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Gastrointestinal tract, hepatic, hindlimb, and renal recovery of CO(2) in vivo.

Whole body oxidative rates of labeled substrates are often measured by collecting expired air and determining the amount of labeled CO(2) that is produced. However, the CO(2) produced may not be completely recovered under all circumstances, and there is a wide variation in values reported under different experimental conditions ( approximately 50-100%). The potential contribution of specific organs to this variation has not been defined. In vivo studies using healthy, postabsorptive, multicatheterized conscious canines were conducted to determine gastrointestinal tract, hepatic, hindlimb, and renal recoveries of NaH(14)CO(3) during a 180-min constant infusion [0.022+/-0.002 (SE) microCi x kg(-1) x min(-1)]. Before the constant infusion period, a bolus infusion of NaH(14)CO(3) (1.76+/-0.16 microCi/kg) was given, and the rate of decay in blood was measured over a 15-min period to determine pool size. The pool size for the distribution of (14)CO(2) was approximately 80% of the total body pool (16.0+/-1.7 liters). Whole body recovery was 97.2+/-6.7%. The recoveries across the liver, gut, leg, and kidney were 99.9+/-1.3, 98.0 +/-1.4, 96.7+/-2.6, and 99.9+/-2.1%, respectively. In conclusion, hepatic, gastrointestinal tract, hindlimb, and renal recoveries of CO(2) in vivo were near 100%, suggesting that CO(2) loss is not greater in gluconeogenic organs and that corrections for incomplete recovery of CO(2), when measuring oxidation of substrates across these organs under normal postabsorptive conditions, would be very minor.

Animals↗

Distribution and characterization of endogenous benzodiazepine receptor ligand (endozepine)-like peptides in the rat gastrointestinal tract.

Endozepine is the generic name for a family of peptides that are capable of displacing benzodiazepines and the 3-carboxylate ester of beta-carboline from their specific binding sites on synaptosomal membranes. The 104-amino acid polypeptide diazepam-binding inhibitor (DBI) and the octadecaneuropeptide (ODN) generated by tryptic digestion of DBI are two members of the endozepine family. In the present study we have used RIA, HPLC, in situ hybridization, and immunohistochemical techniques to identify and localize endozepine-like molecules in the rat gastrointestinal tract. Significant amounts of endozepine-like immunoreactivity (LI) were detected throughout the gut; the highest concentrations were found in the duodenum and antrum. HPLC analysis revealed that the immunoreactive material eluted as a major peak with a higher retention time than that of synthetic ODN. The distribution of the immunoreactive peptide(s) was studied using the peroxidase-antiperoxidase technique at the light microscope level. Endozepine-LI was localized only in the epithelial cell layer of the intestine in both goblet cells and enterocytes. In the stomach, endozepine-LI appeared to be restricted to deep layer of the epithelial cells. The diffuse neuroendocrine cells (amine precursor uptake and decarboxylation system) as well as myenteric and neuronal cells were devoid of immunoreactivity. A good correlation was observed between RIA and immunocytochemical data, in that the esophagus, which contained very low concentrations of endozepine-LI, also exhibited weak immunostaining of secretory cells. In situ hybridization using a 35S-labeled cRNA probe showed that endozepine mRNA was located in the mucosa. Taken together, these results show that in the rat, epithelial cells synthesize endozepine-LI material. Since epithelial cells also contain a high density of peripheral-type benzodiazepine-binding sites, our data indicate that endozepines may play a role in water, electrolyte, and/or mucus regulation in the rat gastrointestinal tract. The occurrence of high levels of endozepine-LI in the rat stomach also suggests that endozepines can be involved in the regulation of gastric acid secretion through modulation of local gamma-aminobutyric acid-ergic neurotransmission.

Animals↗

Role of parenteral antibiotherapy in gastrointestinal tract flora suppression. A study in children treated with high-dose chemotherapy and autologous bone marrow transplantation.

