Lichen aureus induced by an insect bite

Lichen aureus is an uncommon variant of pigmented purpura and presents itself with a chronic and benign course. Clinically, lichen aureus cases are asymptomatic and are found in the lower limbs, presenting themselves as erythematous, brownish or golden macules and/or papules. Its diagnosis is based on clinical and histopathological findings. The prognosis of lichen aureus is generally good. A 34-year-old Filipino male presented himself with a single itchy skin lesion on the right leg present for three months. The lesion started as a small, round, reddish to brownish area and then increased in size over time. A history of an insect bite on the same site was reported. An examination revealed a single annular, golden to brownish macule on the right leg. Based on this clinical and histopathological feature, the skin lesion was diagnosed as lichen aureus. The comprehension of the pathogenesis of lichen aureus is essential for knowing its risk factors.

A pilot study to establish an ovalbumin-induced atopic dermatitis minipig model

Introduction Because minipig skin is similar to human skin in anatomy and physiology, establishing an atopic dermatitis (AD) minipig model seems meaningful. Material and Methods We applied 1-fluoro-2,4-dinitrobenzene (DNFB) or ovalbumin onto the back skin of five Yucatan minipigs aged 8–10 months and 19 kg in median weight. Two minipigs with the same parameters served as controls. Results Both DNFB and ovalbumin mediated epithelial hyperplasia, spongiosis, and immune cell infiltration in the dermis, which is a typical histopathological feature of AD. Moreover, AD upregulated the Th1- and Th2-related cytokine expressions in DNFB- or in ovalbumin-treated skin. Notably, AD-induced minipigs exhibited greater cytokine serum concentrations. Conclusion Histopathological finding and cytokine analysis revealed that DNFB or ovalbumin mediates AD. However, ovalbumin-treated minipig is a more reliable and precise AD model owing to the DNFB-induced severe skin damage. In summary, ovalbumin-treated skin shows similar AD as human in histopathological and molecular analysis.

Two cases of retained medullary cord running parallel to a terminal lipoma

Background: Retained medullary cord (RMC) is a newly defined entity believed to originate from the late arrest of secondary neurulation. Some RMCs contain varying amounts of lipomatous tissues, which need to be differentiated from spinal lipomas, such as filar and caudal lipomas (terminal lipomas). Case Description: We surgically treated two patients with a nonfunctional cord-like structure (C-LS) that was continuous from the cord and extended to the dural cul-de-sac, and ran parallel to the terminal lipoma. In both cases, untethering surgery was performed by resecting the C-LS with lipoma as a column, under intraoperative neurophysiological monitoring. Histopathological examination confirmed that the central canal-like ependyma-lined lumen with surrounding neuroglial and fibrocollagenous tissues, which is the central histopathological feature of an RMC, was located on the unilateral side of the resected column, while the fibroadipose tissues of the lipoma were located on the contralateral side. Conclusion: Our findings support the idea proposed by Pang et al. that entities such as RMC and terminal lipomas are members of a continuum of regression failure occurring during late secondary neurulation, and the coexistence of RMC and terminal lipoma is not a surprising finding. Therefore, it may be difficult in clinical practice to make a distinct diagnosis between these two entities.

Analogous feature of cemento-ossifying fibroma and bone pathology: a clinico-pathological correlation

Intra-osseous pathology of the craniofacial region is microscopically characterized by hypercellular fibroblastic stroma with a variable amount of bone or cementum like calcified structures. The overlapping histopathological features are not limited to lesions under one classification of similar origin rather it imbricates the lesions of entirely different origin as well. The only possible way out then becomes the clinicopathological correlation. Hence, in an out of entire clinical, a radiographic, surgical, and histopathological feature reframes the building block for confirmatory diagnosis of a bone lesion.

Alveolar soft part sarcoma of extremity

Alveolar soft-part sarcoma (ASPS) is an extremely rare connective tissue tumor, predominantly seen in adolescents and young adults, with a female preponderance. Alveolar soft-part sarcoma (ASPS) is a slow growing tumor, but with high likelihood of metastasis, leading to high mortality. A classical histopathological feature of an alveolar pattern from the biopsy of the lesion favors the diagnosis. We report a case of 14 years old male patient who presented with a history of single painless swelling over thigh for which surgical excision was done. Histopathology was suggestive of Alveolar soft-part sarcoma (ASPS). There was no evidence of distant metastases. He was treated with external beam radiotherapy in view of vascular invasion.

Amyloid Proteins and Peripheral Neuropathy

Painful peripheral neuropathy affects millions of people worldwide. Peripheral neuropathy develops in patients with various diseases, including rare familial or acquired amyloid polyneuropathies, as well as some common diseases, including type 2 diabetes mellitus and several chronic inflammatory diseases. Intriguingly, these diseases share a histopathological feature—deposits of amyloid-forming proteins in tissues. Amyloid-forming proteins may cause tissue dysregulation and damage, including damage to nerves, and may be a common cause of neuropathy in these, and potentially other, diseases. Here, we will discuss how amyloid proteins contribute to peripheral neuropathy by reviewing the current understanding of pathogenic mechanisms in known inherited and acquired (usually rare) amyloid neuropathies. In addition, we will discuss the potential role of amyloid proteins in peripheral neuropathy in some common diseases, which are not (yet) considered as amyloid neuropathies. We conclude that there are many similarities in the molecular and cell biological defects caused by aggregation of the various amyloid proteins in these different diseases and propose a common pathogenic pathway for “peripheral amyloid neuropathies”.