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This article discusses the various drugs that affect the equine gastrointestinal tract. Drugs that alter intestinal motility, that protect the gastrointestinal tract, and that alter secretions, as well as analgesics, appetite stimulants, and orally administered antimicrobial agents are reviewed.
INTRODUCTION: Involvement of upper gastrointestinal tract in pemphigus vulgaris is not uncommon. AIM: To study the involvement of upper gastrointestinal tract (UGIT) with the help of esophago-gastro-duodenoscopy (EGD) in patients of vesiculobullous dermatoses with emphasis on pemphigus vulgaris. METHODS: Forty-two patients (M-22, F-20) with vesiculobullous dermatoses, diagnosed on the basis of clinical features and skin histopathology as pemphigus vulgaris (PV)-40 patients and pemphigus foliaceus (PF)-2 patients were included in the study. The EGD was performed and mucosa of the esophagus, stomach and first part of the duodenum were examined. Mucosal biopsies were taken from the lower esophagus in 26 patients of PV and studied after H and E staining. RESULTS: On EGD, esophageal involvement was seen in 67% patients of PV (27/40). Of these, Grade I esophagitis was observed in seven, Grade II in 11, Grade III in four and Grade IV involvement was seen in five patients of PV. Three PV patients had associated esophageal candidiasis. Involvement of esophageal mucosa was also observed in one out of two patients of PF. Gastric mucosa was involved in 52% and duodenal mucosa in 20% of PV patients. Acantholysis was observed in seven out of 26 (27%) esophageal biopsies of PV patients. Two patients of PV vomited a tube-like structure, indicative of 'esophagitis dissecans superficialis'. The involvement of the gastric mucosa in patients with history of oral corticosteroid intake (60%) was compared to the group without history of oral corticosteroids (30%). CONCLUSION: Among PV patients under study, significant involvement of oral (87%), esophageal (67%), gastric (52%) and duodenal mucosa (20%) was observed.
BACKGROUND AND AIMS: To ascertain whether the absorption of L-lysine diatrizoate, a sodium-free salt of the contrast-giving diatrizoic acid from the gastrointestinal tract is increased by surgery, inflammation, and neoplasia. PATIENTS AND METHODS: The prospective study comprised 32 patients who were undergoing radiological examination of the upper gastrointestinal tract with a contrast medium containing L-lysine diatrizoate and 52 further patients who were undergoing examination of the lower gastrointestinal tract in the same way. The concentration of diatrizoic acid was determined by high-pressure liquid chromatography in blood samples taken before and immediately after the radiological examinations. The results were examined in terms of sex, age, surgical history, and any evidence of inflammatory or neoplastic diseases. RESULTS: The serum diatrizoic acid concentration in patients tested after oral administration was 3.62 microg/ml. In patients who had undergone operation the titer was lower than in those who had not been operated on. Serum diatrizoic acid concentration in patients tested after rectal administration was 0.30 microg/ml. In patients suffering from inflammatory conditions or neoplasms the titer was significantly higher than in the other patients. CONCLUSION: The L-lysine salt of diatrizoic acid is absorbed in larger amounts from the upper gastrointestinal tract than from the lower. Absorption is not increased after surgical operations on the viscera. However, inflammatory conditions and neoplasms involving the large bowel increase the uptake of the contrast medium from the intestine.
More than 70% of all carcinoids are localized in the gastrointestinal tract. Carcinoids of the upper, middle and lower intestines have to be distinguished ontogenetically. The classification according to Capella takes into account the size of the tumor (< 0.9 cm; 1-2 cm; > 2 cm), the grade of invasion of other structures, the grade of angioinvasion, the biologic behaviour, the grade of differentiation and the hormonal activity of the tumor. A carcinoid-syndrome is rarely found. Carcinoids of the small intestine occur multiple in 30-50% and in 20-30% a second malignant tumor is seen. In carcinoids of the colon this percentage is even higher (25-40%). The therapy of carcinoids depends on the size of the tumor and consecutively on the risk of metastasis. A local excision or non-oncologic radical operative procedure is justified in carcinoids smaller than 1 cm. In tumors 1-2 cm in size an individual decision has to be made. Larger tumors should be operated according to oncologic standards. Palliative resections, even of the liver, may be indicated to relieve the symptoms of a carcinoid-syndrome or, to prevent ileus or bleeding in the gastrointestinal tract. The prognosis of gastrointestinal carcinoids is heterogenous: The five-year-survival-rate of appendix-carcinoids is 85.9% over all stages. In rectal carcinoids this rate amounts to 72.2%, in carcinoids of the small intestines to 55.4% and in colon-carcinoids to 41.6%. Carcinoids of the stomach have a five-year-survival-rate of 64.3% in the absence of metastases. Within carcinoids of the stomach type III-tumors have the worst prognosis with a median survival time of 6.5 months.
