16 (6%), enterovirus 71 (1%), coxsackievirus A5 (1%) and 12 non-typable enterovirus (12%). Bullous fluid aspirated from 2 patients also grew coxsackievirus A6. Among the patients infected with coxsackievirus A6, 54% (45/81) had bullae, compared to 25% (5/20) of those having non-coxsackievirus A6 infections (P=0.02). Fourteen cases had myoclonic jerks and one boy was diagnosed with febrile convulsions. None had complications or sequelae. Phylogenetic analysis showed the strains in Taiwan in 2010 shared more commonality with strains from Finland in 2009 (GenBank: FJ870502-FJ870508), and were close to those circulating in Japan in 2011 (GenBank: AB649286-AB649291). Conclusions Coxsackievirus A6 infections may cause atypical manifestations of HFMD, including vesicles or papules on faces or bullae on trunks. These features could provide valuable information to distinguish this versatile enterovirus infection from other virus-induced vesiculobullous diseases.