American Journal of the Medical Sciences最新文献

{"title":"Chronic cholecystitis masking as a primary hepatocellular injury","authors":"A Ladner,&nbsp;F Asher","doi":"10.1016/j.amjms.2025.12.027","DOIUrl":"10.1016/j.amjms.2025.12.027","url":null,"abstract":"<div><h3>Case Report</h3><div>Chronic cholecystitis is often diagnosed clinically in patients presenting with recurrent biliary colic pain, coupled with imaging findings suggestive of cholelithiasis. Here, we present a case of chronic cholecystitis with histopathological evidence of cholelithiasis despite the absence of detectable cholelithiasis on imaging.</div><div>A 28-year-old male with no past medical history presented to the emergency department with a 3-week history of diffuse abdominal pain. The pain was sharp and constant and was not associated with meals or physical activity. Associated symptoms included nausea and vomiting, which persisted despite being prescribed ondansetron.</div><div>On physical examination, the patient exhibited diffuse tenderness in the right upper quadrant, epigastric region, and left upper quadrant. Murphy's sign was negative. The initial differential diagnosis included acute cholecystitis, cholangitis, viral hepatitis, pancreatitis, and autoimmune hepatitis.</div><div>Upon admission, liver function tests revealed a hepatocellular injury pattern with aspartate aminotransferase (AST) 628 U/L, alanine aminotransferase (ALT) 624 U/L, alkaline phosphatase (ALP) 60 U/L, total bilirubin 1.73 mg/dL, and direct bilirubin 0.97 mg/dL. The calculated R-factor was 23.3, further suggesting a hepatocellular injury pattern.</div><div>During hospitalization, both total and direct bilirubin levels increased, peaking at 5.70 mg/dL and 4.73 mg/dL, respectively. Initial abdominal ultrasound demonstrated trace gallbladder sludge and nonspecific gallbladder wall thickening. Notably, no intrahepatic or extrahepatic biliary ductal dilation or cholelithiasis was observed.</div><div>Magnetic resonance cholangiopancreatography (MRCP) revealed mild gallbladder wall thickening and gallbladder sludge. A hepatobiliary iminodiacetic acid (HIDA) scan showed signs indicative of chronic acalculous cholecystitis.</div><div>The patient underwent a cholecystectomy, which led to the resolution of his symptoms. He was discharged home the following day. The pathological examination confirmed chronic cholecystitis with cholelithiasis, despite the absence of detectable cholelithiasis on initial abdominal ultrasound, MRCP, and HIDA scan. Three weeks after discharge, a follow-up phone called was made in which the patient stated he was completely symptom free.</div><div>In the absence of cholelithiasis on imaging studies, the diagnosis of cholecystitis can be challenging and may lead to consideration of alternative hepatobiliary or hepatocellular pathologies. It is important to note that markers of hepatocellular injury typically resolve completely within two to four weeks of cholecystectomy. This case highlights the importance of maintaining a high index of suspicion for chronic cholecystitis, especially in young, healthy individuals, when clinical symptoms are suggestive, despite negative imaging findings.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Pages S14-S15"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When a UTI prophylactic turns fatal: a case of chronic nitrofurantoin-induced pulmonary fibrosis","authors":"S Faizia,&nbsp;K Moin,&nbsp;F Mahjabeen,&nbsp;S Siraj,&nbsp;S Saaki,&nbsp;A Qasim","doi":"10.1016/j.amjms.2025.12.025","DOIUrl":"10.1016/j.amjms.2025.12.025","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Case Report&lt;/h3&gt;&lt;div&gt;Background: Nitrofurantoin is a frequently prescribed antibiotic for urinary tract infections, particularly in women with recurrent infections requiring long-term prophylaxis. Although effective, it is associated with pulmonary toxicity, which can manifest as either acute hypersensitivity pneumonitis or chronic fibrotic ILD. Chronic pulmonary toxicity is typically seen after 6–12 months of continuous therapy and may progress to irreversible fibrosis if not recognized early.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Case Presentation&lt;/h3&gt;&lt;div&gt;We report the case of a 59-year-old woman with a history of asthma and recurrent UTIs who presented with several days of progressive shortness of breath and mild chest pain. At her primary care visit, she desaturated into the 80s and was transferred to the ED, started on oxygen. Examination revealed hypoxemia and bilateral inspiratory crackles. Labs were unremarkable. Chest CTA excluded pulmonary embolism but showed severe chronic interstitial thickening. PFT revealed a severe restrictive defect. History revealed daily nitrofurantoin use for 4 years as prophylaxis for recurrent UTIs. The constellation of chronic exposure, restrictive physiology, and radiologic abnormalities strongly supported the diagnosis of nitrofurantoin-induced ILD, presenting as acute hypoxic respiratory failure. We discontinued the drug and recommended to F/U with pulmonology clinic.