In order to determine the effect of parenteral antibiotherapy on the fecal flora in patients with profound and prolonged granulocytopenia, we initiated a prospective study of 62 cases of autologous bone marrow transplantation following high-dose chemotherapy. All patients were children from 2 to 18 years old, isolated in a protective environment, receiving a diet low in viable microbial content but no oral non-absorbable prophylactic antibiotics to decontaminate the gastrointestinal tract. Bacteriological analysis of fecal flora was conducted at least once a week before and during parenteral antibiotherapy, administered at the first greater than 38 degrees C febrile episode in these granulocytopenic patients (granulocyte count less than 0.5 X 10(9)/l). The 58 evaluable patients fell into three groups with regard to the systemic antibiotherapy: group A (n = 16): moxalactam + mezlocillin; group B (n = 15): moxalactam + tobramycin; and group C (n = 27): cefotaxime plus gentamicin. Fecal flora suppression was observed in 51/58 cases (88%) (group A: 15/16, group B: 13/15, group C: 23/27). It always occurred within 5 days of initiating parenteral antibiotherapy and persisted in 88% of the 51 patients over the whole period of systemic antibiotherapy. During the latter, fecal recolonization was observed in seven cases (12%), always by Enterobacteriaceae sensitive to the prescribed systemic antibiotherapy, never responsible for septicemia. Since parenteral antibiotherapy alone was able to suppress the gastrointestinal tract flora, the effects of this treatment should be considered in all trials of digestive tract decontamination.

Adolescent↗

[Microbiocenosis of parietal mucin in the gastrointestinal tract of rats].

The qualitative and quantitative composition of the microbial community in parietal mucin at different areas of the gastrointestinal tract (GIT) of rats was revealed. The pronounced variability in the quantitative and qualitative characteristics of microbiocenosis in parietal mucin of rats at different sections was revealed. The differences were most pronounced in the passage from upper to lower GIT sections, the large intestine found to be the richest biocenosis. The microbial composition of rat feces was faintly associated with the GIT parietal microbiocenosis. The individual areas of GIT mucosa were unique of their microbial characteristics and organization. This makes it possible to regard them as relatively independent biotopes and indicates that it is impossible to evaluate the microbial community by one of the colonic mucosal sifes.

Animals↗

[Pharmacokinetics of site-specific delivery of dexamethasone-dextran prodrug in rat gastrointestinal tract].

AIM: To explore whether dexamethasone-dextran (260,000) has the characteristics of site-specific delivery in rat gastrointestinal tract. METHODS: Dexamethasone prodrug and dexamethasone were administered to rat ig at the dose of 5 mumol.kg-1. The distribution of dexamethasone in the contents and mucosa of different parts of the rat GI tract at different time intervals and its concentration in plasma were determined by HPLC. RESULTS: Dexamethasone was mainly released in the cecum and colon contents and mucosa after oral administration of dexamethasone prodrug. The absorption was reduced significantly. The peak time of the drug in plasma was 8.1 h, and the peak concentration was 32 micrograms.L-1. However, free dexamethasone was found mainly in the contents and mucosa of the stomach, proximal and distal small intestine. The peak time of the drug in plasma was 2.2 h, and the peak concentration was 2120 micrograms.L-1. CONCLUSION: Dexamethasone can be specifically delivered to the large intestine by using dexamethasone-dextran (260,000). It appears that the prodrug has a potential in the treatment of inflammatory bowel disease.

Animals↗

Effects of acetaldehyde on cell regeneration and differentiation of the upper gastrointestinal tract mucosa.

BACKGROUND: The tumor-promoting effect of ethanol on cancer of the upper respiratory-digestive tract is not well understood. Although ethanol itself is not carcinogenic, the first product of ethanol metabolism-acetaldehyde is. Acetaldehyde can be produced from ethanol by oral bacteria, and high concentrations have been observed in human saliva after ethanol consumption. The purpose of this study was to investigate whether acetaldehyde administered orally to rats induces altered differentiation and proliferation in the animals' upper gastrointestinal tracts. METHODS: Twenty Wistar rats were given either water containing acetaldehyde at a concentration of 120 mM or tap water to drink for 8 months. Tissue specimens were then taken from the tongue, epiglottis, and forestomach of each animal and immunohistochemically stained for markers of cellular proliferation (Ki67 nuclear antigen) or differentiation (cytokeratins 1, 4, 10, 11, 14, and 19). The mean epithelial thickness of each sample was measured via light microscopy, using an eyepiece containing grid lines. Differences between the control and acetaldehyde-treated groups were analyzed by use of the unpaired Student's t test. All reported P values are two-sided. RESULTS: Although no tumors were observed, staining for cytokeratins 4 and 14 revealed an enlarged basal layer of squamous epithelia in the rats receiving acetaldehyde. In these animals, cell proliferation was significantly greater than that observed in the control animals for samples from the tongue (P<.0001), epiglottis (P<.001), and forestomach (P<.0001). In addition, the epithelia from acetaldehyde-treated rats were significantly thicker than in epithelia from control animals (P<.05 for all three sites). CONCLUSIONS: Acetaldehyde, administered orally to rats, can cause hyperplastic and hyperproliferative changes in epithelia of the upper gastrointestinal tract. This finding suggests that microbially produced acetaldehyde in saliva may explain the tumor-promoting effect of ethanol on these epithelia.