A histidine auxotroph of Salmonella typhimurium, strain TA1538, will lodge for several months in the gastrointestinal tract of otherwise germ-free rats and of rats additionally associated with bacteria characteristic of the normal flora such as Lactobacillus plantarum and Bacteroides vulgatus. In the presence of the additional flora, the concentration of strain TA1538 is diminished in the stomach but not in the lower gastrointestinal tract or in the feces. Following the ingestion of 2-nitrofluorene, there is an increase in the concentration of revertants in the feces which reflects that observed in the colon and cecum. A dose-response relationship can be demonstrated between the amount of 2-nitrofluorene ingested and the concentration of revertants in the feces. A given dose of 2-nitrofluorene, however, produces fewer revertants in the feces of rats with the additional flora than in the feces of rats associated only with strain TA1538. It is not clear whether the decreased number of revertants in the feces in the presence of the additional flora is a result of metabolic transformations of 2-nitrofluorene by B. vulgatus, which can be demonstrated in vitro, or a result of the displacement of strain TA1538 from the stomach. The rat associated with strain TA1538, or other Ames tester strains, may be useful for detecting carcinogens as mutagens within the gastrointestinal tract and for determining the influence of various constituents of the bacterial flora on the concentration of mutagenic compounds.
Microbial catabolic capacity in digesta from the gastrointestinal tract of pigs fed either dry feed or fermented liquid feed (FLF) was determined with the PhenePlate multisubstrate system. The in vitro technique was modified to analyze the kinetics of substrate catabolism mediated by the standing stock of enzymes (potential rates of fermentation), allowing a quantitative evaluation of the dietary effect on the catabolic capacity of the microbiota. In total, the potential rates of fermentation were significantly reduced in digesta from the large intestine (cecum, P < 0.1; colon, P < 0.01; and rectum, P < 0.0001) of pigs fed FLF compared to pigs fed dry feed. No effect of diet was observed in the stomach (P = 0.71) or the distal part of the small intestine (P = 0.97). The highest rates of fermentation and the most significant effect of diet were observed for readily fermentable carbohydrates like maltose, sucrose, and lactose. Feeding FLF to pigs also led to a reduction in the large intestine of the total counts of anaerobic bacteria in general and lactic acid bacteria specifically, as well as of microbial activity, as determined by the concentration of ATP and short-chain fatty acids. The low-molecular-weight carbohydrates were fermented mainly to lactic acid in the FLF before being fed to the animals. This may have limited microbial nutrient availability in the digesta reaching the large intestine of pigs fed FLF and may have caused the observed reduction in activity and density of the cecal and colonic microbial population. On the other hand, feeding FLF to pigs reduced the viable counts of coliform bacteria (indicator of Escherichia coli and Salmonella spp.) most profoundly in the stomach and the distal part of the small intestine, probably due to the bactericidal effect of lactic acid and low pH. The results presented clearly demonstrate that feeding FLF to pigs had a great impact on the indigenous microbiota, as reflected in bacterial numbers, short-chain fatty acid concentration, and substrate utilization. However, completely different mechanisms may be involved in the proximal and the distal parts of the gastrointestinal tract. The present study illustrates the utility of the PhenePlate system for quantifying the catabolic capacity of the indigenous gastrointestinal tract microbiota.