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Discussion&lt;/h3&gt;&lt;div&gt;Nitrofurantoin-induced pulmonary toxicity, first described in 1962, remains an underrecognized complication. Acute presentations occur within weeks, while chronic toxicity emerges insidiously after prolonged use. The proposed pathogenesis involves oxidative–antioxidative imbalance and toxic metabolite accumulation leading to alveolar injury and fibrosis. The clinical picture is often nonspecific and can mimic asthma, infection, or connective tissue–associated ILD, resulting in diagnostic delays. In our case, the exclusion of alternative etiologies and the temporal association with prolonged nitrofurantoin use supported the diagnosis. Although cessation of the drug typically leads to symptomatic improvement, structural lung damage often persists. There are no specific international guidelines for nitrofurantoin-induced ILD; however, expert consensus on drug-induced ILD recommends structured monitoring after drug withdrawal, including baseline PFT with DLCO and high-resolution CT at diagnosis, followed by reassessment at 3–6 months and annually. Corticosteroid therapy may be considered in severe or progressive cases, although evidence is limited. Re-exposure to nitrofurantoin is contraindicated.&lt;/div&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;div&gt;This case emphasizes the importance of vigilance for nitrofurantoin-induced pulmonary toxicity in patients on long-term prophylaxis. Nonspecific symptoms, frequent misdiagnosis, and delayed recognition place patients at risk of irreversible lung injury. Early suspicion, prompt disc","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Pages S13-S14"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Delayed bilirubin surveillance in a neonate: progression to kernicterus and systemic complications","authors":"K Kaur,&nbsp;E Sack,&nbsp;M Puzdrakiewicz","doi":"10.1016/j.amjms.2025.12.066","DOIUrl":"10.1016/j.amjms.2025.12.066","url":null,"abstract":"<div><h3>Case Report</h3><div>Introduction Neonatal hyperbilirubinemia can lead to severe complications such as kernicterus and bilirubin encephalopathy if not promptly treated. This case involves a 37-week gestation infant who presented with severe hyperbilirubinemia after a home birth, complicated by apnea, seizures, and suspected neonatal tetanus. The case highlights the importance of early bilirubin monitoring and a multidisciplinary approach to management.</div></div><div><h3>Case Presentation</h3><div>The infant, born at 37 weeks via home birth, presented on day 7 of life with cyanosis, lethargy, and apnea. Initial bilirubin levels were 41.9 mg/dL, prompting immediate intervention. An MRI revealed T1 hyperintensity in the globus pallidus, suggesting kernicterus. The infant underwent a double-volume exchange transfusion to reduce bilirubin levels and was started on IV Keppra for suspected seizures. Given the non-sterile cord care during delivery, neonatal tetanus was suspected, and the infant received metronidazole. Despite the mother's initial reluctance, all recommended interventions were initiated, including ongoing neurological monitoring, respiratory support, and nutritional evaluation.</div></div><div><h3>Discussion</h3><div>This case underscores the importance of early bilirubin screening and intervention. The overlapping symptoms of kernicterus, neonatal tetanus, and sepsis made the differential diagnosis challenging. Kernicterus can present with lethargy, hypotonia, and seizures, while neonatal tetanus presents with irritability and muscle rigidity. Early recognition and aggressive treatment, including exchange transfusion and anticonvulsants, were crucial in stabilizing the infant's condition. This case demonstrates the need for timely surveillance and multidisciplinary care to prevent long-term neurological damage in neonates with severe hyperbilirubinemia.