Superficial Perivascular Lymphohistiocytic Infiltrate Research Articles

Persistent Generalized Cutis Marmorata Telangiectatica Congenita with Venectasia.

Persistent Generalized Cutis Marmorata Telangiectatica Congenita with Venectasia.

An Unusual Presentation of Lichen Striatus.

An Unusual Presentation of Lichen Striatus.

Recurrent pregnancy‐associated erythema annulare centrifugum in a single gestation period

Erythema annulare centrifugum (EAC) is reportedly related to many factors such as immunological disorders, infections, malignancies, foods, and drugs. Pregnancy-associated EAC is extremely rare, with only six cases reported in the literature.1-6 To date, there have been no reports of EAC that disappeared and recurred during a single gestation period. A 34-year-old woman visited our department in the 36th week of her first pregnancy with asymptomatic multiple annular erythematous lesions on the legs. On the examination, the erythematous areas were slightly raised and had slight scales (Figure 1A, B). She reported that the eruption had first appeared in week 10 and spontaneously disappeared within 2 months, then reappeared in week 28 and gradually enlarged centrifugally and increased in number. This was confirmed in serial photographs she had taken. Skin biopsy revealed hyperkeratosis, parakeratosis, mild spongiosis in the epidermis, and a superficial perivascular lymphohistiocytic infiltrate (Figure 1C). She was in good health and had not taken any medication or vaccination during the pregnancy. She had a good pregnancy course except that the fetus was in the breech position. The laboratory test results were normal, including complete blood count, renal and hepatic functions indices, immunoglobulins, antinuclear antibodies, anti-SS-A and anti-SS-B antibodies, and rheumatoid factors. She had no evidence of Sjögren syndrome. She delivered a healthy baby by elective cesarean section in week 38. Although all the erythematous lesions had been increasing in number and enlarging until the delivery, they started to disappear within 2 days after the delivery and wholly resolved within 1 month without any treatment. No recurrence was observed during 4 years of follow-up. In all six reported cases of pregnancy-associated EAC, including ours, eruptions appeared during the first pregnancy. The onset of the lesions occurred in week 12 in two cases and weeks 26–33 in four.1-6 The lesions improved in weeks 33–36 in two cases, and at 3 days to 1 month postpartum in four. These findings suggest that the change in maternal hormone levels during pregnancy is a crucial etiological factor.5 The major possible causative candidates include estrogen, progesterone, and human chorionic gonadotropin (hCG).6 The secretion of hCG differs from that of the other hormones and many other placental proteins. hCG is first detected in maternal serum within 9 days after conception. The hCG levels then rise in a logarithmic fashion, peaking at 8–10 weeks after the last menstrual period, followed by a decline to a nadir at 18 weeks, with subsequent levels remaining constant or slightly increasing in some individuals until delivery.7, 8 The concentrations of estrogen and progesterone gradually increase and are maintained at high concentrations until delivery.8 The fact that the initial lesions appeared during early pregnancy, spontaneously disappeared, and then recurred in a single gestation period in our case may suggest that hCG is the most promising causative candidate in our case. However, it is likely that unknown cofactors will exist because EAC never develops in the second pregnancy. EAC during pregnancy resolves when the hormones return to prepregnancy concentrations. We thank Kelly Zammit, BVSc, from Edanz (https://jp.edanz.com/ac) for editing a draft of this manuscript. The authors declare no conflict of interest. Approval of research protocol: Not applicable. Informed Consent: The patient provided informed consent to publish his photographs and case details. Registry and the Registration No. of the study/trial: Not applicable. Animal Studies: Not applicable.