Acetaldehyde↗

Transport of d-galactose by the gastrointestinal tract of the locust, Locusta migratoria.

Due to exoskeleton, the absorption of nutrients in adult insects takes place across the gastrointestinal tract epithelium. In most physiological studies, sugar intestinal absorption has been described as a diffusional process and to date no sugar transporter has been cloned from the digestive tract of insects. In the present work, the existence of a saturable transport system for galactose in the gastric caeca of Locusta migratoria is clearly demonstrated. This transport shows a relatively high affinity for galactose (apparent K0.5=2-3 mM) and is inhibited by glucose, 2-deoxyglucose and with less potency by fructose and alpha-methyl-d-glucoside. The absence of sodium or the presence of phloridzin hardly affects galactose absorption, indicating that it is not mediated by a SGLT1-like transporter. The absence of K+, Cl-, Mg2+ and Ca2+ or changes in the pH do not modify galactose absorption either. Nevertheless, phloretin, cytochalasin B and theophylline (inhibitors of facilitative transporters) decrease sugar uptake around 50%. Xenopus laevis oocytes microinjected with poly A+ RNA isolated from gastric caeca show sodium-independent galactose uptake that is three times higher than in non-injected oocytes, further supporting the existence of a mRNA coding for at least one equilibrative sugar transporter in L. migratoria gastric caeca.

Animals↗

Pathophysiological significance of a reaction in mouse gastrointestinal tract associated with delayed-type hypersensitivity.

AIM: To explore the pathophysiological significance of delayed type hypersensitivity (DTH) reaction in mouse gastrointestinal tract induced by an allergen 2,4-dinitrochlorobenzene (DNCB). METHODS: BALB/c mice were randomly divided into control and DTH(1-6) groups. After sensitized by DNCB smeared on the abdominal skin, the mice were challenged with DNCB by gavage or enema. The weight, stool viscosity and hematochezia were observed and accumulated as disease active index (DAI) score; the gastrointestinal motility was represented by active charcoal propulsion rate; the colon pathological score was achieved by macropathology and HE staining of section prepared for microscopy; and the leukocyte migration inhibitory factor (LMIF) activity was determined by indirect capillary assay of the absorbance (A) of migrated leukocytes. RESULTS: Active charcoal propulsion rates of small intestine in the DNCB gavages groups were significantly higher than that in the control group (P<0.01). The DAI scores and pathological score in DNCB enema groups were also higher than that in the control group (P<0.05), and there were significant rises in LMIF activity in DNCB enema groups as compared with control groups (P<0.01). CONCLUSION: Mouse gastrointestinal DTH reaction could be induced by DNCB, which might facilitate the mechanism underlying the ulcerative colitis.

Animals↗

Radiologic, endoscopic, and surgical considerations of melanoma metastatic to the gastrointestinal tract.

Malignant melanoma is the most common malignancy to metastasize to the gastrointestinal tract. In a retrospective computer-assisted data search of over 2500 patients with melanoma registered over the past 10 years, 110 patients have been identified to have premortem gastrointestinal metastatic disease (metastatic disease identified at least 6 months before death). The small intestine (35%), colon (14.5%), and stomach (7%) are the most common sites for metastases. Polypoid or ulcerating masses and intramucosal nodules are typical radiologic presentations for gastric and colonic lesions, while over 50% of the small bowel metastases are polypoid masses that many times act as leading points for intussusception. Endoscopic studies are helpful in the preoperative diagnosis of these lesions. In a subset of 38 patients with symptomatic small bowel metastatic disease, complete resections were performed in 26% of patients, with palliative bypasses being performed in 40%, despite the fact that over 50% of the patients had documented visceral metastasis in other body sites. The operative morbidity rate was 15% with no operative deaths. Ninety percent of patients gained relief of symptoms, and overall survival from the time of confirmed small bowel disease averaged 17.3 months, with a range of 6 months to 9 years. It would seem that patients with melanoma with gastrointestinal metastatic disease can benefit from aggressive radiologic and endoscopic procedures for diagnosis and staging. Only through surgical interventions for symptomatic gastrointestinal disease can the quality of life be improved and life expectancy be extended.