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Page S39"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding fibromyocytes' contributions to atherosclerosis: from senescence induction to promoting formation of necrotic core","authors":"M Li,&nbsp;S Sukhanov,&nbsp;P Delafontaine","doi":"10.1016/j.amjms.2025.12.009","DOIUrl":"10.1016/j.amjms.2025.12.009","url":null,"abstract":"<div><h3>Purpose</h3><div>Smooth muscle cells (SMC), an important cellular component of atherosclerosis, exhibit variant phenotypes after trans differentiation. The synthetic SMC phenotype was defined as fibromyocytes (FM). SMC-specific knockout of <em>TCF21</em> transcription factor inhibited SMC phenotypic modulation but did not change atherosclerotic plaque burden in mouse model. TCF21 gene was associated with increased cardiovascular risk in genome wide RNA-Seq study suggesting pro-atherogenic role of FM. Cell senescence is an irreversible cell proliferation arrest associated with vascular aging, and the progression of atherosclerosis. We hypothesize that FM promotes cellular senescence and exacerbates formation of plaque's necrotic core contributing to atherosclerotic plaque progression.</div></div><div><h3>Methods</h3><div>We analyzed single-cell RNA seq (scRNAseq) dataset obtained for atherosclerotic human coronary artery, atherosclerotic mouse aortas (Apoe-null mice on high-fat diet), and spatial transcriptomics (ST) data set obtained for atherosclerotic pig coronary artery. Senescence module score was calculated based on expression level of senescent genes using gene set enrichment algorithm. Differentially expressed genes (DEGs) were identified in FM versus SMC and module score was calculated for each cell phenotype based on the DEGs expression. Spearman coefficients were calculated to align each gene expression pattern with FM and senescence score distribution.</div></div><div><h3>Results</h3><div>Gene expression profiling of atherosclerotic specimens obtained from humans, pigs and mice revealed that FM exhibited higher senescence module scores compared to SMC suggesting increased FM susceptibility to developing senescence. Cell type ratios were estimated for ST spots by deconvolution of porcine ST data using human scRNA-seq data. FM was the most abundant cell type in the porcine coronary plaque's fibrous cap (FC). Thick FC prevents plaque from rupture and FC thinning is an index of plaque vulnerability. Complement factor H (CFH) and versican (VCAN) were identified in data sets as top genes expressed in FM and highly correlated with senescence module score: expression level of CFH and VCAN were 13 and 7.5 folds higher in FM compared to SMC, respectively. VCAN is highly expressing in senescent cells promoting senescence to neighboring cells. CFH inhibits immune cell-mediated efferocytosis to clear dying cells, which may exacerbate formation of necrotic core.</div></div><div><h3>Conclusions</h3><div>Our results identified high levels of FM in FC in advanced coronary plaque and indicate that FM are prone to develop senescence. Upregulation of VCAN and CFH in FM is potential mechanism to promote senescence and extension of necrotic core. These findings revealed novel role of FM in plaque progression and destabilization and identified FM as novel cellular target for development of innovative anti-atherosclerotic therapy.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Pages S2-S3"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175530","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Knockout of RECK in vascular smooth muscle cells alters circulating cholesterol levels and atherosclerosis formation","authors":"W Ditta ,&nbsp;G Kaplan ,&nbsp;M Zhang ,&nbsp;R Iwai ,&nbsp;S Danchuk ,&nbsp;S Sukhanov ,&nbsp;T Yoshida ,&nbsp;P Delafontaine ,&nbsp;S Chen ,&nbsp;B Chandrasekar ,&nbsp;Y Higashi","doi":"10.1016/j.amjms.2025.12.007","DOIUrl":"10.1016/j.amjms.2025.12.007","url":null,"abstract":"<div><h3>Purpose</h3><div>Arterial smooth muscle cells (SMCs) play a multifaceted role in atherosclerosis, driving disease progression and stabilizing plaque. Reversion-inducing cystein-rich protein with kazal motif (RECK) is a membrane-anchored glycoprotein that inhibits matrix metalloproteinases. Our previous study demonstrated RECK suppresses SMC migration and proliferation. Given these functions, the absence of RECK in SMCs may disrupt vascular homeostasis and accelerate plaque development. In this study, we investigated the impact of smooth muscle cell–specific knockout of RECK (SMC-RECK-KO) on atherosclerotic disease progression. We hypothesized that RECK-KO in smooth muscle cells would cause an increase in atherosclerotic progression.</div></div><div><h3>Methods</h3><div>SMC-RECK-KO mice on an Apoe-deficient background were fed a Western diet for 12 weeks starting at 8 weeks old. Plasma was collected for total cholesterol measurement. Atherosclerotic burden was quantified by oil-red-O staining on aorta en face preparations. Necrotic core size and fibrous cap thickness were evaluated on aortic root cross-sections stained with Masson's trichrome. Aortic valve cross-sections were immunostained for α-smooth muscle actin (SMCs) and Mac3 (macrophages) to assess plaque composition.