Post-Transplant Fecal Carriage of Antibiotic Resistant and B-Lactamases-Producing Enterobacteriales among Renal Transplant Recipients.

BACKGROUND: The intestinal colonization and transmission of antibiotic-resistant Enterobacteriales to renal transplant recipients may pose a threat to them because they are profoundly immunocompromised and vulnerable to infection. Hence, it is crucial to identify these antibiotic-resistant fecal Enterobacteriales harboring high-risk populations. The objective of this study was to determine antibiotic resistance as well as ß-lactamases production in fecal Enterobacteriales among renal transplant recipients. METHODS: The stool samples, one collected from each transplant recipient, were processed for isolation and identification of Enterobacteriales and were tested for their antibiotic susceptibility, extended-spectrum ß-lactamase, and metallo-ß-lactamase production by standard methods. RESULTS: A total of 103 Enterobacteriales comprising of Escherichia coli (86.4%), Klebsiella species (11.7%), and Citrobacter species (1.9%) were isolated and more than 60% of the E. coli were found resistant to ceftazidime and ciprofloxacin and around half of the Klebsiella species were resistant to ceftazidime and fluroquinolones. The extended-spectrum ß-lactamase production was seen in 3.4% and 8.3% and metallo-ß-lactamase production in 24.7% and 33.3% of E. coli and Klebsiella species, respectively. The high proportion of ß-lactamase-producers were resistant to piperacillin-tazobactam, meropenem, gentamicin, and amikacin than ß-lactamases non-producers. CONCLUSION: Since the antibiotic resistance is higher in fecal Enterobacteriales, each renal transplant recipient should be screened for these highly resistant intestinal colonizers after transplantation in order to prevent infections and to reduce the rate of transplant failure due to infections.

A Comparative Study of Pain in Patients Planned for Tooth Extraction and Dental Implant Insertion.

Introduction: A variation in dental pain following tooth extraction and implant placement has been observed. The present study aimed to compare pain in patients undergoing tooth extraction and implant placement. Materials and Methods: Eighty-four patients underwent tooth extraction and implant placement in maxillary central incisor. Pain (VAS) was recorded at 24 h, 24 h, and 48 h. Results: The mean pain value (VAS) at 24 h post-operatively after tooth extraction was 6.1 and after implant insertion was 2.9. At 48 h after tooth extraction was 4.3 and after implant insertion was 1.1 and after 72 h after tooth extraction was 2.4 and after implant insertion was 0.27. A significant difference was observed between both procedures at different intervals of time (P < 0.05). Conclusion: The pain experienced by patients during dental implant insertion was comparatively less as compared to dental tooth extraction.

Mean Warm Ischemia Time among Kidney Transplant Patients in a Tertiary Care Centre: A Descriptive Cross-sectional Study.

Introduction: In renal transplantation, warm ischemia time is the interval from the removal of a procured kidney from ice storage to initiating graft reperfusion. Successful kidney transplantation depends on warm ischemia time. The study aims to find the mean warm ischemia time among kidney transplant patients in a tertiary care centre. Methods: This descriptive cross-sectional study was conducted among kidney transplant patients in a tertiary care centre. Data from 15 December 2012 to 15 October 2022 were collected between 1 December 2022 to 4 January 2023 from the hospital records. Ethical approval was taken from the Nepal Health Research Council (Reference number: 1341). All first-time living-related kidney transplant recipients were included in the study. All the patients undergoing kidney transplants from brain-dead donors were excluded from the study. Convenience sampling method was used. Point estimate and 95% Confidence Interval were calculated. Results: Among 230 patients, the mean warm ischemia time was 35.45±7.35 min. The mean first warm ischemia time was 4.28±2.05 min and the mean second warm ischemia time was 31.27±7.04 min. The mean age of the recipients was 35.14±10.49 years (range 14-64), of which 173 (75.20%) were male and 57 (24.80%) were female. Conclusions: The mean warm ischemia time among kidney transplant patients in a tertiary care centre was similar to the studies done in similar settings. Keywords: kidney transplantation; prevalence; warm ischemia.

Kidney transplantation from brain-dead donors in Nepal: Report of first six cases.

