Steroid-induced generalized pustular psoriasis: case report and reviewKaili R Barnes BS1*, Aliyah Parker BS1*, Danielle Tartar MD2, Barton L. Wise MD31UC Davis Health, School of Medicine, Sacramento, CA2UC Davis Health, Department of Dermatology, Sacramento, CA3UC Davis Health, Division of Rheumatology; Department of Orthopaedic Surgery, Sacramento, CA *These authors contributed equally to this work. Correspondence: Aliyah Parker, 4301 X St, Sacramento, CA, UC Davis Health, ahnparker@ucdavis.edu Author Details: Kaili R Barnes BS1krbarnes@health.ucdavis.edu Aliyah Parker BS1ahnparker@health.ucdavis.edu Danielle Tartar MD2dtartar@health.ucdavis.edu Barton L. Wise MD, MSc3blwise@health.ucdavis.edu

AbstractA conservative internal approach combining calcium hydroxide medication and MTA obturation can effectively arrest Class 3 external cervical resorption, promote hard tissue regeneration, and preserve periodontal structures over nearly ten years.Keywords : Calcium hydroxide, Case report, Endodontic, External cervical resorption, Mineral trioxide aggregate

Title: The Effectiveness of Ultrasound Biofeedback as a Muscle Retraining Tool Post PatellarTendon Debridement Surgery: A Case ReportAuthors: Faizeen Ahmed1 , Jane Borghehammar1, Bhupinder Singh1Affiliations: 1 Department of Physical Therapy, Midwestern University, Downers Grove, IL60515. * Corresponding author: Bhupinder Singh, PT, PhD, Tel: 630-515-6462, e-mail:bsingh@midwestern.edu

Title pageRunning Title: Trichoblastic Carcinosarcoma: a rare biphasic cutaneous malignancyAuthors: Gianfranco Emilio Tunesi MD1, Riccardo Roesel MD1, Giulia Bozzo MD2, Francesca Prestinari MD3, Lucia Ferrari MD4

Authors: Hattan Dagestani MD, Rawan BinKhunayn MD, Wesam Bin Obaid MDCorresponding Authors:1. Hattan Dagestani MD Email: dagestaniha@mngha.med.sa Ministry of National Guard Health Affairs, Women’s Health Hospital, Riyadh, Kingdom of Saudi Arabia2. Rawan BinKhunayn MD Email: Rawan.mbk1@gmail.com Ministry of National Guard Health Affairs, Women’s Health Hospital, Riyadh, Kingdom of Saudi Arabia3. Wesam Bin Obaid MD Email: BinObaidWe@mngha.med.sa Ministry of National Guard Health Affairs, Women’s Health Hospital, Riyadh, Kingdom of Saudi Arabia

IntroductionMELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is a rare mitochondrial disorder first described in 1984. It is caused by heteroplasmic mutations in mitochondrial DNA (mtDNA). Mitochondria are responsible for numerous essential functions, including adenosine triphosphate (ATP) production; however, these mutations impair oxidative phosphorylation, resulting in energy failure and tissue dysfunction, particularly in organs with high metabolic demand. The condition is maternally inherited, and its clinical expression is highly heterogeneous, largely determined by the degree of heteroplasmy. Onset occurs during childhood in up to 75% of patients. Disease severity correlates with the proportion of mutated mtDNA, and the underlying mechanisms include accumulation of mutant genomes, impaired ATP synthesis, excessive production of reactive oxygen species, and calcium dysregulation.Neurological manifestations predominate in MELAS syndrome. Stroke-like episodes (SLE) are a hallmark feature, occurring in more than 80% of cases. Unlike ischemic stroke, they are not caused by vascular occlusion: brain magnetic resonance angiography is typically normal, whereas magnetic resonance spectroscopy often demonstrates reduced N-acetylaspartate signals and lactate accumulation. SLE result from mitochondrial dysfunction, oxidative stress, and lactate buildup in plasma and cerebrospinal fluid, leading to vascular dysregulation and neuronal hyperexcitability. They do not conform to vascular territories, may produce transient or permanent deficits, and ultimately contribute to progressive neurodegeneration through cytotoxic edema and neuronal necrosis. Seizures, either focal or generalized, are another common feature, affecting 70–90% of patients. They stem from increased neuronal excitability and lowered seizure thresholds, further exacerbating neuronal injury, and are often resistant to therapy. Other systemic manifestations are frequent and include sensorineural hearing loss, peripheral neuropathy, myopathy, hypertrophic cardiomyopathy, arterial hypertension, and nephropathy, such as focal segmental glomerulosclerosis or tubulointerstitial nephritis, which may progress to chronic kidney disease. Lactic acidosis is also a cardinal feature, present in approximately 90% of patients, and is often reflected by elevated lactate concentrations in cerebrospinal fluid.1–3Beyond neurological involvement, systemic and endocrine manifestations also contribute significantly to the disease burden. Endocrine involvement is a recognized but variable complication of mitochondrial disorders. Diabetes mellitus is particularly common in MELAS, affecting up to one third of patients, and results from mitochondrial dysfunction in pancreatic β-cells, leading to impaired insulin secretion. Mitochondrial diabetes may present with either a type 1 or type 2 phenotype, and progressive insulinopenia can develop. The mean age of onset has been reported as approximately 38 years4,5However, acute hyperglycemic crises, and specifically hyperglycemic hyperosmolar state (HHS), remain exceptionally rare and are only scarcely documented in the literature1,2,5–8It is not yet clear whether specific preventive measures are warranted in MELAS patients.5Current mitochondrial disease management guidelines recommend annual HbA1c screening to monitor for the development of diabetes.6