</div></div><div><h3>Results</h3><div>Compared with RECK-flox controls, SMC-RECK-KO mice exhibited a 102.7% increase in plaque burden (P &lt; 0.0001). Masson's trichrome staining demonstrated significantly reduced fibrous cap thickness (P = 0.006) and enlarged necrotic core size (P = 0.012) in SMC-RECK-KO mice. In addition, SMC-RECK-KO plaques showed a 57.5% reduction in macrophage content (P = 0.019) and a decreasing trend in SMC number, consistent with accelerated atherosclerotic progression. Circulating total cholesterol was also markedly lower in SMC-RECK-KO mice compared with RECK-flox controls (972.1 ± 91.5 mg/dL vs. 631.3 ± 62.7 mg/dL, P = 0.001).</div></div><div><h3>Conclusions</h3><div>Our findings suggest that SMC-RECK-KO exacerbated atherosclerotic burden and advanced plaque progression, while reducing circulating total cholesterol levels. This suggests that RECK may influence the onset of atherosclerosis in ways beyond traditional lipid metabolism. This study highlights RECK as a potential therapeutic target to treat cardiovascular diseases and calls for further investigation into its role in the mechanisms of atherosclerosis.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Pages S1-S2"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When a sore throat turns deadly: a rare cause of sepsis","authors":"MJ Rodriguez,&nbsp;D Smith,&nbsp;B Ozier,&nbsp;S Sanne,&nbsp;J Martinez","doi":"10.1016/j.amjms.2025.12.036","DOIUrl":"10.1016/j.amjms.2025.12.036","url":null,"abstract":"<div><h3>Case Report</h3><div>Introduction: Lemierre syndrome is a rare condition characterized by septic thrombophlebitis of the internal jugular vein (IJV). Diagnosis requires the presence of an oropharyngeal infection, positive blood cultures, evidence of thrombophlebitis, and metastatic infection such as septic emboli. It occurs infrequently, with an incidence of approximately 3.6 cases per million, most often affecting young females.</div></div><div><h3>Case</h3><div>A 20-year-old female with no past medical history presented with shortness of breath and back pain. She arrived by plane about a week ago from out of state and started having flu-like symptoms and a sore throat that was improving with over-the-counter medications. However, over the past few days she had upper back pain causing significant dyspnea. The patient denied any chest pain or lower extremity swelling. The patient was tachycardic and tachypneic (42 bpm) with an oxygen saturation of 92% on room air, improved with supplemental oxygen. However, her breathing was concerning and on her oropharyngeal exam, it was noted that she had uvular deviation. A septic work-up and broad-spectrum antibiotics were initiated. Imaging found that she had pulmonary septic emboli with acute tonsillitis, left neck venous thrombosis and bilateral pleural effusions. The patient was admitted to the intensive care unit and otolaryngology was consulted. Unfortunately, her respiratory status continued to deteriorate despite noninvasive ventilation, necessitating intubation. She subsequently developed septic shock requiring two vasopressors and experienced a prolonged hospital course, including re-intubation, administration of lytics for her effusions and prolonged antibiotics.</div></div><div><h3>Discussion</h3><div>This case demonstrates the importance of a thorough physical exam, as uvular deviation was an exam finding that prompted further imaging of her neck. Obtaining early consultation with Otolaryngology is urgent to evaluate the extent of soft tissue edema that can lead to airway compromise necessitating early airway management and to assess for necrotizing infections that require surgical intervention. Fusobacterium necrophorum, alongside other common oropharyngeal pathogens such as oral Streptococci should prompt antibiotic coverage with piperacillin-tazobactam, carbapenems, or ceftriaxone and metronidazole. Ampicillin-sulbactam should be avoided because of higher resistance rates. In this case, the patient's blood cultures grew Arcanobacterium haemolyticum which is a gram-positive facultative bacillus. Up to 97% of cases can develop septic emboli, therefore, a risk-benefit analysis is important regarding embolization and a decision for anticoagulation. Data is limited, so there is no strong evidence to favor starting anticoagulation, but can be considered in high-risk patients with extensive thrombosis or extension.