Introduction: and importance: Kidney transplantation is one of the best treatment options for patients with end-stage renal disease. More than 90% of patients awaiting renal transplantation die without getting the kidney for transplantation. Brain dead donor kidney transplantation can bridge this gap proficiently. We aim to report details of the first six patients who had undergone brain-dead donor kidney transplantation in the history of transplantation in Nepal. Case presentation: We conducted a descriptive analysis of clinical data of six adult recipients with kidney transplantation from three brain-dead donors. We described postoperative complications, length of stay, graft function which was documented with serum creatinine, acute rejection episode, delayed graft function, and patient/graft survival of recipient. Recipients were between 15 and 56 years old. Three patients experienced delayed graft function. Urinary tract infection was observed in two patients, both of whom were treated with antibiotics. One patient had acute graft rejection. None of our patients required reoperation. Length of hospital stay ranged from 9 to 32 days. The postoperative graft function was 100% in all patients. There was no graft loss, and no death was observed during follow-up. Clinical discussion: Following the initiation of the brain-dead donor transplantation program, a lot of work needs to be done to make it a regular practice. Thus, this program needs support from all sections of society and government. This can be the only solution to decrease the huge gap between the supply and demand of organs in Nepal. Conclusion: This case reports indeed revealed impressive success in initiating a brain-dead donor kidney transplantation program in a developing country that in terms of quality, meets comprehensive standard with acceptable graft function and patient/graft survival in under limited resources healthcare setting.

Living donor kidney paired exchange: An observational study.

Background: Kidney transplantation is the treatment of choice for patients with end-stage renal disease (ESKD). Kidney paired donation (KPD) provides the chance to match an incompatible donor/recipient pair with another donor and recipient in a similar condition. We aimed to compare the outcomes of pair exchange kidney transplantation with traditional live donor kidney transplantation in our context. Method: A review of medical records of 62 patients (31 pairs) who underwent two-way conventional living kidney pair exchange from July 2016 to June 2021 was done. The control group was considered those 62 patients who had undergone classic live donor kidney transplantation (LDKT) during the study period. The patient's demographics, intraoperative and postoperative variables including delayed graft function, length of hospital stay, graft survival, patient survival, and rejections rates were compared between the groups (KPD and LDKT). Results: The majority of recipients were male (77.4 and 80.6%) while donors were female (77.4 and 69.4%) in KPD and the LDKT groups. Mean ages were 37 years (range: 19-59) and 37 years (range: 17-65) for the recipient's in KPD and the LDKT. KPD transplantation was performed in 62 recipients to avoid blood group incompatibility. There were no significant differences in outcomes comprising delayed graft function (1.6 and 3.2%), graft survival (100% in both groups), patient survival (95.2 and 96.8%), and rejections rates (1.6 and 1.6%) between KPD and LDKT group (P > 0.005). The length of stay was similar (5.9 and 5.7 days) in KPD and LDKT groups (P > 0.005). Conclusions: The outcomes of KPD were comparable with classic LDKT in terms of delayed graft function, length of hospital stay, graft survival, patient survival, and rejections rates in our study. Therefore, the kidney paired donation program should be encouraged and promoted in centers where the ABO-incompatible transplant is expensive with added risk and the rate of deceased donor transplantation is very low.

Class switching of carbonic anhydrase isoforms mediates remyelination in CA3 hippocampal neurons during chronic hypoxia.

Chronic exposure to hypoxia results in cerebral white matter hyperintensities, increased P300 latency, delayed response and impairment in working memory. Despite burgeoning evidence on role of myelination in nerve conduction, the effect of chronic hypoxia on myelination of hippocampal neurons has been less studied. The present study provides novel evidence on alterations in myelination of hippocampal CA3 neurons following chronic hypoxic exposure. Sprague Dawley rats exposed to global hypobaric hypoxia simulating altitude of 25,000 ft showed progressive demyelination in CA3 hippocampal neurons on 14 days followed by remyelination on 21 and 28 days. The demyelination of CA3 neurons was associated with increased apoptosis of both oligodendrocyte precursor cells (OPCs) and mature oligodendrocytes (OLs), peroxidation of myelin lipids, and nitration induced reduced expression of Carbonic Anhydrase II (CAII). Prolonged hypoxic exposure of 21 and 28 days on the other hand resulted in peroxisome proliferator-activated receptor alpha (PPARα) induced upregulation of Carbonic Anhydrase IV (CAIV) expression in mature oligodendrocytes through iNOS mediated mechanisms along with reduction in lipid peroxidation and remyelination. Inhibition of carbonic anhydrase activity on the other hand prevented remyelination of CA3 neurons. Based on these findings we propose a novel iNOS mediated mechanism for regulation of myelination in hypoxic hippocampal neurons through class switching of carbonic anhydrases.

