Biomarkers of Brain Dysfunction in Perinatal Iron Deficiency.

Iron deficiency in the fetal and neonatal period (perinatal iron deficiency) bodes poorly for neurodevelopment. Given its common occurrence and the negative impact on brain development, a screening and treatment strategy that is focused on optimizing brain development in perinatal iron deficiency is necessary. Pediatric societies currently recommend a universal iron supplementation strategy for full-term and preterm infants that does not consider individual variation in body iron status and thus could lead to undertreatment or overtreatment. Moreover, the focus is on hematological normalcy and not optimal brain development. Several serum iron indices and hematological parameters in the perinatal period are associated with a risk of abnormal neurodevelopment, suggesting their potential use as biomarkers for screening and monitoring treatment in infants at risk for perinatal iron deficiency. A biomarker-based screening and treatment strategy that is focused on optimizing brain development will likely improve outcomes in perinatal iron deficiency.

Simultaneous Presentation of Takayasu Arteritis and Crohn's Disease in a Middle-Aged Patient: Are they two sides of the same coin?

Autoimmune disorders have a wide spectrum of symptoms, often with multiorgan involvement. Multiple autoimmune disorders also often occur concurrently in the same patient. These two possibilities must be distinguished in patients with multiorgan involvement to ensure early diagnosis and treatment. Here, we report a case of a previously healthy man who presented with simultaneous Takayasu arteritis and Crohn's disease. He presented with heart failure with reduced ejection fraction and severe aortic regurgitation. An echocardiogram demonstrated a greatly dilated aorta, and a diagnosis of Takayasu arteritis was made, confirmed with CT aortogram. Inpatient treatment was begun, but the patient subsequently developed bloody diarrhoea a few days after admission. Colonoscopy done to locate the source of bleeding showed colonic ulcers; a biopsy confirmed a diagnosis of Crohn's disease. The patient was successfully managed with medical management of heart failure, steroids, mesalamine and azathioprine, and has been in remission for the last 2 years.

Prognostic Performance of Hematological and Serum Iron and Metabolite Indices for Detection of Early Iron Deficiency Induced Metabolic Brain Dysfunction in Infant Rhesus Monkeys.

BACKGROUND: The current pediatric practice of monitoring for infantile iron deficiency (ID) via hemoglobin (Hgb) screening at one y of age does not identify preanemic ID nor protect against later neurocognitive deficits. OBJECTIVES: To identify biomarkers of iron-related metabolic alterations in the serum and brain and determine the sensitivity of conventional iron and heme indices for predicting risk of brain metabolic dysfunction using a nonhuman primate model of infantile ID. METHODS: Simultaneous serum iron and RBC indices, and serum and cerebrospinal fluid (CSF) metabolomic profiles were determined in 20 rhesus infants, comparing iron sufficient (IS; N = 10) and ID (N = 10) infants at 2 and 4 mo of age. RESULTS: Reticulocyte hemoglobin (RET-He) was lower at 2 wk in the ID group. Significant IS compared with ID differences in serum iron indices were present at 2 mo, but Hgb and RBC indices differed only at 4 mo (P < 0.05). Serum and CSF metabolomic profiles of the ID and IS groups differed at 2 and 4 mo (P < 0.05). Key metabolites, including homostachydrine and stachydrine (4-5-fold lower at 4 mo in ID group, P < 0.05), were altered in both serum and CSF. Iron indices and RET-He at 2 mo, but not Hgb or other RBC indices, were correlated with altered CSF metabolic profile at 4 mo and had comparable predictive accuracy (area under the receiver operating characteristic curve scores, 0.75-0.80). CONCLUSIONS: Preanemic ID at 2 mo was associated with metabolic alterations in serum and CSF in infant monkeys. Among the RBC indices, only RET-He predicted the future risk of abnormal CSF metabolic profile with a predictive accuracy comparable to serum iron indices. The concordance of homostachydrine and stachydrine changes in serum and CSF indicates their potential use as early biomarkers of brain metabolic dysfunction in infantile ID.