A document by Christian Damien Tchuisseu Ngapjang. Click on the document to view its contents.

A case report of renal pathological changes of PGNMID

A Case Report of a Large Occult Intraorbital Branch Foreign Body

IntroductionCongenital Dyserythropoietic Anemia Type II (CDA-II) is a rare autosomal recessive disorder characterized by ineffective erythropoiesis, typically caused by biallelic mutations in the SEC23B gene [1]. This gene encodes a crucial component of the COPII coat protein complex responsible for intracellular protein transport [2]. Clinically, CDA-II presents with lifelong anemia of variable severity, jaundice, and hepatosplenomegaly [1]. However, arriving at a correct diagnosis is often challenging due to significant phenotypic heterogeneity and clinical overlap with more common hereditary anemias [3]. In regions where disorders like thalassemia are endemic, the similar presentation of chronic, transfusion-dependent anemia frequently leads to misdiagnosis, delaying appropriate management [4].This diagnostic delay can lead to severe and preventable long-term complications. Patients often develop significant iron overload, not only from repeated transfusions but also from increased intestinal absorption driven by the profound ineffective erythropoiesis. Other sequelae include growth retardation, gallstones, and, in resource-limited settings, transfusion-transmitted infections. While the morphological hallmark of CDA-II is the presence of binucleated erythroblasts in a hypercellular bone marrow, this finding is not entirely specific and modern diagnostic standards rely on molecular confirmation [5]. The transition from a morphology-based diagnosis to a genetically confirmed one is critical for guiding management and preventing irreversible organ damage.Here, we report the case of a 13-year-old girl from South Asia with a classic CDA-II phenotype whose diagnosis was delayed for years due to the regional prevalence of thalassemia. This case illustrates the severe morbidity that accumulates from a delayed diagnosis, including growth failure, extreme iron overload, and transfusion-acquired hepatitis C. It underscores the limitations of relying solely on morphological findings in a complex diagnostic landscape and highlights the critical need for increased awareness and access to definitive genetic testing in resource-constrained environments to improve patient outcomes.

Case Image

IntroductionThe widespread use of high-resolution, cross-sectional imaging has led to a dramatic increase in the incidental detection of pancreatic cystic lesions (PCLs), confronting clinicians with a high-stakes diagnostic challenge [1]. The central task is to accurately risk-stratify these lesions, distinguishing benign, non-neoplastic entities from pancreatic cystic neoplasms (PCNs) that harbor malignant potential [2]. This distinction is critical, as misclassification can lead either to unnecessary, high-morbidity pancreatectomy for benign cysts or, conversely, a missed opportunity to resect a pre-malignant or early-stage malignant tumor [3].Among the most frequent and consequential diagnostic dilemmas is the differentiation between a pancreatic pseudocyst (PPC)—a non-neoplastic, encapsulated fluid collection arising from pancreatitis—and a mucinous cystic neoplasm (MCN). PPCs are the most common PCL, accounting for approximately 75% of cases, and are defined by a fibrous wall devoid of an epithelial lining [5]. In contrast, MCNs are true neoplasms characterized by mucin-producing epithelial cells and an underlying ovarian-like stroma, carrying a significant risk of malignant transformation that prompts recommendations for surgical resection [6]. Despite these distinct pathologies, their radiological features can overlap substantially; large or complex PPCs containing debris can mimic the septations, wall thickening, and internal complexity characteristic of an MCN, creating significant diagnostic ambiguity from imaging alone [5].When initial imaging is inconclusive, a multimodal diagnostic algorithm is essential [3]. Endoscopic ultrasound (EUS) with fine-needle aspiration (FNA) allows for high-resolution morphologic assessment and cyst fluid acquisition [7]. Subsequent analysis of the cyst fluid for tumor markers, such as carcinoembryonic antigen (CEA), and cytology provides critical data to resolve the differential [8]. While high levels of CEA are strongly suggestive of a mucinous lesion, elevated amylase points towards a pseudocyst, and cytology can confirm malignancy, each test has known limitations [8].However, extreme clinical presentations, such as a cyst of massive size, can heavily bias initial interpretation towards neoplasia, creating a significant diagnostic pitfall that may lead to premature closure. In this report, we present the case of a patient with a 1.85-liter pancreatic cyst whose immense size and complex features on imaging were highly suggestive of an MCN. We detail the systematic application of a multimodal diagnostic approach that successfully averted a misdiagnosis, underscoring the principle that even in the face of atypical features, a stepwise, evidence-based evaluation is paramount to ensure correct diagnosis and guide appropriate management.