Conscious Abstinence from Smokeless Tobacco Evokes Higher Withdrawal Response and Impairs Cognitive Performance Independent of Sympathetic Response.

INTRODUCTION: High consumption of smokeless tobacco in adult Indian population increases the risk of developing oral cancers leading to high morbidity and mortality. Though the influence of abstinence from smoking on cognitive performance has been widely studied, the effect of smokeless tobacco on cognitive performance and its association with withdrawal symptoms is less understood. This study comparatively investigates the effect of short-term conscious abstinence and distraction during abstinence from smokeless tobacco consumption on the craving, withdrawal symptoms, sympathetic response, and cognitive performance in tobacco addicts. METHODS: Age, sex, education and socioeconomic status matched control (N = 15) and smokeless tobacco addicts (N = 60) were recruited from residential areas in Bhubaneswar for the study. Following randomization of the addicts, conscious abstinence (N = 30) was induced by informed abstinence from tobacco consumption for 8 hours, while distracted cessation (N = 30) was induced by involving the participants in a cognitively engaging task for 8 hours during uninformed tobacco abstinence. RESULTS: The results of the study show higher withdrawal symptoms and reduced cognitive performance in volunteers with conscious abstinence which was positively correlated. The decreased cognitive performance in conscious cessation was independent of tobacco-induced increase in the LF:HF ratio and cotinine concentration in saliva. CONCLUSION: While conscious abstinence results in higher withdrawal symptoms, distraction during abstinence lowers these symptoms. Inclusion of distraction sessions during cessation can, therefore, be a new element in tobacco control strategies.

Micronucleus and Its Significance in Effusion Fluids.

BACKGROUND: Micronucleus (MN) is an extranuclear body within the cell formed due to failure of incorporation of whole chromosomes or their fragments during cell division. MN scoring can be done to identify malignant effusions. AIMS: This study aimed to score micronuclei to distinguish malignant effusion from benign effusions and to correlate MN score with type of malignant effusion. METHODS AND MATERIALS: A retrospective study was conducted on 30 malignant and 30 benign effusions. The number of micronucleated cells per 1,000 cells was counted in effusion smears stained with Papanicolaou stain under oil immersion (1,000×). RESULTS: The mean MN score in malignant effusions was 3.77 with standard deviation (SD) of 2.13. The mean MN score in benign effusions was 0.50 with SD of 0.57. The difference in MN score between malignant and benign effusions is statistically significant (P < 0.001). A cut-off MN score of 6.5 was seen to distinguish malignant and benign effusions with 100% specificity and 100% sensitivity in this study. CONCLUSIONS: MN score is higher in malignant effusions when compared with benign effusions. This can be used to differentiate malignant effusions from benign effusions in low resource setting.

Identification of Key Genes in Purine Metabolism as Prognostic Biomarker for Hepatocellular Carcinoma.

BACKGROUND: Deregulated purine metabolism is critical for fast-growing tumor cells by providing nucleotide building blocks and cofactors. Importantly, purine antimetabolites belong to the earliest developed anticancer drugs and are still prescribed in clinics today. However, these antimetabolites can inhibit non-tumor cells and cause undesired side effects. As liver has the highest concentration of purines, it makes liver cancer a good model to study important nodes of dysregulated purine metabolism for better patient selection and precisive cancer treatment. METHODS: By using a training dataset from TCGA, we investigated the differentially expressed genes (DEG) of purine metabolism pathway (hsa00230) in hepatocellular carcinoma (HCC) and determined their clinical correlations to patient survival. A prognosis model was established by Lasso-penalized Cox regression analysis, and then validated through multiple examinations including Cox regression analysis, stratified analysis, and nomogram using another ICGC test dataset. We next treated HCC cells using chemical drugs of the key enzymes in vitro to determine targetable candidates in HCC. RESULTS: The DEG analysis found 43 up-regulated and 2 down-regulated genes in the purine metabolism pathway. Among them, 10 were markedly associated with HCC patient survival. A prognostic correlation model including five genes (PPAT, DCK, ATIC, IMPDH1, RRM2) was established and then validated using the ICGC test dataset. Multivariate Cox regression analysis found that both prognostic risk model (HR = 4.703 or 3.977) and TNM stage (HR = 2.303 or 2.957) independently predicted HCC patient survival in the two datasets respectively. The up-regulations of the five genes were further validated by comparing between 10 pairs of HCC tissues and neighboring non-tumor tissues. In vitro cellular experiments further confirmed that inhibition of IMPDH1 significantly repressed HCC cell proliferation. CONCLUSION: In summary, this study suggests that purine metabolism is deregulated in HCC. The prognostic gene correlation model based on the five purine metabolic genes may be useful in predicting HCC prognosis and patient selection. Moreover, the deregulated genes are targetable by specific inhibitors.