Colonic Neoplasms↗

Fetal exposure to intact immunoglobulin E occurs via the gastrointestinal tract.

BACKGROUND: Consideration of the evolutionary significance of IgE might provide insight into the immunological interactions occurring in utero and during early post-natal life that regulate later atopic disease. OBJECTIVE: We postulated that the fetal gut is exposed to intact amniotic fluid IgE that might interact with local IgE receptors. METHODS: IgE levels in matched maternal blood and amniotic fluid (n = 47) or breast milk (n = 15) collected from pregnant women in the UK (Southampton) and Brazil (Sao Paulo) were studied. Expression of IgE receptors, Fc epsilon RI and Fc epsilon RII (CD23), in fetal gastrointestinal tract (n = 19) and skin (n = 11) was examined immunohistochemically. RESULTS: Human amniotic fluid at 16-18 weeks' gestation contained intact IgE at levels that increased as maternal circulating levels increased (Spearman's rho = 0.897; P < 0.001). Circulating IgE levels from women in Sao Paulo, Brazil, associated positively not only with term (> 37 weeks' gestation) amniotic fluid (rho = 0.993; P < 0.001) but also breast milk IgE levels (rho = 0.785; P = 0.001). Maternal levels of IgE did not change significantly over pregnancy and fetal circulating levels of IgE were very low (< 0.6 IU/mL). Low-affinity IgE receptors (CD23) were expressed in lymphoid follicles of the fetal gut from 16 weeks of gestation (6/8), but not from 11 to 16 weeks (0/11) or in the skin. CONCLUSION: Amniotic fluid contains intact IgE that might bind to CD23+ cells within the lymphoid follicles of the fetal gastrointestinal tract. The evolutionary significance of these interactions might be to prepare the immune system for helminthic parasite exposure at birth via IgE-mediated antigen focusing, or "education" of the developing immune system about the prevailing extrauterine environment. However, at present in societies where helminthosis is not a significant health issue, this pathway may still be operational and associated with the development of atopic disease.

Amniotic Fluid↗

Intestinal protein supply alters amino acid, but not glucose, metabolism by the sheep gastrointestinal tract.

This study was intended to establish the extent which amino acids (AAs) and glucose are net metabolized by the gastrointestinal tract (GIT) of ruminant sheep when intestinal protein supply is varied. Wether sheep (n = 4, 33 +/- 2.0 kg) were fitted with catheters for measurement of net absorption by the mesenteric (MDV) and portal-drained (PDV) viscera and a catheter inserted into the duodenum for casein infusions. Sheep received a fixed amount of a basal diet that provided adequate metabolizable energy (10.9 MJ/d) but inadequate metabolizable protein (75 g/d) to support 300-g gain per day. Four levels of casein infusion [0 (water), 35, 70, and 105 g/d], each infused for 5.5 d, were assigned to sheep according to a 4 x 4 Latin square design. [methyl-(2)H(3)]leucine was infused (8 h) into the duodenum while [1-(13)C]leucine plus [6-(2)H(2)]glucose were infused (8 h) into a jugular vein. With the exception of glutamate and glutamine, net absorption of AAs increased linearly (P < 0.05, R(2) = 0.46-1.79 for MDV; P < 0.05, R(2) = 0.6-1.58 for PDV) with casein infusion rate. Net absorption by the PDV accounted for <100% of the additional supplies of leucine, valine, and isoleucine (0.6-0.66, P < 0.05) from casein infusion, whereas net absorption by the MDV accounted for 100% of the additional essential AA supply. Glucose absorption (negative) and utilization of arterial glucose supply by the GIT remained unchanged. There was a positive linear (P < 0.05) relation between transfer of plasma urea to the GIT and arterial urea concentration (MDV, P < 0.05, r = 0.90; PDV, P < 0.05, r = 0.93). The ruminant GIT appears to metabolize increasing amounts of the branched-chain AAs and certain nonessential AAs when the intestinal supply of protein is increased.

