Refractory Postinflammatory Hyperpigmentation Treated Fractional CO2 Laser

Objective: Postinflammatory hyperpigmentation is a reactive hypermelanosis of the skin that occurs as a consequence of an inflammatory process, such as acne, eczema, drug reactions, burns, chemical peelings, and laser applications. Although topical agents remain to be the first-line treatment of postinflammatory hyperpigmentation, treatment of recalcitrant cases is challenging. The Q-switched ruby laser, the low-dose Q-switched neodymium-doped yttrium aluminum garnet laser, and the fractional 1550nm erbium-doped fiber laser have been reported to improve postinflammatory hyperpigmentation. Design/setting/participants: The authors present a case of refractory postinflammatory hyperpigmentation successfully treated with two sessions of fractional CO₂ laser in a 24-year-old woman with Fitzpatrick skin type III. Results: After two treatment sessions with a one-month interval, the lesion totally cleared without any complications. Conclusion: Although many laser systems, including fractional CO₂ lasers, can cause postinflammatory hyperpigmentation, they also can be very efficacious tools by using conservative laser settings and by providing appropriate post-treatment care in recalcitrant postinflammatory hyperpigmentation treatment.Postinflammatory hyperpigmentation (PIH) is a reactive hypermelanosis of the skin. It appears as asymptomatic macules or patches that may be different in size and distribution depending on the causative pathology. Characteristically, it occurs as a consequence of an inflammatory process, such as acne, eczema, drug reactions, burns, chemical peelings, and laser applications. Increased amounts of arachidonic acid metabolites, cytokines, inflammatory mediators, and histamine in the inflammatory process may stimulate the melanocytes causing an increase in the melanin synthesis and transfer of pigment to the surrounding keratinocytes. In PIH, there is either excess melanin production or an abnormal distribution of melanin pigment deposited in the epidermis and/or dermis.1Treatment of PIH consists of a variety of medications and procedures. These include topical bleaching agents, such as hydroquinone, azelaic acid, kojic acid, retinoids, vitamin C, chemical peels, laser therapy, and sunscreens.1,2 The Q-switched ruby laser, the low-dose Q-switched neodymium-doped yttrium aluminum garnet (Nd:YAG) laser, and the fractional 1550nm erbium-doped fiber laser have been reported to improve PIH.1-4 Here, the authors present a case of refractory PIH treated with fractional CO₂ laser.     

Palmitic Acid and DGAT1 Deficiency Enhance Osteoclastogenesis,while Oleic Acid‐Induced Triglyceride Formation Prevents It

Both obesity and diabetes mellitus are associated with alterations in lipid metabolism as well as a change in bone homeostasis and osteoclastogenesis. We hypothesized that increased fatty acid levels affect bone health by altering precursor cell differentiation and osteoclast activation. Here we show that palmitic acid (PA, 16:0) enhances receptor activator of NF‐κB ligand (RANKL)‐stimulated osteoclastogenesis and is sufficient to induce osteoclast differentiation even in the absence of RANKL. TNFα expression is crucial for PA‐induced osteoclastogenesis, as shown by increased TNFα mRNA levels in PA‐treated cells and abrogation of PA‐stimulated osteoclastogenesis by TNFα neutralizing antibodies. In contrast, oleic acid (OA, 18:1) does not enhance osteoclast differentiation, leads to increased intracellular triglyceride accumulation, and inhibits PA‐induced osteoclastogenesis. Adenovirus‐mediated expression of diacylglycerol acyl transferase 1 (DGAT1), a gene involved in triglyceride synthesis, also inhibits PA‐induced osteoclastogenesis, suggesting a protective role of DGAT1 for bone health. Accordingly, Dgat1 knockout mice have larger bone marrow‐derived osteoclasts and decreased bone mass indices. In line with these findings, mice on a high‐fat PA‐enriched diet have a greater reduction in bone mass and structure than mice on a high‐fat OA‐enriched diet. Thus, we propose that TNFα mediates saturated fatty acid‐induced osteoclastogenesis that can be prevented by DGAT activation or supplementation with OA. © 2014 American Society for Bone and Mineral Research.     