Methanolic root extract of Codonopsis clematidea prevents hypoxia induced procoagulant state by inhibition of GPIb receptor regulated Lyn kinase activation.

BACKGROUND: The prevalence of procoagulant state under prolonged hypoxic exposures and the complications and lack of specificity associated with use of existing anti-thrombotic agents have necessitated the search for safer and natural therapeutics. Codonopsis, a widely studied medicinal herb, has been reported to decrease whole blood viscosity but the bioactive ingredients involved, and their mechanism of action therein however remain to be investigated. PURPOSE: The present study aimed at evaluating the efficacy of C. clematidea root extract and mechanism of action of its bioactive constituent flavonoid, Kaempferol, in ameliorating hypobaric hypoxia induced procoagulant state. METHODS: Fingerprinting analysis of methanolic extract of C. clematidea root was performed by RP-HPLC. In vitro toxicity study was conducted using HUVEC cell line and in vivo acute and sub-acute toxicity were done according to OECD guidelines (section-4, number-420 and 407 respectively). Adult male Sprague-Dawley rats weighing 230-250 g were exposed to global hypoxia simulating an altitude of 7600 m (282 mmHg), in animal decompression chamber for 3, 7, 14 and 21 days for in vivo studies. Dose optimisation of the extract was done by quantification of Thromboxane A2 in the serum of hypoxic rats. C. clematidea root extract was also evaluated for its in vitro and in vivo antioxidant properties. Procoagulant changes were studied by biochemical plasma coagulation assays and expression analysis of the signalling molecules of the platelet activation cascade like vWF, platelet activation marker CD41, GpIb-IX-V (CD42), Lyn kinase, p-PI3K, p-ERK and p-PLCγ were conducted to investigate C. clematidea mediated signalling mechanisms. RESULTS: Methanolic extract of C. clematidea root showed improved antioxidant status and improvement in bleeding time and in vitro coagulation assays like pT, aPTT, INR. Decreased concentrations of D-Dimers along with that of platelet activation marker CD41 and serum concentration of Thromboxane A2 were observed in C. clematidea root extract supplemented hypoxic animals. Phosphorylation of Lyn kinase, was reduced despite increase in concentration of activating ligand vWF. CONCLUSION: C. clematidea root extract was effective in preventing hypoxia induced platelet activation and resultant procoagulant state by inhibiting Lyn kinase, a serine threonine kinase effector of vWF signalling cascade.

Hypoxia-mediated alteration in cholesterol oxidation and raft dynamics regulates BDNF signalling and neurodegeneration in hippocampus.

Brain-derived neurotrophic factor (BDNF) which is primarily associated with neuronal survivability, differentiation and synaptic plasticity has been reported to mediate neurodegeneration in hypoxia through its p75 Neurotrophin receptors (p75NTR). The molecular events promoting BDNF-mediated pro-death signalling in hypoxia, however, still remain an enigma. This study attempts towards deciphering the signalling cascades involved in alteration of BDNF isoforms and its cognate receptor subtypes leading to neurodegeneration in hypoxia. Adult Sprague-Dawley rats were exposed to global hypobaric hypoxia simulating an altitude of 7620 m at standard temperature and humidity. Chronic hypoxic exposure for 7 days resulted in higher expression of pro-BDNF and alteration in N-linked glycosylation in hippocampus along with increased expression of endoplasmic reticulum stress markers viz., glucose-regulated protein (Grp78), calnexin and changes in the endoplasmic reticulum morphology. Our findings reveal enriched expression of p75NTR in lipid rafts and higher expression of tyrosine receptor kinase ß (Trkß) in non-raft regions following hypoxic exposure. Further investigations on membrane properties revealed decline in membrane fluidity along with increased cholesterol oxidation resulting in reduced translocation of Trkß from non-raft to raft regions. Supplementation of vitamin E during hypoxic exposure on the other hand reduced cholesterol oxidation and increased translocation of Trkß from non-raft to raft regions and promoted neuronal survival. Hence, our findings suggest a novel mechanism of cholesterol oxidation-induced alteration in raft dynamics which is promotes p75 receptor-mediated death signalling in hippocampal neurons during chronic hypoxia.

