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Lipoid proteinosis (LP) or Hyalinosis Cutis et Mucosae or Urbach-Wiethe disease is a rare autosomal recessive genodermatosis characterized by an amorphous hyaline material deposition in the skin mucosa and viscera. The clinical symptoms of this disease often begin in childhood, which persist throughout life. Skin manifestations include inflammation, scaling, acne, and eventually ulceration, and hyaline amorphous deposits in these areas of the wound cause a waxy and thick appearance on the skin. In addition, wounds leave atrophic scars like chickenpox.Herein, we present the first case of LP in the north of Iran; although LP is a sporadic disease, it occurs all around the world, with about 400 cases worldwide having been reported thus far.We report the case of a 28-year-old female patient with a history of skin lesions on her face, scalp, extremities, and buttock, as well as hoarse cry, respiratory problems, dysphagia, and migraine since childhood. There was no evidence of other clinical presentations. A biopsy was taken from the lesions, and the patient was diagnosed with LP. A laryngeal laser was performed for the patient, and peeling creams were used for her skin lesions.According to previous findings, there has been no case report of LP with systemic symptoms in the north of Iran.

Tinea capitis (TC) is the most common dermatophyte scalp infection in children and an unusual dermatophytosis in adults. The clinical appearance of tinea capitis is highly variable and depends on the causative organism, type of hair invasion, and degree of the host inflammatory response. The commonly observed features are patchy hair loss with varying degrees of scaling and erythema. The clinical signs may be subtle and diagnosis may be challenging. We report the case of an adult patient with tinea capitis mimicking alopecia areata. The patient was initially diagnosed with alopecia areata and completed one month of treatment without clinical benefits. In view of no clinical signs of tinea capitis, a biopsy was performed. A scalp punch biopsy revealed an endothrix dermatophytosis. The patient’s medication was switched to 250 mg terbinafine daily for 8 weeks and 2% ketoconazole shampoo. The patient completed two months of therapy with maintenance of hair regrowth and resolution of symptoms and scales.

Background Baboon syndrome is a rare, type IV hypersensitivity reaction causing a maculopapular rash. Tamoxifen is an antineoplastic agent, working as an estrogen receptor antagonist, also called a selective estrogen receptor modulator. A variety of rashes were reported with Tamoxifen use to‐date except baboon syndrome. The Tamoxifen‐induced baboon syndrome seems to be reversible, as discontinuation of the drug improves clinical outcomes. Aim Herein, we present the first case of Tamoxifen‐induced baboon syndrome which occurred 8 years after initiation of Tamoxifen use. Patients A 44‐year‐old woman presented with papulovesicular eruption on her body and erythema on her face for a duration of 6 months. There was no evidence of ocular or mucosal involvement. She was diagnosed with breast cancer and treated with tamoxifen 10 mg twice daily over the past 8 years. She was not taking other medications or over‐the‐counter supplements at the time of presentation. The patient underwent urgent skin biopsies of two lesions on her buttock and thigh. No organisms were seen on Gram stain. The patient's skin biopsy revealed extensive hyperorthokeratosis, minimal parakeratosis, hypergranulosis, and lichenoid interface dermatitis in the irregularly acanthotic epidermis supporting diagnosis of fixed drug eruption. Following a multidisciplinary discussion, the patient was diagnosed with baboon syndrome or symmetrical drug‐related intertriginous and flexural exanthema (SDRIFE) associated with Tamoxifen. Results Hence, Tamoxifen was immediately discontinued and treated with oral steroid along with topical agents. She showed improvement of clinical abnormalities within days after discontinuation of Tamoxifen. Conclusions Given the widespread use of Tamoxifen in the management of patients with breast cancer, it is important that healthcare professionals monitor for rare, however clinically significant, and potentially life‐threatening dermatological manifestations of Tamoxifen use, such as baboon syndrome.

Background AA is an acquired dermatosis distributed universally, with multifactorial etiology. It affects the hair follicle with or without nail involvement, resulting in an acute nonscarring alopecia with a relapsing course.1 Being a relatively common skin disease, LPP (lichen planopilaris) is initiated by a chronic lymphocytic inflammation that selectively destructs the hair follicles and eventually leads to scarring alopecia. Also, even though there is enough literature available for the co-existence of AA and LPP with each other and their association with other autoimmune conditions, there are only very few reports on the anatomical concomitance of both disorders.3 AIMS: Although the incidence of not only one but two autoimmune diseases in an immunosuppressed individual is very unusual, we hereby report a case of co-localization of AA and LPP in a patient receiving immunosuppression due to a previous history of SLE (Systemic lupus erythematosus). Patients A 37-year-old woman, housewife, presented to our office with general alopecia on the scalp since about two years ago (Figure 1), particularly on the vertex which was accompanied by mild itching and trichodynia. She had a history of hypothyroidism and lupus erythematosus arthritis. She had been receiving long-term treatment with prednisolone, hydroxychloroquine, azathioprine, and levothyroxine but had not been treated for hair loss. Despite being on all of the above-mentioned immunosuppressants, the patient developed AA and LPP which are both immune-mediated diseases. Results In addition to continuing her oral immunosuppressants, the patient was treated with Minoxidil 5% and Clobetasol solution as well as a higher dose of Azathioprine than she was receiving beforehand. Approximately, 3 months into the treatment, the follicular hyperkeratosis and scalp erythema resolved. Also, hair growth could be seen on AA spots. Conclusion Our case report is indicating the possibly mutual immunopathogenesis of these two T cell-mediated disorders. Furthermore, we want to bring attention to the probability of new autoimmune diseases occurring even during treatment with immunosuppressive medications.

