Mast Cells Trigger Disturbed Bone Healing in Osteoporotic Mice

Mast cells are important tissue-resident sensor and effector immune cells but also play a major role in osteoporosis development. Mast cells are increased in numbers in the bone marrow of postmenopausal osteoporotic patients, and mast cell–deficient mice are protected from ovariectomy (OVX)-induced bone loss. In this study, we showed that mast cell–deficient Mcpt5-Cre R-DTA mice were protected from OVX-induced disturbed fracture healing, indicating a critical role for mast cells in the pathomechanisms of impaired bone repair under estrogen-deficient conditions. We revealed that mast cells trigger the fracture-induced inflammatory response by releasing inflammatory mediators, including interleukin-6, midkine (Mdk), and C-X-C motif chemokine ligand 10 (CXCL10), and promote neutrophil infiltration into the fracture site in OVX mice. Furthermore, mast cells were responsible for reduced osteoblast and increased osteoclast activities in OVX mice callus, as well as increased receptor activator of NF-κB ligand serum levels in OVX mice. Additional in vitro studies with human cells showed that mast cells stimulate osteoclastogenesis by releasing the osteoclastogenic mediators Mdk and CXCL10 in an estrogen-dependent manner, which was mediated via the estrogen receptor alpha on mast cells. In conclusion, mast cells negatively affect the healing of bone fractures under estrogen-deficient conditions. Hence, targeting mast cells might provide a therapeutic strategy to improve disturbed bone repair in postmenopausal osteoporosis. © 2021 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).     

Jejunal perforation in mentally retarded patient due to an ingested chicken bone

We report a mentally retarded case with jejunal perforation by ingested chicken bone. Foreign body ingestion constructs a health threat for mentally retarded people. Under guidance of the literature, travel of the bones in the gastrointestinal tract, diagnosis and treatment strategies are evaluated.     

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.     

A case of thrombocytopenia associated with the use of hydroxychloroquine following open heart surgery

INTRODUCTION

Thrombocytopenia is a common problem occurring in patients and drug-induced thrombocytopenia is a significant cause of thrombocytopenia.

PRESENTATION OF CASE

We present an unusual case of thrombocytopenia that was considered to be associated with the use of hydroxychloroquine in the late term following open heart surgery.

DISCUSSION

The drug-induced thrombocytopenia, mechanical destruction of the platelets, and hemodilution are common causes of low platelet count. Although drug-induced immune thrombocytopenia has a mild clinical course in most cases (in this case it has severe clinical course), some patients may experience life-threatening hemorrhages. The decision to discontinue the drug that is deemed to be responsible from the drug-induced thrombocytopenia (DITP) relies on the clinical condition of the patient. The diagnosis is mostly established by discontinuation, exclusion, and correlation because the tests performed to detect drug-dependent antibodies (DDAbs) for the diagnosis of DITP are time-consuming, and these tests are also not commonly available. The authors of the current study diagnosed DITP by discontinuation of the drug. We suggest that the use of hydroxychloroquine could be severe thrombocytopenia occurring after open heart surgery.

CONCLUSION

The medication history must be carefully reviewed in patients presenting with thrombocytopenia, and if the medications could cause thrombocytopenia must be discontinued.