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Page S19"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The seronegative puzzle: cryoglobulinemic GN in a patient with Sjögren's Syndrome","authors":"S Yunas,&nbsp;R Velagapudi,&nbsp;H Ibrahim,&nbsp;R Marathi,&nbsp;T Yen,&nbsp;Y Obi,&nbsp;M Atari,&nbsp;N Dossabhoy,&nbsp;M Tio","doi":"10.1016/j.amjms.2025.12.034","DOIUrl":"10.1016/j.amjms.2025.12.034","url":null,"abstract":"<div><h3>Case Report</h3><div>We report a case of seronegative cryoglobulinemic glomerulonephritis (GN) in the setting of Sjogren's Syndrome.</div><div>A 64-year-old female with a history of hypertension and rheumatoid arthritis previously treated with methotrexate and hydroxychloroquine was admitted with a 2-month history of persistent nausea, emesis, and 24-pound weight loss. She was also found to have an elevated serum creatinine (sCr) of 1.8 mg/dL (unknown baseline), microscopic hematuria, and nephrotic syndrome with a urine protein-to-creatinine ratio of 5.4 g/g. Initial serologic work-up obtained showed +ANA (1:320; speckled nuclear pattern), +SSA (&gt;8 u), +SSB (&gt;8 u), elevated CRP (5.13 mg/dL), +rheumatoid factor (68.2 IU/mL), decreased C3 and C4 (61 mg/dL and 2 mg/dL, respectively), +IgM kappa M protein (0.022 g/dL) with free light chain ratio of 1.4. Pertinent negatives included cryoglobulin, hepatitis C virus antibody, ANCA, PLA2R, dsDNA serologies. Kidney biopsy demonstrated membranoproliferative GN with diffuse and global endocapillary hypercellularity. Two glomeruli had cellular crescents and few glomeruli showed intraluminal Periodic Acid Schiff positive pseudo-thrombi consistent with cryoplugs on light microscopy. Immunofluorescence showed IgM dominant diffuse global granular mesangial and capillary loop staining with slight clonal shift (kappa &gt; lambda) on both frozen and paraffin-embedded tissues. Electron microscopy on paraffin-embedded tissue showed possible subendothelial deposits with short fibrillary substructures. Given concerns for crescentic cryoglobulinemic GN, the patient received pulse-dose methylprednisolone. Further investigations yielded the following negative results- cyclic citrullinated peptide, MYD88 gene mutation, blood cultures, and urine culture. CT chest/abdomen/pelvis was negative for lymphadenopathy. Esophagogastroduodenoscopy showed moderate chronic gastritis with immunohistochemical stain negative for lymphoma. Bone marrow biopsy was negative for malignancies or plasma cell dyscrasias. The patient was ultimately diagnosed with type II cryoglobulinemic GN in the setting of Sjogren's Syndrome and was treated with steroid taper following pulsed dosing and rituximab infusion. While hospitalized, patient's sCr peaked to 3.7 and downtrended, discharged with a sCr of 1.4.</div><div>Sjogren's Syndrome has variable renal manifestations including interstitial nephritis, renal tubular acidosis, GN, and nephrolithiasis. In cases of mixed cryoglobulinemic GN such as this, it is important to exclude active infections, lymphomas, and plasma cell dyscrasias.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Page S18"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WITHDRAWN","authors":"","doi":"10.1016/j.amjms.2025.12.032","DOIUrl":"10.1016/j.amjms.2025.12.032","url":null,"abstract":"","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Page S17"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Subcutaneous fat necrosis with extensive hematoma following therapeutic hypothermia","authors":"A Barkemeyer ,&nbsp;L Barbiero ,&nbsp;J Surcouf ,&nbsp;A Martin","doi":"10.1016/j.amjms.2025.12.054","DOIUrl":"10.1016/j.amjms.2025.12.054","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Case Report&lt;/h3&gt;&lt;div&gt;Subcutaneous fat necrosis (SCFN) is an uncommon but often self-limited panniculitis. In term neonates it can be associated with a perinatal stress event, particularly in neonates who undergo therapeutic hypothermia. There are several known complications of SCFN including hypercalcemia which can be severe as well as hypoglycemia, thrombocytopenia, anemia, and hypertriglyceridemia. We present the case of an infant with a rare complication of SCFN who developed a hematoma requiring surgical debridement and skin grafting.&lt;/div&gt;&lt;div&gt;A term male infant was born via emergent Cesarean Section due to non-reactive fetal heart tones. At delivery, the infant had a nuchal cord, body cord, and thick meconium. He required significant resuscitation with APGARS of 0/0/3/7. The infant met criteria for therapeutic hypothermia due to concern for hypoxic ischemic encephalopathy and was transferred to our Level IV NICU. His initial hospital course was consistent with severe multi-organ dysfunction.