Clinical features and eosinophilia in pityriasis rubra pilaris: A multicenter cohort

Clinical features and eosinophilia in pityriasis rubra pilaris: A multicenter cohort

SDRIFE-like reaction induced by an intradermal skin test with clindamycin: A case report

Systemic contact dermatitis (SCD) occurs when an individual sensitized to a contact allergen is exposed to that same allergen or a cross-reacting molecule through a systemic route (transcutaneous, transmucosal, oral, intravenous, intramuscular, or inhalated). Baboon syndrome is the most pathognomonic form of SCD, which consists of delayed exanthema affecting intertriginous surfaces (buttocks, upper inner thighs, axillae, etc.). It was described for the first time in 1984, and its name is due to the erythema that occurs in intergluteal folds and thighs, reminiscent of the red bottoms of baboons. Despite the most frequent location being upper inner thighs and buttocks, it can also involve other intertriginous parts of the body. The first cases were observed after exposure to mercury, nickel, and ampicillin. Since then, over 100 cases of similar eruptions under different names have been described. In 2004, the acronym SDRIFE (symmetric drug-related intertriginous and flexural exanthema) was accepted to refer to those cases associated with systemic drugs with typical lesions of baboon syndrome with unknown history of previous skin sensitization. Five clinical criteria were established for diagnosis: (1) occurrence after exposure to systemic drugs, (2) sharply demarcated erythema in the buttocks and/or V-shaped erythema of the thighs, (3) involvement of at least one other flexural fold, (4) symmetry, and (5) the absence of systemic symptoms. Most frequently, it is caused by antibiotics, especially b-lactams. A 72-year-old woman, without atopic history, was referred to our unit to be studied. She developed a generalized pruritic maculopapular rash without systemic symptoms 6 hours after the intake of ibuprofen and clindamycin for arm cellulitis. Treatment was administered with antihistamines and systemic corticosteroids with improvement of the lesions. The condition resolved completely within a few weeks, with a scaly rash and desquamation, but without residual lesions. She had previously tolerated ibuprofen, but it was the first time she was treated with clindamycin. We performed the patch test (PT) on her upper back with ibuprofen (5% in petrolatum) with readings on day 2 (D2) and day 4 (D4) with negative results. An intradermal (ID) test with 0.03 c.c. of clindamycin (30 mg/mL) was carried out with positive readings on D2. In addition, the patient had erythema in antecubital folds, and retroauricular and occipital regions with generalized pruritus (Figure 1). ID tests in 10 healthy controls were negative. To investigate the sensitivity of the PT versus ID test, we asked our patient for permission to perform a PT with clindamycin, even after the positive ID test with the drug, and she accepted. We performed the PT with clindamycin (1% in petrolatum) with positive readings on D2 and D4. A skin biopsy of the ID lesion was taken (Figure 2) in which preserved thickness, foci of spongiosis, and some necrotic keratinocytes were found in the epidermis. In the dermis, edema, blood extravasation, and a perivascular inflammatory infiltrate, predominantly lymphocytic with some eosinophils, were seen. After written informed consent, a single-blind oral challenge test (OCT) was performed with ibuprofen at gradually increasing doses, at 1-hour intervals up to 600 mg, following the protocol of the European Academy of Allergy and Clinical Immunology drugs committee, with negative result. We describe a case of SDRIFE-like reaction as a complication of an ID test. Usually skin testing is an essential and safe tool for the diagnosis, but the risk of inducing a systemic reaction exists. Although the PT was positive in our patient, it can be negative in one-third to one-half of the patients with SDRIFE. Perhaps this could be due to reduced absorption of systemically administered drugs when applied to the skin by PT. We thought ID with delayed reading would be more accurate for diagnosis than PT, but it may have more risks for patients. The OCT or re-challenge test is positive in almost all reported cases of SDRIFE and at this time is the most reliable way to confirm the diagnosis. There are a few reports in the literature that document SDRIFE due to clindamycin, but we have not found any reports of positive delayed prick or ID tests with clindamycin in patients with SDRIFE. Delayed rashes after the OCT with clindamycin have also been described. Histopathology most commonly demonstrates a superficial perivascular lymphohistiocytic infiltrate sometimes including neutrophils, eosinophils, or mast cells with or without epidermal spongiosis, and necrotic keratinocytes can also be observed, compatible with the findings in the biopsy of the ID test of our patient. The pathogenesis of SDRIFE is not yet known with certainty, although the clinical manifestations and results of skin tests suggest that it could be due to a type IV hypersensitivity mechanism. In our patient, the observed clinical manifestations as well as the results of skin tests and the morphological findings of the

Favre-Racouchot syndrome.