Pneumoperitoneum often occurs after the perforation of the gastrointestinal tract. However, pneumoperitoneum without the perforation has been reported as one of the complications of collagen diseases, the cause of which is usually the rupture of pneumatosis cystoides intestinalis (PCI). PCI is sometimes observed in the patients with scleroderma and mixed connective tissue disease but rarely in the patients with systemic lupus erythematosus. We reported here a case of systemic lupus erythematosus developed the pneumoperitoneum without the perforation of gastrointestinal tract. A 51-year-old female who had been diagnosed as systemic lupus erythematosus and taken steroid for 12 years, visited our hospital because of general malaise. She had no abdominal symptoms but the roentgenographic examinations revealed the pneumoperitoneum. The laparotomy was performed and there were no findings of the perforation of the gastrointestinal tract. Because PCI is hardly recognized macroscopically after the rupture and the pneumoperitoneum due to PCI is often asymptomatic, we considered the cause of the pneumoperitoneum in this case was the rupture of PCI. The mechanisms of the formation of PCI in patients with collagen diseases were also discussed in this paper.
Because of improvement in survival rate of patients with abdominal cancer, gastrointestinal complications following external radiation therapy are becoming more frequent. Thus, an increased number of patients are commonly investigated with imaging because of suspected radiation-induced injury of the gastrointestinal tract. This pictorial review highlights the spectrum of CT and barium study manifestations of radiation-induced injury of the gastrointestinal tract. The major role of CT in the evaluation and management of patients with radiation injury of the gastrointestinal tract is highlighted. Emphasis is placed on CT imaging signs that may help in distinguishing between radiation-induced injury and recurrent disease.
The UDP glucuronosyltransferases (UGT) of the gastrointestinal (GI) tract have a crucial role in protection against the toxic effects of lipophilic chemicals in the environment. UGTs such as UGT1A7, UGT1A8, and UGT1A10 are exclusively expressed in gastrointestinal tissues, each with a unique tissue distribution pattern that is subject to interindividual variation. The factors regulating this tissue-specific expression and that contribute to variability are beginning to be elucidated. Studies on the UGT1A7, 1A8, 1A9, and 1A10 gene promoters in Caco-2 cells, an in vitro model of enterocytes of the gastrointestinal tract, have identified the caudal homeodomain transcription factor, Cdx2, as an important regulator of the UGT1A8 and 1A10 gene proximal promoters. This transcription factor is found exclusively in the small intestine and colon: it is absent in the gastric epithelium and the esophagus. Cdx2 regulates the UGT1A8 and 1A10 promoters in cooperation with hepatocyte nuclear factor 1alpha (HNF1alpha). It is noteworthy that UGT1A7 is not expressed in gastrointestinal tissue distal to the gastric mucosa and does not contain a Cdx2 binding site in its proximal promoter. Transcription factors, including Sp1, which differentially bind to the initiator regions of the UGT1A8, 1A9, and 1A10 promoters, also contribute to the differences in expression of these UGTs in Caco-2 cells. The identification of important regulatory regions of UGT genes expressed in the gastrointestinal tract, and the transcription factors that bind to these regions, will aid in the elucidation of factors that contribute to interindividual differences in gastrointestinal UGT expression. In turn, this will lead to further understanding of interindividual variation in the capacity of the GI tract to metabolize lipophilic chemicals and to act as a barrier to dietary toxins and orally administered drugs.
The multiple actions of somatostatin are mediated by specific membrane-bound receptors present in all somatostatin target tissues, such as brain, pituitary, pancreas, and gastrointestinal tract. Three different types of tissues in the human gastrointestinal tract express somatostatin receptors: (1) the gastrointestinal mucosa, (2) the peripheral nervous system, and (3) the gut-associated lymphoid tissue, where the receptors are preferentially located in germinal centers. In all these cases, somatostatin binding is of high affinity and specific for bioactive somatostatin analogs. Somatostatin receptors are also expressed in pathological states, particularly in neuroendocrine tumors of the gastrointestinal tract. Ninety percent of the carcinoids and a majority of islet-cell carcinomas, including their metastases, usually have a high density of somatostatin receptors. Only 10 percent of the colorectal carcinomas and none of the exocrine pancreatic carcinomas, however, contain somatostatin receptors. The somatostatin receptors in tumors are identified with in vitro binding methods or with in vivo imaging techniques; the latter allow the precise localization of the tumors and their metastases in the patients. Since somatostatin receptors in gastroenteropancreatic tumors are functional, their identification can be used to assess the therapeutic efficacy of octreotide to inhibit excessive hormone release in the patients.