&lt;/div&gt;&lt;div&gt;On DOL 2, the infant was found to have erythematous indurated plaques to the back and posterior shoulders most consistent with SCFN. Therapeutic hypothermia was continued. In the following days, the erythematous skin evolved to a violaceous color and became more nodular. On DOL 9, there was an acute change with the development of large, fluctuant, violaceous nodules overlying the back and bilateral posterior shoulders with a large central mass measuring ∼15cm x 15cm. This was associated with a concomitant drop in hemoglobin and platelets requiring multiple blood products. An ultrasound of the mass was obtained showing extensive subcutaneous fat edema with scattered fluid. On DOL 10, following correction of coagulopathy, general surgery incised the large central nodule which evacuated 250 mL of serous fluid and blood. Pathology was significant for SCFN with hematoma. The infant was followed closely by plastic surgery to determine the need for soft tissue reconstruction. On DOL 13, the patient underwent debridement of non-viable tissue with placement of a wound vac. Over the next month, the infant underwent six wound vac exchanges with placement of dermal regeneration template on DOL 16. A split thickness skin graft was performed on DOL 34. The wound vac was ultimately removed prior to discharge on DOL 45. He has since followed up in dermatology and plastic surgery clinics and, by 7 weeks of age, the skin graft was noted to be well healing and closed.&lt;/div&gt;&lt;div&gt;This unique case of SCFN complicated by the development of a significant hematoma contributes to a small collection of existing literature on this rare complication of SCFN. Secondary hematomas require multidisciplinary care and may need intensive, repeated surgical intervention. Therapeutic hypothermia is critical in the management of term infants (&gt;36 weeks) status post a significant HIE event to optimize long term neurodevelopmental outcomes. Awareness of rare sequelae is i","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Page S30"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reversible pediatric dilated cardiomyopathy due to severe iron deficiency anemia","authors":"JD Canonigo,&nbsp;JM Mack,&nbsp;D Fiedorek","doi":"10.1016/j.amjms.2025.12.072","DOIUrl":"10.1016/j.amjms.2025.12.072","url":null,"abstract":"<div><h3>Case Report</h3><div>Purpose: Iron deficiency anemia (IDA) is the most common nutritional deficiency worldwide and remains a significant cause of morbidity in children. In the United States, up to 15% of children aged 1–3 years have iron deficiency, and approximately 5% meet criteria for IDA. While typically associated with neurodevelopmental delays and infection risk, severe IDA can rarely cause dilated cardiomyopathy (DCM) through chronic hypoxia, impaired myocardial energetics, and high-output physiology. We present a toddler with profound IDA who developed decompensated heart failure during transfusion, illustrating the link between IDA and reversible pediatric DCM.</div></div><div><h3>Case</h3><div>A 2-year-old male with developmental delay and a cow's milk–dominant diet presented with lethargy, pallor, and tachypnea. Laboratory studies showed profound IDA (hemoglobin 1.8 g/dL, ferritin 8.3 ng/mL, MCV 50 fL). He was started on 20 mL/kg of pRBCs in aliquots. After the first aliquot, he developed acute respiratory distress with pulmonary edema and cardiomegaly; after the second, he progressed to hypoxemic respiratory failure requiring intubation.</div><div>Echocardiography demonstrated severe left ventricular dilation with depressed systolic function and valvular regurgitation. Notably, baseline cardiomegaly and chamber enlargement suggested an underlying chronic DCM. He was managed with inotropes, diuretics, cautious transfusions, and intravenous iron.</div><div>Following IV iron therapy, ventricular systolic function rapidly and dramatically improved. By hospital day 11, echocardiography showed normalization, allowing extubation and discontinuation of inotropes. He was discharged on oral iron and diuretics, and at one-month follow-up remained asymptomatic with sustained normal function.</div></div><div><h3>Discussion</h3><div>This case underscores the need for vigilance when transfusing profoundly anemic children, as underlying ventricular dysfunction may predispose to circulatory overload. Most importantly, the rapid normalization of cardiac function following IV iron suggests that IDA was the direct cause of this patient's cardiomyopathy. Early screening and nutritional intervention are essential to prevent severe IDA, while careful transfusion and multidisciplinary management are critical in cases of decompensation.</div></div>","PeriodicalId":55526,"journal":{"name":"American Journal of the Medical Sciences","volume":"371 ","pages":"Pages S42-S43"},"PeriodicalIF":1.8,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146175556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}