Kaempferol Inhibits Extra-synaptic NMDAR-Mediated Downregulation of TRkß in Rat Hippocampus During Hypoxia.

Cognitive dysfunction on chronic exposure to hypobaric hypoxia has been attributed to a myriad of survival and degenerative factors. Downregulation of Trkß and compromised survival signaling has been ascribed as a major contributing factor for hypoxic neurodegeneration. The mechanisms leading to downregulation of Trkß in hypoxia, however, remain to be elucidated. The present study aimed at investigating the upstream signaling mechanisms leading to Trkß downregulation in hypoxia and the potential of Kaempferol in ameliorating these changes. Our results showed a duration-dependent increase in hypoxic neurodegeneration as measured by Fluoro-Jade C staining of hippocampal CA3 neurons. Protein expression studies revealed strong correlation of Trkß with NR1 and NR2b expression on exposure to hypoxic stress. Administration of Kaempferol during hypoxic stress revealed its neuroprotective effect and Morris Water Maze test also highlighted its efficacy in improving spatial learning and memory. Further elucidation of the signaling mechanisms using specific inhibitors and in vitro silencing experiments confirmed involvement of extra-synaptic N-methyl-d-aspartate receptor (NMDAR) i.e. NR2b receptor subunit in downregulation of Trkß under hypoxic conditions. ChIP assay showed involvement of E47 transcription factor in NR2b mediated Trkß downregulation. Selective inhibition of signaling intermediate MLK2 by CEP11004 and inhibition of extra-synaptic NMDAR during hypoxic stress prevented Trkß downregulation in the hippocampus of hypoxic rats. Administration of Kaempferol also inhibited phosphorylation of E47 and hypoxia-induced downregulation of Trkß. The present study establishes the role of extra-synaptic NMDAR in hypoxia-induced downregulation of Trkß and the efficacy of Kaempferol in inhibiting extra-synaptic NMDAR-mediated signaling.

Salidroside mediated stabilization of Bcl -xL prevents mitophagy in CA3 hippocampal neurons during hypoxia.

Chronic hypoxic stress results in deposition of lipofuscin granules in the CA3 region of hippocampal neurons which contributes to neurodegeneration and accelerated neuronal aging. Oxidative stress and mitophagy during hypoxia are crucial to cause aggregation of these lipofuscin granules in hypoxic neurons. Salidroside, a glucoside derivative of ß-Tyrosol, has been reported to protect hypoxic neurons through maintenance of mitochondrial activity. The present study is aimed at investigating the potential of Salidroside in preventing mitophagy during chronic hypoxia and identification of the molecular targets and underlying signaling mechanisms. In-silico analysis for interaction of salidroside with Bcl-xL was carried out using VLife MDS software. The prophylactic efficacy of Salidroside for amelioration of global hypoxia induced neuronal aging was studied in adult male Sprague-Dawley rats exposed to hypobaric hypoxia simulating an altitude of 7600 m for 21 days. Salidroside was supplemented at a daily dose of 25 mg kg-1b.w. p.o. during hypoxic exposure. Ultra-structural and immune-histological studies were conducted to study lipofuscin aggregation and mitophagy. In-silico findings on salidroside mediated stabilization of Bcl-xL were validated by investigating its effect on downstream signaling molecules involved in mitophagy. Administration of Salidroside reduced deposition of lipofuscin in hypoxic CA3 hippocampal neurons and prevented mitophagy. Salidroside stabilizes Bcl-xL in hypoxic neurons resulting in inhibition of PGAM5 phosphatase activity and maintenance of FUNDC1 in phosphorylated state. Salidroside mediated inhibition of pFUNDC1 dephosphorylation prevents FUNDC1-LC3 II interaction which is crucial for mitophagy. The present study demonstrates potential of Salidroside in preventing lipofuscin deposition during chronic hypoxic stress.