An extremely rare case of recurrent pleomorphic myxoidliposarcoma with response to eribulin chemotherapy - A case report.

Pleomorphic myxoid liposarcoma (PML) is a newly recognized entity with aggressive clinical behavior and a tendency to recur. It has histological features of both myxoid and pleomorphic liposarcoma and lacks the molecular and structural chromosomal abnormalities associated with myxoid and pleomorphic liposarcoma. The data about their response to chemotherapy is quite sparse. We report a case of incidentally detected pleomorphic myxoid liposarcoma of the mediastinum in a 32-year-old gentleman. After resection and adjuvant chemotherapy with doxorubicin and ifosfamide, there was no evidence of residual disease at the end of treatment. During a routine follow-up 5 months later, he was found to have a recurrence of the disease with histological confirmation. He received a trabectedin given its activity in myxoid liposarcoma. However, he had toxicities and progression leading to its discontinuation. Subsequently, eribulin was started as the next line of therapy. After 4 cycles of chemotherapy, response assessment was suggestive of partial response, which is still maintained after 7 cycles of eribulin. This is the first report of this entity responding to a newer chemotherapy regimen.

Anemia, Iron Supplementation, and the Brain.

The developing brain is particularly vulnerable to extrinsic environmental events such as anemia and iron deficiency during periods of rapid development. Studies of infants with postnatal iron deficiency and iron deficiency anemia clearly demonstrated negative effects on short-term and long-term brain development and function. Randomized interventional trials studied erythropoiesis-stimulating agents and hemoglobin-based red blood cell transfusion thresholds to determine how they affect preterm infant neurodevelopment. Studies of red blood cell transfusion components are limited in preterm neonates. A biomarker strategy measuring brain iron status and health in the preanemic period is desirable to evaluate treatment options and brain response.

Intranasal insulin treatment partially corrects the altered gene expression profile in the hippocampus of developing rats with perinatal iron deficiency.

Perinatal iron deficiency (FeD) targets the hippocampus and leads to long-term cognitive deficits. Intranasal insulin administration improves cognitive deficits in adult humans with Alzheimer's disease and type 2 diabetes and could provide benefits in FeD-induced hippocampal dysfunction. To objective was to assess the effects of intranasal insulin administration intranasal insulin administration on the hippocampal transcriptome in a developing rat model of perinatal FeD. Perinatal FeD was induced using low-iron diet from gestational day 3 until postnatal day (P) 7, followed by an iron sufficient (FeS) diet through P21. Intranasal insulin was administered at a dose of 0.3 IU twice daily from P8 to P21. Hippocampi were removed on P21 from FeS control, FeD control, FeS insulin, and FeD insulin groups. Total RNA was isolated and profiled using next-generation sequencing. Gene expression profiles were characterized using custom workflows and expression patterns examined using ingenuity pathways analysis (n = 7-9 per group). Select RNAseq results were confirmed via qPCR. Transcriptomic profiling revealed that mitochondrial biogenesis and flux, oxidative phosphorylation, quantity of neurons, CREB signaling in neurons, and RICTOR-based mTOR signaling were disrupted with FeD and positively affected by intranasal insulin treatment with the most benefit observed in the FeD insulin group. Both perinatal FeD and intranasal insulin administration altered gene expression profile in the developing hippocampus. Intranasal insulin treatment reversed the adverse effects of FeD on many molecular pathways and could be explored as an adjunct therapy in perinatal FeD.

Nonhematopoietic Umbilical Cord Blood Stem Cell Administration Improves Long-term Neurodevelopment After Periventricular-Intraventricular Hemorrhage in Neonatal Rats.