Amino Acids↗

Mucosal vaccination increases endothelial expression of mucosal addressin cell adhesion molecule 1 in the human gastrointestinal tract.

Homing of leukocytes to various tissues is dependent on the interaction between homing receptors on leukocytes and their ligands, addressins, on endothelial cells. Mucosal immunization results in homing of antigen-specific lymphocytes back to the mucosa where they first encountered the antigen. However, it is unknown whether this homing of antigen-specific cells is mediated by an altered endothelial addressin expression after vaccination. Using different immunization routes with an oral cholera vaccine, we show that the endothelial expression of mucosal addressin cell adhesion molecule 1 (MAdCAM-1) is increased in the gastric and upper small intestinal mucosae after immunization through various local routes in the upper gastrointestinal tract. In contrast, rectal immunization did not influence the levels of MAdCAM-1 in the gastric or duodenal mucosa. Furthermore, we show that MAdCAM-1 can be induced on human endothelial cells by tumor necrosis factor alpha (TNF-alpha) and gamma interferon. The vaccine component cholera toxin B subunit (CTB) increased MAdCAM-1 expression on endothelial cells in cultured human gastric explants, an effect that seemed to be mediated by TNF-alpha. In conclusion, MAdCAM-1 expression is increased in the upper gastrointestinal tract after local immunizations with a vaccine containing CTB. This strongly suggests the involvement of MAdCAM-1 in the preferential homing of mucosal lymphocytes to their original site of activation.

Adult↗

Prostaglandin synthesis along the gastrointestinal tract of the rabbit: differences in total synthesis and profile.

In the present study we systematically investigated the synthesis of prostaglandins in the mucosa and the muscle layer along the length of the rabbit gut. Homogenates of mucosa and muscle layer were incubated with (14C)-labelled arachidonic acid, and prostaglandin formation was determined using thin-layer chromatography. With respect to total prostaglandin synthesis the highest values in the mucosa were measured in fundus, antrum and colon, whereas the prostaglandin synthesis in the muscle layer was maximal in the small bowel, particularly the ileum. In the mucosa, the prostaglandins E2 and F2a predominated, and there were minor differences along the gastrointestinal tract. In the muscle layer of the stomach, high amounts of 6-keto prostaglandin F1a, the stable degradation product of prostacyclin were produced, while small and large bowel homogenates synthesized mostly F2a. Consistently the prostaglandins A2/B2 were a major product in most locations. In addition, PG E2 catabolism to 15-keto PG E2 and 13,14-dihydro-15-keto PG E2 in the absence of NAD was slow. No significant changes in total prostaglandin synthesis and prostaglandin profile were detected between 24 hrs fasted and normally fed rabbits at any part of the gastrointestinal tract.

Animals↗

Degradation of Cry1Ab protein from genetically modified maize in the bovine gastrointestinal tract.

Immunoblotting assays using commercial antibodies were established to investigate the unexpected persistence of the immunoactive Cry1Ab protein in the bovine gastrointestinal tract (GIT) previously suggested by enzyme-linked immunosorbent assay (ELISA). Samples of two different feeding experiments in cattle were analyzed with both ELISA and immunoblotting methods. Whereas results obtained by ELISA suggested that the concentration of the Cry1Ab protein increased during the GIT passage, the immunoblotting assays revealed a significant degradation of the protein in the bovine GIT. Samples showing a positive signal in the ELISA consisted of fragmented Cry1Ab protein of approximately 17 and 34 kDa size. Two independent sets of gastrointestinal samples revealed the apparent discrepancy between the results obtained by ELISA and immunoblotting, suggesting that the antibody used in the ELISA reacts with fragmented yet immunoactive epitopes of the Cry1Ab protein. It was concluded that Cry1Ab protein is degraded during digestion in cattle. To avoid misinterpretation, samples tested positive for Cry1Ab protein by ELISA should be reassessed by another technique.

Animal Feed↗

Mouse R-cadherin: expression during the organogenesis of pancreas and gastrointestinal tract.