BACKGROUND AND STUDY AIMS: Endoscopic laser therapy involves a risk of perforation, mainly because the depth of tissue destruction is not visible. Magnetic resonance (MR) imaging is capable of showing temperature changes, and is therefore suitable for monitoring thermal therapies such as laser. This animal study assessed the feasibility of real-time MR monitoring of endoscopic laser applications in the gastrointestinal tract. MATERIALS AND METHODS: The procedures were carried out using an MR-compatible endoscope in three live pigs in a 0.5-Tesla interventional MR system. Nd:YAG laser applications were performed in the lower gastrointestinal tract (n = 7) and upper gastrointestinal tract (n = 5), and were monitored using real-time color-coded T1-weighted gradient echo sequences. The postmortem macroscopic tissue coagulation sizes were compared with the lesion diameters seen on real-time MR. RESULTS: The endoscope did not cause any artifacts during continuous MR imaging. Ten of the twelve laser lesions were visible with temperature-sensitive MR imaging, and their sizes correlated well with the diameters of the postmortem macroscopic coagulation zones (r = 0.76, P = 0.009). Two laser lesions were not visible on MR due to technical limitations inherent with the healthy animal model. CONCLUSIONS: The formation of endoscopic laser lesions in the porcine gastrointestinal tract can be accurately visualized using real-time temperature-sensitive MR imaging. This new technique has the potential to spare healthy tissue while ensuring full treatment coverage of the targeted lesion with fewer therapy sessions.
Several pharmacological and electrophysiological studies have shown that the opioid receptors are widely distributed in the gastrointestinal tract. Despite such consensus, there are conflicting findings regarding their effects in intestinal function, and their precise site of action remained unclear. The aim of the present study was therefore to delineate the cellular localization of mu and kappa opioid receptors in rat gastrointestinal tract using polyclonal antibodies generated to C-terminal end of the cloned mu (63 amino acids) and kappa (41 amino acids) receptors. The distribution of mu differs from that of kappa receptors within the gastrointestinal wall, with a greater abundance of mu receptor-like immunoreactive fibres in all intestinal layers. Numerous neurons expressing mu receptor-like proteins were found in the submucosal plexus with comparatively few in the myenteric plexus. In contrast, a higher number of neurons expressing kappa receptor-like immunoreactivity were visualized in the myenteric plexus with a small number in the submucosal plexus. A high number of immunopositive neurons were found in the myenteric plexus of the stomach and the proximal colon with both antibodies. In the submucosal and mucosal layers. mu receptor-immunoreactive fibres were more abundant and distributed around the crypts, blood vessels and lymphatic nodes. Interestingly, numerous mu and fewer kappa receptor-immunoreactive interstitial cells are localized in the region of myenteric plexus and at the internal border of the circular muscle. Finally, smooth muscle cells did not demonstrate any mu- nor kappa-receptor immunoreactivity. These findings suggest that in the rat gastrointestinal tract, mu and kappa opioid receptors may directly influence neuronal and interstitial cell activity. This appears not to be the case for the smooth muscle cells. In the muscular layers, the anatomical data point to mu receptor actions being mediated by nerve terminals, whereas kappa receptor effects may be mediated by both nerve terminals and somatodendritic synaptic mechanisms. In contrast, in the submucosal and mucosal layers, mu receptors predominate and are localized on both nerve terminals and somatodendritic synaptic elements.
The factors controlling growth and maturation in the porcine gastrointestinal tract are not well understood. Epidermal growth factor (EGF) is a polypeptide that has been implicated in the control of gastrointestinal tract growth, maturation, and protection in other species. Immunoreactive EGF (IR-EGF) and EGF receptors (EGF-R) were histochemically identified in formalin-fixed tissues of the upper digestive tract of 1-, 3-, 7-, 14-, 21-, and 28-day-old pigs. The ductal epithelium consistently contained IR-EGF in the parotid salivary gland of pigs of all ages and in the mandibular salivary gland in pigs greater than or equal to 7 days old. Immunoreactive EGF was detected in the mucosal epithelium of the esophagus and nonglandular portion of the stomach, and in the pancreas and liver in all pigs. Gastric gland IR-EGF was inconsistently detected in pigs less than 14 days old and was consistently observed in all older pigs. Enterocyte EGF immunoreactivity was usually weak and was variably detected in the duodenum of pigs less than or equal to 7 days old and in the jejunum of pigs less than or equal to 14 days old, but was consistently observed in older pigs. Ileal immunoreactivity was erratic. Immunoreactive EGF-R were identified in the esophageal epithelium of all pigs, and in the nonglandular gastric and glandular gastric mucosa of all pigs, except for two 7-day-old pigs and one 7-day-old pig, respectively. Immunoreactive EGF-R were detected in the duodenal, jejunal, and ileal enterocytes of pigs of all ages examined.