Prevalence and risk factors of hypertension in acclimatized lowlanders staying at high altitude for different durations.

Hypoxic exposure at high-altitude (HA) modulates blood pressure (BP). High prevalence of hypertension among native highlanders (NH) has been reported. However, information on prevalence and determinants of hypertension in acclimatized young lowlanders (ALL) staying at HA for different durations is sparse. We aimed to determine the prevalence of hypertension in ALL staying at HA for different durations and its association with cardiovascular risk factors. Male volunteers were categorized on the basis of their duration of stay at HA; Lowlanders (LL) (0 months; n = 151), ALL (1-24 months; n = 519) and NH (n = 103). ALL were sub grouped into ALL 1 (1-6 months; n = 165), ALL 2 (6-12 months; n = 181), and ALL 3 (12-24 months; n = 173). BP, sympathetic activity, arterial stiffness, lipid profile, and homocysteine were estimated. Regression analysis was performed to determine association of risk factors with hypertension. Prevalence of hypertension among ALL was highest with 17.53% followed by NH (11.6%) and LL (9.27%). Prevalence of hypertension in ALL sub group was in order ALL 1 < ALL 2 < ALL 3. Hypertension was significantly associated with sympathetic dominance (p < 0.001) in ALL 1. Hypertension in ALL 2 was associated with dyslipidemia (p < 0.01) while in ALL 3 hypertension was associated with hyperhomocysteinemia (hHCY, p < 0.001), arterial stiffness and dyslipidemia (p < 0.01). In conclusion, our report suggests higher prevalence of hypertension in ALL. The association of studied risk factors and hypertension in different ALL sub groups varied significantly. Our findings suggest the need for a differential clinical approach to control hypertension in ALL considering their duration of stay at HA.

Estrogen Receptor ß Mediated Neuroprotective Efficacy of Cicer microphyllum Seed Extract in Global Hypoxia.

Hypoxia induced oxidative stress and neurodegeneration in the hippocampus has been implicated for memory impairment in conditions like stroke, ischemia and hypobaric hypoxia. The present study, aimed at investigating the potential of ethanolic extract of Cicer microphyllum seeds (CSE) for amelioration of global hypoxia induced neurodegeneration in CA1 region of hippocampus. CSE supplementation considerably reduced neurodegeneration and dendritic atrophy in CA1 neurons along with improvement of memory in hypoxic rats. This effect of CSE was partly attributed to its antioxidant activity resulting in reduction of lipid peroxidation, protein oxidation and DNA damage during exposure to chronic hypoxia. CSE also promoted dendritic arborization through activation of estrogen receptor beta (ERß) and phosphorylation of extracellular signal regulated kinase (ERK1/2) which was independent of brain derived neurotrophic factor (BDNF) mediated signalling mechanisms. Extra nuclear activation of ERK1/2 by ERß resulted in phosphorylation of cyclic AMP response element binding protein (CREB) leading to increased expression of PSD-95.These molecular alterations translated to behavioural changes in CSE administered hypoxic animals that performed better in Morris Water Maze Task as compared to vehicle treated hypoxic animals. Toxicological studies show NOEAL > 2000 mg/kg b.w. for oral administration of CSE indicating its safety for consumption. Our findings not only suggest the neuroprotective potential of CSE in hypoxia but also provide evidence for involvement of estrogen receptor and pCREB mediated nootropic effect of the extract.

Inflammatory pseudotumor of kidney masquerading as renal carcinoma.

Inflammatory pseudotumor also known as inflammatory fibroblastic tumor is a rare benign tumor, which commonly affects the lung. It is very rarely seen in the genitourinary tract. As the preoperative diagnosis, clinically and radiologically is inconclusive, it is imperative to surgically remove and confirm it on histopathologic examination. We report a case of inflammatory pseudotumor in a 51-year-old male who presented with flank pain and was treated with nephrectomy.

Fraser syndrome.

Fraser syndrome or cryptophthalmos is a rare autosomal recessive disorder characterized by major features such as cryptophthalmos, syndactyly and abnormal genitalia. The diagnosis of this syndrome can be made on clinical examination and perinatal autopsy. We present the autopsy findings of a rare case of Fraser syndrome in a male infant.