Favre-Racouchot syndrome.

Is acquired symmetrical acrokeratoderma a new dermatosis? Two case reports and Chinese literature review

A series of cases characterized by symmetrical acral hyperkeratosis, mainly involving the dorsal surface of the hands, feet, and wrists, but sparing the palmoplantar areas, as well as rapid immersion upon exposure to water have been recently described in China, but similar disorders have not been reported in the English literature. The clinicopathologic features of two cases of acquired symmetrical acrokeratoderma were reported and 27 Chinese patients were reviewed. The disorder typically occurred in young or middle aged men. Brown to black hyperkeratotic patches were symmetrically distributed particularly on the wrists and dorsum of hands, fingers, and feet, but without involvement of palms and soles. The lesions became whitish with mild swelling immediately after contact with water and improved generally in winter. Histopathologic examination revealed epidermal hyperkeratosis, acanthosis, and papillomatous hyperplasia, as well as superficial perivascular lymphohistiocytic infiltrate. Main ultrastructural features of the immersed lesion were epidermal hyperkeratosis and spongiosis with partial split of the desmosomes. This disorder may be a new dermatosis, and the term "acquired symmetrical acrokeratoderma" could exactly reflect its clinicopathologic characteristics.

Antineoplastic therapy-induced palmar plantar erythrodysesthesia ('hand-foot') syndrome. Incidence, recognition and management.

Palmar plantar erythrodysesthesia (PPE) is a distinctive and relatively frequent toxic reaction related to some chemotherapeutic agents. Doxorubicin, cytarabine, docetaxel, and fluorouracil are the most frequently implicated agents. PPE seems to be dose dependent and both peak drug concentration and total cumulative dose determine its occurrence. PPE presents as a painful erythema, often preceded by paresthesia, located on the palms and soles in the context of treatment with chemotherapy. Histologically, PPE shows few specific findings. Mild spongiosis, scattered necrotic and dyskeratotic keratinocytes and vacuolar degeneration of the basal layer is seen. Dermal changes in most cases include dilated blood vessels, papillary edema, and a sparse superficial perivascular lymphohistiocytic infiltrate can be found in varying degrees in the epidermis. Withdrawal or dose reduction of the implicated drug usually gives rise to amelioration of the symptoms. Supportive treatments such as topical wound care, elevation, and cold compresses may help to relieve the pain. Use of systemic corticosteroids, pyridoxine (vitamin B6), blood flow reduction, and, recently, topical 99% dimethyl-sulfoxide have been used with variable outcomes. It could be of interest to consider them as preventive measures when drugs with a strong association with PPE are going to be administered.

Brunsting-Perry Cicatricial Pemphigoid Precipitated by Trauma

To the Editor.— A 78-year-old Hispanic man was without previous skin lesions until he sustained a hot oil burn to his left cheek. He was seen in the emergency department at the Brooklyn (NY) Veterans Administration Medical Center, noted to have a small crusted lesion on the left cheek, diagnosed as having a second-degree thermal burn, and treated with topical silver sulfadiazine cream. When seen in the dermatology clinic 1 week later, his lesions were resolving and showed only crusts on an erythematous base with slight scarring. No further care was recommended. One week later, he returned to the clinic with multiple small, tense blisters in a ring around the previously involved area (Fig 1). Tzanck preparation and herpes simplex cultures were negative. Histopathologic findings revealed a subepidermal blister and superficial perivascular lymphohistiocytic infiltrate with multiple eosinophils (Fig 2). Direct immunofluorescence showed heavy fibrillar deposits of IgG at the dermoepidermal