Periventricular-intraventricular hemorrhage (PIVH) is common in extremely low gestational age neonates (ELGAN) and leads to motor and behavioral impairments. Currently there is no effective treatment for PIVH. Whether human nonhematopoietic umbilical cord blood-derived stem cell (nh-UCBSC) administration reduces the severity of brain injury and improves long-term motor and behavioral function was tested in an ELGAN-equivalent neonatal rat model of PIVH. In a collagenase-induced unilateral PIVH on postnatal day (P) 2 model, rat pups received a single dose of nh-UCBSCs at a dose of 1 × 106 cells i.p. on P6 (PIVH + UCBSC group) or were left untreated (Untreated PIVH group). Motor deficit was determined using forelimb placement, edge-push, and elevated body swing tests at 2 months (N = 5-8). Behavior was evaluated using open field exploration and rearing tests at 4 months (N =10-12). Cavity volume and hemispheric volume loss on the PIVH side were determined at 7 months (N = 6-7). Outcomes were compared between the Untreated PIVH and PIVH + UCBSC groups and a Control group. Unilateral motor deficits were present in 60%-100% of rats in the Untreated PIVH group and 12.5% rats in the PIVH + UCBSC group (P = 0.02). Untreated PIVH group exhibited a higher number of quadrant crossings in open field exploration, indicating low emotionality and poor habituation, and had a cavitary lesion and hemispheric volume loss on the PIVH side. Performance in open field exploration correlated with cavity volume (r2 = 0.25; P < 0.05). Compared with the Untreated PIVH group, performance in open field exploration was better (P = 0.0025) and hemispheric volume loss was lower (19.9 ± 4.4% vs 6.1 ± 2.6%, P = 0.018) in the PIVH + UCBSC group. These results suggest that a single dose of nh-UCBSCs administered in the subacute period after PIVH reduces the severity of injury and improves neurodevelopment in neonatal rats.

Reticulocyte Hemoglobin Equivalent has Comparable Predictive Accuracy as Conventional Serum Iron Indices for Predicting Iron Deficiency and Anemia in a Nonhuman Primate model of Infantile Iron Deficiency.

BACKGROUND: Infantile iron deficiency (ID) causes anemia and compromises neurodevelopment. Current screening relies on hemoglobin (Hgb) determination at 1 year of age, which lacks sensitivity and specificity for timely detection of infantile ID. Low reticulocyte Hgb equivalent (RET-He) indicates ID, but its predictive accuracy relative to conventional serum iron indices is unknown. OBJECTIVES: The objective was to compare diagnostic accuracies of iron indices, red blood cell (RBC) indices, and RET-He for predicting the risk of ID and IDA in a nonhuman primate model of infantile ID. METHODS: Serum iron, total iron binding capacity, unsaturated iron binding capacity, transferrin saturation (TSAT), Hgb, RET-He, and other RBC indices were determined at 2 wk and 2, 4, and 6 mo in breastfed male and female rhesus infants (N = 54). The diagnostic accuracies of RET-He, iron, and RBC indices for predicting the development of ID (TSAT < 20%) and IDA (Hgb < 10 g/dL + TSAT < 20%) were determined using t tests, area under the receiver operating characteristic curve (AUC) analysis, and multiple regression models. RESULTS: Twenty-three (42.6%) infants developed ID and 16 (29.6%) progressed to IDA. All 4 iron indices and RET-He, but not Hgb or RBC indices, predicted future risk of ID and IDA (P < 0.001). The predictive accuracy of RET-He (AUC = 0.78, SE = 0.07; P = 0.003) for IDA was comparable to that of the iron indices (AUC = 0.77-0.83, SE = 0.07; P ≤ 0.002). A RET-He threshold of 25.5 pg strongly correlated with TSAT < 20% and correctly predicted IDA in 10 of 16 infants (sensitivity: 62.5%) and falsely predicted possibility of IDA in only 4 of 38 unaffected infants (specificity: 89.5%). CONCLUSIONS: RET-He is a biomarker of impending ID/IDA in rhesus infants and can be used as a hematological parameter to screen for infantile ID.

Clinico-Pathological Correlation in Dermatological Disorders: A Retrospective Audit of 332 Skin Biopsies from a Tertiary Care Center.

