Is cutaneous microbiota a player in disease pathogenesis? Comparison of cutaneous microbiota in psoriasis and seborrheic dermatitis with scalp involvement.

Background Knowledge about cutaneous microbiota in psoriasis vulgaris and seborrheic dermatitis is limited, and a comparison of microbiota in the two diseases was not yet previously undertaken. Aims/Objectives This study aimed to compare the scalp lesional and non-lesional microbiota in psoriasis vulgaris and seborrheic dermatitis with that in a healthy control group. Methods Fifty samples were taken with sterile swabs from patients' and controls' scalps, and 16S rRNA gene sequencing analyses were performed. Results Alpha and beta diversity analyses showed that bacterial load and diversity were significantly increased in psoriasis vulgaris and seborrheic dermatitis lesions compared to the controls. As phyla, Actinobacteria decreased and Firmicutes increased, while as genera, Propionibacterium decreased; Staphylococcus, Streptococcus, Aquabacterium, Neisseria and Azospirillum increased in lesions of both diseases. Specifically, Mycobacterium, Finegoldia, Haemophilus and Ezakiella increased in psoriasis vulgaris and Enhydrobacter, Micromonospora and Leptotrichia increased in seborrheic dermatitis lesions. Mycobacterium, Ezakiella and Peptoniphilus density were higher in psoriasis vulgaris compared to seborrheic dermatitis lesions. The bacterial diversity and load values of non-lesional scalp in psoriasis vulgaris and seborrheic dermatitis lay between those of lesional areas and controls. Limitations The small sample size is the main limitation of this study. Conclusion Higher bacterial diversity was detected in lesions of both psoriasis and seborrheic dermatitis compared to the controls, but similar alterations were observed when the two diseases were compared. Although these differences could be a result rather than a cause of the two diseases, there is a need to analyze all members of the microbiota and microbiota-host interactions.

Effect of low-dose acitretin treatment on pituitary hormones in psoriasis vulgaris: A retrospective study.

BACKGROUND: It has been reported that retinoids may lead to hormonal alterations. AIM: In this retrospective study, we aimed to study the effect of acitretin on pituitary hormones in psoriasis patients. METHODS: Out of 50 patients intended to be studied, blood samples of 43 patients could be tested before and after 3 months of acitretin therapy (0.2 to 0.5 mg/kg/day). RESULTS: Patients mean ± standard deviation ages and female/male ratio were 46 ± 17 years and 19/24, respectively. After treatment with acitretin, gamma-glutamyltransferase, alkaline phosphatase, total cholesterol and triglyceride levels increased significantly (P < 0.05). After treatment, total protein, free thyroxine (T4) levels decreased significantly (P < 0.05). No significant differences were observed between before-after acitretin treatment regarding pituitary hormone levels in psoriasis patients (P > 0.05). LIMITATIONS: The retrospective nature of the study, inability to retest blood samples of 7 patients at 3 months post treatment, low dose and short duration of acitretin treatment were limitations of this study. CONCLUSION: This study showed that pituitary hormones were not affected except free T4 (thyroid hormone) by acitretin treatment. Further experimental and clinical studies are needed to clarify the effect of acitretin on pituitary hormones.

Sneddon syndrome associated with Protein S deficiency.

Sneddon syndrome (SS) is rare, arterio-occlusive disorder characterized by generalized livedo racemosa of the skin and various central nervous symptoms due to occlusion of medium-sized arteries of unknown. Seizure, cognitive impairment, hypertension, and history of repetitive miscarriages are the other symptoms seen in this disease. Livedo racemosa involves persisting irreversible skin lesions red or blue in color with irregular margins. Usually, SS occurs in women of childbearing age. Protein S deficiency is an inherited or acquired disorder associated with an increased risk of thrombosis. We present a 33-year-old woman with SS with diffuse livedo racemosa, recurrent cerebrovascular diseases, migraine-type headache, sinus vein thrombosis, and protein S deficiency. Protein S deficiency and with Sneddon syndrome rarely encountered in the literature.