The relationship of Prohepcidin levels with anemia and inflammatory markers in non-diabetic uremic patients: a controlled study

Introduction: Hepcidin, a small peptide hormone synthesized in the liver, plays central role in regulation of iron metabolism. Hepcidin generation in chronic kidney disease (CKD) is dependent on iron status, anemia, inflammation, and hypoxia and erythropoietin levels. In our study, the relationship between Prohepcidin levels and inflammation and iron indices in non-diabetic uremic patients was investigated. Methods: This study has a cross-sectional design which includes four groups: Non-diabetic 21 patients with stage 4 CKD (predialysis), 20 hemodialysis (HD) and 21 peritoneal dialysis (PD) patients and 17 healthy volunteers as the control group. Complete blood count, iron, total iron binding capacity (TIBC), ferritin, high-sensitive C-reactive protein (hsCRP), fibrinogen, parathyroid hormone, interleukin (IL)-6 and Prohepcidin levels were recorded. Results: Serum Prohepcidin levels in the predialysis, HD, PD and the control groups were 119.6?±?45.1?ng/mL, 140.2?±?41.8?ng/mL, 148.2?±?35.0?ng/mL and 93.8?±?21.9?ng/mL, respectively (p?r?=?0.345, p?=?0.002), creatinine (r?=?0.465, p?r?=?0.253, p?=?0.025), hsCRP (r?=?0.275, p?=?0.019), duration of dialysis treatment (r?=?0.443, p?r?=?0.467, p?r?=?0.615, p?r?=??0.286, p?r?=??0.573, p?r?=??0.473, p?r?=??0.351, p?=?0.002) and hematocrit (r?=??0.342, p?=?0.002) levels. Discussion: Prohepcidin levels increase with deepening anemia and show positive correlation with inflammatory markers. Therapeutic interventions regarding Prohepcidin action on inflammatory status may play a role in the treatment of anemia due to inflammation. Functional iron deficiency is frequent in uremic patients. It may be beneficial to measure Prohepcidin level together with ferritin among these patients.     

Cerebro-facio-thoracic dysplasia: expanding the phenotype

We report a further two patients with cerebro-facio-thoracic dysplasia, a rare autosomal recessive condition with thoracic costovertebral dysplasia, developmental delay and characteristic facial features. One of our patients has the additional features of large, bilateral colobomas of the optic nerve, ptosis, small conical teeth and severe left-sided talipes. He also has hypermobile joints, especially in his hands and anterior subluxation of the shoulders. The second patient has hypodensity of the grey matter on magnetic resonance imaging, which is the second report of this finding in cerebro-facio-thoracic dysplasia. In addition, he has hypoplasia of the corpus callosum. These cases illustrate the expanding phenotype of this condition, and support the hypothesis that this is an autosomal recessive condition.     

Evaluation of albendazole efficiency and complications in patients with pulmonary hydatid cyst

 Open in a separate windowOBJECTIVESThis study investigated the efficacy and complications of albendazole use after surgery in patients with pulmonary hydatid cysts.METHODSOne hundred fifty-three consecutive patients who met the study criteria out of 215 patients who received prophylaxis with albendazole after surgery for isolated pulmonary hydatid cysts in our clinic between January 2011 and December 2020 were analysed retrospectively.RESULTSEighty-six out of 153 (56.2%) of cases were male and 67 (43.8%) were female. The average age was 24.6 ± 17.4 (between 3 and 71 years), 76 of them (49.7%) were 18 years old and younger, while 77 (50.3%) were adults. All cases were approached transthoracically and a total of 170 operations were performed on the 153 cases. Fever, weakness and dizziness were reported in only one patient who was given albendazole treatment. A partial increase in liver enzymes was observed in 16 cases (10.5%) after albendazole treatment. Mild leukopoenia and neutropenia were observed in only one of the cases. In 1 case, a second operation was performed 30 months later due to recurrence. Albendazole treatment was not required to be discontinued in any of the cases. Mortality was not observed in any of the cases. Factors such as mean age, cyst size and hospitalization period did not have a statistically significant effect on any changes in liver enzymes tests following albendazole therapy (P > 0.05).CONCLUSIONSAlbendazole treatment can safely be used for postoperative prophylaxis in patients with pulmonary hydatid cysts in a controlled manner without causing serious complications.Subj collection152.     

Liver immunity,autoimmunity, and inborn errors of immunity

The liver is the front line organ of the immune system.The liver contains the largest collection of phagocytic cells in the body that detect both pathogens that enter through the gut and endogenously produced antigens.This is possible by the highly developed differentiation capacity of the liver immune system between self-antigens or non-self-antigens,such as food antigens or pathogens.As an immune active organ,the liver functions as a gatekeeping barrier from the outside world,and it can create...