Background: Skin biopsy is a frequently employed tool by the dermatologists with several factors that are known to influence its diagnostic yield as well as interpretation. The objective of our study was to analyze the clinico-pathological concordance and discordance rates in various dermatological conditions and study the factors affecting the same. Materials and. Methods: We retrospectively analyzed 332 biopsies conducted over a period of 1 year and looked for clinico-pathological correlation and tabulated the results. Results: The overall concordance rate observed in the present study was 70.48% (234 out of 332). Out of 234 concordant cases, 175 of them (74.8%) were concordant with the first differential diagnosis mentioned on the histopathology requisition form, thus revealing an acceptable level of clinico-pathological correlation. The concordance was observed to be 66.87% when only one differential was mentioned on the requisition forms, whereas it increased to 73.96% when more than one diagnosis was offered (P = <0.00001). However, the adequacy of clinical description on the histopathological requisition form was not observed to significantly impact the clinico-pathological correlation in the present study. Conclusion: An acceptable level of clinico-pathological concordance was observed in the present study thus reinforcing skin biopsy as an indispensable tool in the dermatological practice. However, continuous effort in the form of regular audits in the department, interdepartmental discussions between pathologists and clinicians, and repeat biopsies in case of discordancy would help in identifying and addressing the deficiencies that impact the diagnostic yield of histopathology and which would ultimately result in better patient care.

Comparative evaluation of the antibacterial activity of red diode laser therapy and 0.2% chlorhexidine against Aggregatibacter actinomycetemcomitans on implant healing abutments: An ex vivo study.

Aims: The intraoral microbiota has a high potential to undergo dysbiosis, causing inflammatory changes with respect to the tissues surrounding either a natural tooth or an implant. Thus, the longevity of implant prosthesis depends on a thorough implant decontamination protocol. Among all the techniques available for doing so, laser is garnering increasing popularity, owing to minimal bleeding, high efficiency, and faster healing. However, limited literature exists regarding the superiority of lasers over chlorhexidine (CHX), the indisputable gold standard antibacterial chemical agent. The aim of this study was to compare the percentage of bacterial reduction of Aggregatibacter actinomycetemcomitans from implant healing abutments post red diode laser therapy versus 0.2% CHX treatment. Settings and Design: The current study had an ex vivo, observational, case-control design. Materials and Methods: Patients reporting for the second stage of the implant surgery were taken as the source of data and the healing abutments, the clinical samples. Eleven patients were chosen with one intraoral implant serving as the test site for laser treatment and another, the control site for CHX treatment. Microbiological analysis was performed via quantitative real time polymerase chain reaction to compare the bacterial reduction percentage after each treatment. Statistical Analysis Used: Repeated measures ANOVA and independent sample t test were used. Results: The mean bacterial viability of the test group (laser) was 1.2%-1.6%, and 0.6%-1.4% for the control group (CHX). The former caused a mean bacterial reduction of 96.1% while the latter, 96.3%. Both the treatments caused a highly statistically significant reduction of viable bacterial counts (P = 0.001). However, when compared, there was no statistically significant difference in the bacterial reduction, when compared in between the two (P = 0.902). Conclusion: Laser treatment is at par with chemical implant surface decontamination. It can help bypass the complications of CHX and revolutionize the protocols for implant surface decontamination.

Iron supplementation and the risk of bronchopulmonary dysplasia in extremely low gestational age newborns.