Thyroidectomy appears to reduce the serotonin content in the rat brain, whereas hyperthyroidism has the opposite effect. As it is not known whether the serotonin-producing cells of the gastrointestinal tract are influenced by these conditions, the effects of thyroparathyroidectomy and induced hyperthyroidism were studied experimentally, particularly as regards the serotonin- and gastrin-immunoreactive cells of the gastrointestinal tract. Immunocytochemical and quantification techniques were used to localize and determine the numbers of serotonin and gastrin cells. In thyroparathyroidectomized rats the intestine was significantly shorter and the mucosa thinner than in sham-operated and untreated controls, whereas the converse was found in the hyperthyroid rats. Following thyroparathyroidectomy, there were fewer gastrin-immunoreactive cells in antrum and the serotonin-immunoreactive cells were significantly less dense throughout the gastrointestinal tract. In hyperthyroid rats, gastrin-immunoreactive cells were more numerous, as were the serotonin-immunoreactive cells in the small intestine, whereas these cells were fewer in antrum and caecum. In conclusion, the thyroid gland exerts a significant influence on the gastrointestinal tract and on the serotonin-and gastrin-immunoreactive cells. The observed alterations may reflect a direct effect of the thyroid hormones, although indirect factors must also be considered.
The regional distribution and relative frequency of endocrine cells in the gastrointestinal tract of the camel, Camelus bactrianus, were investigated using immunohistochemical methods. Ten types of immunoreactive (IR) endocrine cells were identified in this study. Among these cell types, only serotonin- and somatostatin-IR cells were detected in almost all regions of the gastrointestinal tract. Most of the cell types showed peak density in the pyloric gland region. The others showed restricted distribution: gastrin, cholecystokinin (CCK), motilin, bovine pancreatic polypeptide (BPP), and (gastric) substance P in the stomach; gastrin, CCK, BPP, gastric inhibitory polypeptide (GIP), glucagon, peptide tyrosine tyrosine (PYY) and substance P in the small intestine; and CCK, motilin, BPP, and PYY in the large intestine. Fundamentally the distribution pattern of endocrine cells in the gastrointestinal tract of the camel is similar to that of cattle. The distribution and frequency of endocrine cells in the glandular sac region are the same as those of the cardiac gland.
At present, there is little information on the phylogenetic diversity of microbial species that inhabit the gastrointestinal tracts of wildlife. To increase understanding in this area, we initiated a characterization of the bacterial diversity in the digestive tracts of three wild African ruminant species namely eland (Taurotragus oryx), Thompson's gazelle (Gazella rufifrons) and Grant's gazelle (Gazella granti), together with a domesticated ruminant species, zebu cattle (Bos indicus), and a non-ruminant species, zebra (Equus quagga). Bacterial diversity was analysed by PCR amplification, sequencing and phylogenetic analysis of 16S ribosomal DNA (rDNA) sequences. A total of 252 full-length 16S rDNA sequences averaging 1,500 base pairs (bp) in length, and an additional 27 partial sequences were obtained and subject to phylogenetic analysis. Using a 98% criterion for similarity, all except for one of the sequences were derived from distinct phylotypes. At least 24 distinct operational taxonomic units (OTU's) could be identified, with the majority of these sequences representing hitherto uncharacterized species and genera. The sequences were generally affiliated with four major bacterial phyla, the majority being members of the Firmicutes (low G+C Gram-positives) related to the genera Clostridium and Ruminococcus. By contrast, with earlier studies using 16S rDNA sequences to assess biodiversity in Bos taurus dairy cattle, Gram-negative bacteria in the Bacteroidales (Prevotella-Bacteroides group) were poorly represented. The lack of redundancy in the 16S rDNA dataset from the five African ungulate species, and the presence of novel sequences not previously described from the gastrointestinal tract of any animal species, highlights the level of diversity that exists in these ecosystems and raises the question as to the functional role of these species in the gastrointestinal tract.