IntroductionNeurofibromatosis type 1 (NF1) is one of the most common autosomal dominant genetic disorders, with an estimated prevalence of 1 in 2,500 to 3,000 individuals worldwide. It results from pathogenic variants in the NF1 gene on chromosome 17, leading to haploinsufficiency and dysregulation of the RAS/MAPK signaling pathway, which manifests as a multisystem condition with variable expressivity(1). Characteristic features include café-au-lait macules, axillary freckling, cutaneous neurofibromas, Lisch nodules, optic pathway gliomas, and skeletal abnormalities, with nearly half of cases arising de novo(2). Oral manifestations in NF1, such as gingival hyperplasia, mandibular enlargement, and increased risk of periodontitis or salivary gland dysfunction, become more prominent with age and may contribute to reduced quality of life, though they are often underrecognized in routine dental care(3).Oral lichen planus (OLP) is a chronic T-cell-mediated inflammatory mucocutaneous disorder affecting approximately 0.5-2% of the general population, predominantly middle-aged women, with a potential for malignant transformation to oral squamous cell carcinoma in 1-2% of cases(4). Clinically, it presents as bilateral white reticular striae, erosions, or plaques on the buccal mucosa, often accompanied by symptoms of discomfort or burning sensation, and histopathologically characterized by basal cell degeneration, band-like lymphocytic infiltrate, and Civatte bodies(5). While autoimmune and environmental triggers are implicated, the precise pathogenesis involves dysregulated immune responses, including exosome-mediated cytokine release (e.g., IL-6, TNF-α), highlighting the need for non-invasive biomarkers for early detection(6).To date, direct associations between OLP and NF1 remain exceedingly rare, with only isolated reports describing verruciform xanthoma in NF1 patients exhibiting clinical features mimicking OLP, suggesting possible overlapping inflammatory pathways influenced by NF1-related fibrosis(7). This case report aims to describe the clinical, histopathological, and genetic features of biopsy-confirmed erosive OLP in a 22-year-old woman with familial NF1 harboring a pathogenic NF1 variant (c.2850+1delG), representing a novel documentation of this comorbidity and underscoring the importance of multidisciplinary surveillance in NF1 patients.

A document by Huda Al Akrabi. Click on the document to view its contents.

Title:

Neurological and Systemic Complications of Dengue Expanded Syndrome: A Case ReportHimel Kumar Biswas, Monisha Basak*, Amrita Saha*Corresponding Author: Monisha Basak, Resident Medical Officer, Department of Internal Medicine, Square Hospitals Ltd., Dhaka Bangladesh, Email: monishabasak3@gmail.com

IntroductionThe presence of a single abdominal wall hernia is a common surgical problem, but the synchronous presentation of multiple, distinct hernias in a single patient represents a significant diagnostic and therapeutic challenge [1]. Such cases may signal an underlying systemic predisposition to fascial weakness, a concept increasingly described as ”abdominal wall failure,” rather than a series of coincidental events [2]. There is substantial evidence that a deficiency in type 1 collagen, inadequate collagen cross-linking, or other connective tissue abnormalities may underpin the development of multiple hernias, creating a generalized vulnerability to herniation [2]. This perspective shifts the clinical paradigm from treating an isolated defect to managing a systemic condition with local manifestations.While reports of double or even triple hernias exist, they often involve bilateral presentations of a single type, such as inguinal hernias [3]. The combination of hernias across different anatomical zones—such as the groin, the umbilical region, and a prior surgical site—is less commonly documented and complicates surgical planning [4]. A key clinical pitfall is the presence of occult or ”hidden” hernias, where a larger, more symptomatic hernia obscures the detection of smaller, concurrent defects during physical examination [5]. Failure to identify all existing hernias preoperatively can lead to persistent patient symptoms, the need for repeat operations, and an increased risk of recurrence [6].Herein, we present the rare case of a 56-year-old male with three concurrent hernias: a right indirect inguinal hernia, an umbilical hernia, and an incisional hernia at the site of a previous appendectomy. This case highlights the critical importance of maintaining a high index of suspicion for multiple defects and underscores the utility of preoperative imaging for comprehensive surgical planning. Furthermore, we use this case to explore the potential for a unifying pathophysiological mechanism and discuss the surgical strategy for managing such complex abdominal wall disease in a single operative setting.

A document by RISHI RAM BANJADE. Click on the document to view its contents.