BACKGROUND: The aim of this study was to determine the relationship between iron exposure and the development of bronchopulmonary dysplasia (BPD). METHODS: A secondary analysis of the PENUT Trial dataset was conducted. The primary outcome was BPD at 36 weeks gestational age and primary exposures of interest were cumulative iron exposures in the first 28 days and through 36 weeks' gestation. Descriptive statistics were calculated for study cohort characteristics with analysis adjusted for the factors used to stratify randomization. RESULTS: Of the 941 patients, 821 (87.2%) survived to BPD evaluation at 36 weeks, with 332 (40.4%) diagnosed with BPD. The median cohort gestational age was 26 weeks and birth weight 810 g. In the first 28 days, 76% of infants received enteral iron and 55% parenteral iron. The median supplemental cumulative enteral and parenteral iron intakes at 28 days were 58.5 and 3.1 mg/kg, respectively, and through 36 weeks' 235.8 and 3.56 mg/kg, respectively. We found lower volume of red blood cell transfusions in the first 28 days after birth and higher enteral iron exposure in the first 28 days after birth to be associated with lower rates of BPD. CONCLUSIONS: We find no support for an increased risk of BPD with iron supplementation. TRIAL REGISTRATION NUMBER: NCT01378273. https://clinicaltrials.gov/ct2/show/NCT01378273 IMPACT: Prior studies and biologic plausibility raise the possibility that iron administration could contribute to the pathophysiology of oxidant-induced lung injury and thus bronchopulmonary dysplasia in preterm infants. For 24-27-week premature infants, this study finds no association between total cumulative enteral iron supplementation at either 28-day or 36-week postmenstrual age and the risk for developing bronchopulmonary dysplasia.

Tandem mass tag proteomic and untargeted metabolomic profiling reveals altered serum and CSF biochemical datasets in iron deficient monkeys.

The effects of early-life iron deficiency anemia (IDA) extend past the blood and include both short- and long-term adverse effects on many tissues including the brain. Prior to IDA, iron deficiency (ID) can cause similar tissue effects, but a sensitive biomarker of iron-dependent brain health is lacking. To determine serum and CSF biomarkers of ID-induced metabolic dysfunction we performed proteomic and metabolomic analysis of serum and CSF at 4- and 6- months from a nonhuman primate model of infantile IDA. LC/MS/MS analyses identified a total of 227 metabolites and 205 proteins in serum. In CSF, we measured 210 metabolites and 1,560 proteins. Data were either processed from a Q-Exactive (Thermo Scientific, Waltham, MA) through Progenesis QI with accurate mass and retention time comparisons to a proprietary small molecule database and Metlin or with raw files imported directly from a Fusion Orbitrap (Thermo Scientific, Waltham, MA) through Sequest in Proteome Discoverer 2.4.0.305 (Thermo Scientific, Waltham, MA) with peptide matches through the latest Rhesus Macaque HMDB database. Metabolite and protein identifiers, p-values, and q-values were utilized for molecular pathway analysis with Ingenuity Pathways Analysis (IPA). We applied multiway distance weighted discrimination (DWD) to identify a weighted sum of the features (proteins or metabolites) that distinguish ID from IS at 4-months (pre-anemic period) and 6-months of age (anemic).

Autosomal recessive inheritance of a novel missense mutation of ITGB4 for Epidermolysis-Bullosa pyloric-atresia: a case report.

Epidermolysis-Bullosa (EB), a rare Mendelian disorder, exhibits complex phenotypic and locus-heterogeneity. We identified a nuclear family of clinically unaffected parents with two offsprings manifesting EB-Pyloric-Atresia (EB-PA), with a variable clinical severity. We generated whole exome sequence data on all four individuals to (1) identify the causal mutation behind EB-PA (2) understand the background genetic variation for phenotype variability of the siblings. We assumed an autosomal recessive mode of inheritance and used suites of bioinformatic and computational tools to collate information through global databases to identify the causal genetic variant for the disease. We also investigated variations in key genes that are likely to impact phenotype severity. We identified a novel missense mutation in the ITGB4 gene (p.Ala1227Asp), for which the parents were heterozygous and the children homozygous. The mutation in ITGB4 gene, predicted to reduce the stability of the primary alpha6beta4-plectin complex compared to all previously studied mutations on ITGB4 reported to cause EB.

Smokeless Tobacco Exposure and Fetal Iron Status: An Analytical Study.