Members of the cadherin protein family of cell adhesion molecules are thought to regulate many morphogenetic events during the development of multicellular organisms. We are interested in which cell-cell interactions cadherins regulate during pancreas morphogenesis. Expression and function of E-cadherin in the pancreas have previously been characterized. Recently, R-cadherin cDNA was isolated and the expression patterns of R- and N-cadherin cDNA was isolated and the expression patterns of R- and N-cadherin mRNAs in the pancreas have been described. In the present study, we have investigated the expression of R-cadherin in the pancreas and gastrointestinal tract using specific anti-R-cadherin antibodies. During early stages of pancreas development (E10.5) R-cadherin is expressed in most hormone-producing cells in addition to in primitive duct-like cells. Later, at E18.5, when islets start to form, R-cadherin is not expressed in intraislet endocrine cells, but is instead found in intraductule endocrine and exocrine cells. In adult islets of Langerhans R-cadherin is absent from endocrine cells, but is present in ductule-like cells. Furthermore, the molecule is expressed in exocrine cells: apically and basolaterally on epithelial duct and ductule cells and apically on acinar cells. Interestingly, there appears to be a correlation between the downregulation of R-cadherin expression in intraductule endocrine cells and the migration out of the duct epithelium to form islets. In the gastrointestinal tract R-cadherin is expressed in the pit region of gastric glands and in absorptive cells of the small intestine. The subcellular localization in these tissues is on both the apical and basolateral surfaces. The potential function of R-cadherin, in particular its role in pancreas development, is discussed.

Animals↗

Supplementation with alpha-tocopherol or a combination of alpha-tocopherol and ascorbic acid protects the gastrointestinal tract of iron-deficient rats against iron-induced oxidative damage during iron repletion.

Recently we have shown the susceptibility of Fe-deficient rat intestine to oxidative damage during Fe repletion. The role of dietary antioxidants like ascorbic acid, alpha-tocopherol and a combination of both in counteracting the oxidative stress was tested in this study. Five groups of thirteen weanling WKY female rats were fed with an Fe-deficient diet for a period of 5 weeks. Another set of thirteen rats received an Fe-sufficient diet and served as the control group (Con). Oral administration of either vehicle (D), 8 mg Fe alone (D+) or in the presence of 24 mg ascorbic acid (D+ + C), 40 mg alpha-tocopherol (D+ + E) or a combination of both (D+ + C + E) per d for 15 d was carried out in Fe-depleted rats. The impact of this treatment protocol on Fe status, oxidative stress and antioxidant status at the site of Fe absorption was assessed. It was observed that though the indicators of Fe status were normalised on Fe supplementation, the oxidative stress as reflected by the levels of both thiobarbituric-acid reactive substances (TBARS) and protein carbonyls were significantly greater in D+ and D+ + C compared to D+ + E, D+ + C + E and Con groups. The mucosal cell DNA damage was seen in D+, D+ + C and D+ + E groups on electrophoresis. Functional integrity as assessed by the activities of alkaline phosphatase and lys-ala-dipeptidyl aminopeptidase were normalized in all the groups treated with the antioxidant(s). There were significant positive alterations in some of the endogenous antiperoxidative systems and in serum caeruloplasmin activity in D+ + E and D+ + C + E groups. Paradoxically, serum ascorbate levels were significantly lower in D+ + C than in D+ + E and D+ + C + E groups. This could be due to the protection offered by alpha-tocopherol in the presence of Fe. It is concluded that supplementation of alpha-tocopherol alone or in combination with ascorbic acid protects the gastrointestinal tract of Fe-deficient rats against Fe-mediated oxidative damage during Fe repletion. However, ascorbic acid alone does not protect the gastrointestinal tract against Fe-induced oxidative stress.

Administration, Oral↗

Leukaemic lesions of the gastrointestinal tract.

This study is based on the clinical records and post-mortem findings of 264 patients with leukaemia. Gross leukaemic lesions in the gastrointestinal tract were found in 39 patients, an overall incidence of 14.8%. The incidence in all types of acute leukaemia was 18.4%, in chronic leukaemias 9.6%, and in myeloid leukaemia 10.9%. The ileum, stomach, and proximal colon were the sites most commonly affected. Four types of lesion were found: raised leukaemic nodules, leukaemic plaques, diffuse infiltrations with a convoluted brain-like appearance of the mucosal folds, and a multiple leukaemic polyposis. The clinical and pathological features of these lesions are described, and references are given to similar cases reported in the literature.

Acute Disease↗