Erythema induratum (EI) is a rare chronic disease, which occurs with cutaneous tuberculosis (TB). Nodular vasculitis, much rarer than erythema induratum, describes the same condition but without cutaneous TB, with lesions usually in the lower legs and rarely on the breasts. We report the case of a 46-year-old female with a history of crusted skin and necrotic lesions two years before, which, once self-limited, multiplied one month before and transferred to uncommon sites of the body, such as the breast. There was no evidence of other clinical presentations, and a chest X-ray gave no pathological findings. A biopsy was taken from the lesions, and the patient was diagnosed with erythema induratum without cutaneous tuberculosis, that is, nodular vasculitis. After treatment with calcineurin-inhibiting tacrolimus ointment, topical corticosteroids, and immunosuppressive oral azathioprine, the lesions improved.

Background Acute Generalized Exanthematous Pustulosis (AGEP)is a rare, severe skin reactionmainly caused by medications such as antibiotics, anti fungals, Calcium channel blockers and Anti malarias. Although it resolves spontaneously in most patients, systemic corticosteroids are neededin severe cases. Aims In order to determine the drug that is causing this condition, patch testing must be performed. Hydroxychloroquine is a medication that is used for the treatment of rheumatic and dermatologic conditions. And although it has been rarely seen to cause this reaction, we report a case of Hydroxychloroquine-induced (HCQ) AGEP which was confirmed by Patch testing. Patients A woman 49 years of age with an18 month history of mild, untreated Rheumatoid Arthritis experienced an acute episode of arthritis in her right elbow. Upon going to a rheumatologist, Prednisolone 5 mg BID and HCQ 200 mg daily were administered for a 30-day period. But after only 17 days of this treatment, the patient developed generalized erythema and painful pustular eruptions. Prednisolone dosage was changedto 7.5 mg per day andHCQ was discontinued one day afterthe appearance of eruptions. The diffuse erythema started improving a week after the patient's hospitalization.Considering the factthat our patient was receiving multiple potentially causative medications, patch testing was necessary to distinguish the drug responsible for this reaction. Results After the patch testing was done, HCQ-induced AGEP was confirmed. Conclusions Patch testing is the gold standard of determining the responsible drug for an AGEP reaction. It should also be kept in mind that HCQ, although rarely, can cause this condition.

BACKGROUND Fixed Drug Eruption (FDE) is a drug reaction involving the skin and less commonly the mucosal membranes. Tamsulosin is an alpha-1 adrenergic receptor blocker used to treat benign prostatic hyperplasia. Dizziness and headache are among its most common side effects (Singapore Med J, 2018;59:336). Although cutaneous drug eruption has been reported with other alpha-1 adrenergic receptor blockers. AIMS Drug rash due to Tamsulosin is relatively uncommon (Singapore Med J, 2018;59:336). In this case we report an incidence of fixed drug eruption due to Tamsulosin. PATIENTS A 54 year old male, with benign prostatic hyperplasia was referred to our office for evaluation of certain eruptions, having developed his hyper-pigmented patches after 2 weeks of using oral 0.4 mg Tamsulosin per day. Based on the clinical course and the skin biopsy we diagnosed the condition as Tamsulosin associated fixed drug eruption. The most important therapeutic measure was discontinuing Tamsulosin medication. Following this, his eruptions improved remarkably in a few days without complications. RESULTS According to previous findings, there has been no case report on fixed drug eruption caused by Tamsulosin. CONCLUSION Our case is a relatively mild form of fixed drug eruption. Therefore it should be kept in mind that a severe cutaneous drug eruption might occur after Tamsulosin administration.

Addison’s disease or chronic adrenocortical insufficiency, can remain unrecognized for a long time. It usually presents with non-specific symptoms, which are often ignored or misdiagnosed as a sign of other more common diseases. In this case report we focused on subtle findings of diffuse hyperpigmentation. We present a study on 2 skin biopsies from a 38-year-old woman in whom hyperpigmentation lesions were first found on the face and after two months, in the oral cavity. Addison’s disease usually presents with non-specific symptoms and this can be a rare case because it presents with hyperpigmentation as its only sign and has no other clinical symptoms.There are a few diagnosed cases of this disease with hyperpigmentation only.