Objectives: To compare the cord serum ferritin and fetal iron status in newborns with and without maternal occupational smokeless tobacco exposure and determine the influencing factors. Methods: This cross-sectional study included mother-infant dyads with occupational tobacco exposure (exposed) and an unexposed group. Umbilical cord serum ferritin was compared in both groups. Fetal nicotine absorption was established by cord cotinine. Results: A total of 140 newborns each were analyzed in each group. There was no significant mean difference (MD) (P = 0.900) between the cord serum ferritin in the tobacco exposed and unexposed group. Fetal nicotine absorption was seen in 43.6% of the exposed group. Cord serum ferritin was 14.1 µg/L (95% confidence interval [(95% CI:-43.1, 14.9); P=0.338] lower in this group compared with the group without fetal nicotine absorption. A higher adjusted MD for ferritin was present for maternal hypertension (12.5 [95% CI: -75.5, 100.5]; P = 0.777) and gestational diabetes mellitus (21.4 [95% CI: -54.0, 96.9]; P = 0.571) in the group with fetal nicotine absorption. Fetal nicotine absorption exaggerated fetal iron depletion in maternal anemia [aOR 4.8 (95%CI: 1.2, 19.0); P=0.025]. Conclusion: Cord serum ferritin and fetal iron status were comparable in tobacco exposed and unexposed groups. In those with fetal nicotine absorption, cord ferritin levels reflect the fetal inflammatory state.

Multiomic profiling of iron-deficient infant monkeys reveals alterations in neurologically important biochemicals in serum and cerebrospinal fluid before the onset of anemia.

The effects of iron deficiency (ID) during infancy extend beyond the hematologic compartment and include short- and long-term adverse effects on many tissues including the brain. However, sensitive biomarkers of iron-dependent brain health are lacking in humans. To determine whether serum and cerebrospinal fluid (CSF) biomarkers of ID-induced metabolic dysfunction are concordant in the pre/early anemic stage of ID before anemia in a nonhuman primate model of infantile iron deficiency anemia (IDA). ID (n = 7), rhesus infants at 4 mo (pre-anemic period) and 6 mo of age (anemic) were examined. Hematological, metabolomic, and proteomic profiles were generated via HPLC/MS at both time points to discriminate serum biomarkers of ID-induced brain metabolic dysfunction. We identified 227 metabolites and 205 proteins in serum. Abnormalities indicating altered liver function, lipid dysregulation, and increased acute phase reactants were present in ID. In CSF, we measured 210 metabolites and 1,560 proteins with changes in ID infants indicative of metabolomic and proteomic differences indexing disrupted synaptogenesis. Systemic and CSF proteomic and metabolomic changes were present and concurrent in the pre-anemic and anemic periods. Multiomic serum and CSF profiling uncovered pathways disrupted by ID in both the pre-anemic and anemic stages of infantile IDA, including evidence for hepatic dysfunction and activation of acute phase response. Parallel changes observed in serum and CSF potentially provide measurable serum biomarkers of ID that reflect at-risk brain processes prior to progression to clinical anemia.

Perinatal iron deficiency as an early risk factor for schizophrenia.

Growing evidence indicates that a suboptimal intrauterine environment confers risk for schizophrenia. The developmental model of schizophrenia posits that aberrant brain growth during early brain development and adolescence may interact to contribute to this psychiatric disease in adulthood. Although a variety of factors may perturb the environment of the developing fetus and predispose for schizophrenia later, a common mechanism has yet to be elucidated. Micronutrient deficiencies during the perinatal period are known to induce potent effects on brain development by altering neurodevelopmental processes. Iron is an important candidate nutrient to consider because of its role in energy metabolism, monoamine synthesis, synaptogenesis, myelination, and the high prevalence of iron deficiency (ID) in the mother-infant dyad. Understanding the current state of science regarding perinatal ID as an early risk factor for schizophrenia is imperative to inform empirical work investigating the etiology of schizophrenia and develop prevention and intervention programs. In this narrative review, we focus on perinatal ID as a common mechanism underlying the fetal programming of schizophrenia. First, we review the neural aberrations associated with perinatal ID that indicate risk for schizophrenia in adulthood, including disruptions in dopaminergic neurotransmission, hippocampal-dependent learning and memory, and sensorimotor gating. Second, we review the pathophysiology of perinatal ID as a function of maternal ID during pregnancy and use epidemiological and cohort studies to link perinatal ID with risk of schizophrenia. Finally, we review potential confounding phenotypes, including nonanemic causes of perinatal brain ID and future risk of schizophrenia.

An eye-opening case of periorbital oedema: a clinicodiagnostic dilemma.

Cutaneous metastasis (CM), a rare occurrence, can produce a variety of skin lesions. Signet-ring cell carcinoma (SRCC) is a very aggressive tumour with low survival rate irrespective of location. We report a case of SRCC with CM presenting with asymptomatic progressive unilateral angio-oedema-like findings. A high index of suspicion and low threshold for biopsy are crucial for early diagnosis of CM as the prognosis is poor, especially when the primary cancer is SRCC.

Pathological Lung Patterns of COVID-19 and its Clinical Correlation to Disease Severity.

Introduction: Coronavirus disease-2019 (COVID-19) infection can result in pulmonary complications ranging from mild illness to severe life-threatening disease. There are limited studies correlating the association between the clinical course of COVID-19 and histopathological findings. This study aimed to examine the postmortem histopathological changes in lung tissue of COVID-19-positive patients and to correlate those changes with disease severity. Materials and methods: This prospective observational study was conducted in adult COVID-19-positive patients. Postmortem core needle biopsy (CNB) of the lung was done using ultrasonography guidance within 1 hour of death. Histopathological analyses were performed by two expert pulmonary pathologists. The demographic and clinical data of the patients were recorded to correlate them with histopathological findings. Results: In total, 48 patients were assessed for inclusion, and 21 patient relatives consented for the study. The median duration of illness was 21 (range 9-38) days, the predominant histopathological finding was diffuse alveolar damage (DAD) in most patients (19/21), followed by pneumonia (13/21). Exudative, intermediate, and advanced DAD patterns were seen in 9.5%, 52.4%, and 28.6% of cases, respectively. Advanced DAD was associated with a longer duration of disease. The pneumonia findings were associated with positive respiratory and blood cultures. The microvascular thrombus was seen only in one patient. Conclusion: The predominant pathological findings in our patients were DAD and pneumonia. The DAD type correlated with the duration of illness, and we attributed pneumonia findings to secondary infection. The incidence of microvascular thrombi was low, and it might reflect the effect of treatment with anticoagulation. How to cite this article: Maddani SS, Rao R, Deepa HC, Noronha AK, Chaudhuri S, Vishwas P. Pathological Lung Patterns of COVID-19 and its Clinical Correlation to Disease Severity. Indian J Crit Care Med 2022;26(12):1285-1292.

Utility of Immunofluorescence Antigen Mapping in Hereditary Epidermolysis Bullosa.

BACKGROUND: Epidermolysis bullosa (EB) is characterized by blisters and erosions on the trauma-prone areas of the body. It occurs as a result of mutation in the genes encoding structural proteins. Transmission electron microscopy (TEM) is considered the gold standard test in the laboratory diagnosis of EB. However, this test requires a lot of expertise and is not widely available. Immunofluorescence antigen mapping (IFM) is considered a suitable alternative with comparable sensitivity and specificity. However, there is paucity of studies analyzing the utility of IFM in the diagnosis of EB. AIMS AND OBJECTIVES: To study the utility of IFM in the laboratory diagnosis of EB. MATERIALS AND METHODS: A cross-sectional study was conducted involving 179 biopsy specimens of patients with EB. IFM was carried out using a panel of monoclonal antibodies against K14, laminin 332, type IV collagen, and type VII collagen. RESULTS: Diagnosis of EB simplex (EBS), junctional EB (JEB), and dystrophic EB (DEB) was made in 104, 28, and 26 biopsy specimens, respectively. The overall concordance rate was 41.3% with higher concordance rates in EBS. CONCLUSION: The present study is conducted to assess the efficacy of IFM in the diagnosis of EB with large sample size. Our study serves to establish IFM as an important tool in the diagnostic armamentarium of EB as the prognosis mainly rests on diagnosing the type of EB.