Although the gastrointestinal tract represents the most common site of extranodal lymphoma, primary follicular lymphoma of the gastrointestinal tract is an uncommon and poorly defined disease. We report the clinical and pathologic features of 26 patients with primary gastrointestinal follicular lymphoma. Ten of 26 patients (38.5%) were stage IIE, and 16 patients (61.5%) were stage IE. Of the 26 patients, 13 were female and 13 were male. The age range was 26-81 years (median 54.5 years). Abdominal pain was the most common presenting symptom, seen in 12 of 24 patients (50%). Nodularity of the mucosal surface was the most common endoscopic finding, seen in 10 of 14 patients (71.4%). The majority of cases (22 of 26, 84.6%) involved small bowel, four involved colorectum alone, and two involved the ileocecal valve. Within the small bowel the duodenum was the most commonly involved site (10 cases). Transmural involvement by follicular lymphoma was identified in 11 of the 16 patients who underwent surgical resection; five showed involvement of mucosa and submucosa only. The most common histologic grade was grade 1. Thirteen of 26 cases were grade 1, ten grade 2, and three grade 3. Twenty-one of 26 cases showed a predominantly follicular growth pattern, four mixed follicular and diffuse, and one predominantly diffuse. All cases were positive for CD20 and BCL2 and negative for CD3, CD5, CD23, CD43, and cyclin D1. Twenty-four of 26 were positive for CD10. Four of four cases showed cytogenetic or molecular genetic evidence of t(14;18). Initial treatment modalities included surgery plus chemotherapy (nine cases), surgery alone (seven cases), chemotherapy alone (four cases), observation alone (four cases), and chemotherapy and abdominal radiation (one case). One case presented with rectal polyps and was treated with polypectomy. A complete response was observed in 15 of 22 cases that received treatment, and of the 15 cases, five recurred 27-60 months after the initial diagnosis. Recurrence and progression were associated with histologic transformation to diffuse large cell lymphoma in one case. No significant correlation was identified between treatment response and various clinical and pathologic features. Overall, none of the 26 patients died of lymphoma. One patient died of a concomitant pancreatic carcinoma. Of the remaining 25 patients, 14 were disease free and 11 were alive with disease at a mean follow-up of 43 months. The estimated 5-year disease-free survival was 62%, and median disease-free survival was 69 months. The estimated 5-year relapse-free survival was 54%, and the median relapse-free survival was 63 months.
Severe gastrointestinal necrosis and strictures after an iron overdose are well described. However, mucosal injury in patients receiving therapeutic iron has received only scant recognition despite its wide use. We studied the clinical and histologic features of 36 upper gastrointestinal tract biopsies from 33 patients (24 gastric, 9 esophageal, 1 gastroesophageal junction, and 2 duodenal) containing characteristic brown crystalline iron material, and evaluated the amount and tissue distribution of the iron. In addition, we investigated the prevalence of iron-associated mucosal injury in upper gastrointestinal endoscopic examinations. The majority of the biopsies (32 of 36, 89%) contained luminal crystalline iron adjacent to the surface epithelium or admixed with luminal fibrinoinflammatory exudate. Thirty biopsies (83%) showed crystalline iron deposition in the lamina propria, either covered by an intact epithelium, subjacent to small superficial erosions, or admixed with granulation tissue. Three biopsies (8%) demonstrated iron-containing thrombi in mucosal blood vessels. Erosive or ulcerative mucosal injury was present in 30 of 36 biopsies (83%). The amount of iron accumulation in cases with mucosal injury was greater than in cases without mucosal injury (mean grades, 2.4+ vs. 1.3+ on a 1+ to 3+ scale; p = 0.002). Iron medication was confirmed in 25 of 33 patients (76%) 22 patients were receiving ferrous sulfate. Approximately half of the patients (17 of 33, 51%) also had underlying infectious, mechanical, toxic, or systemic medical conditions that could have initiated or exacerbated tissue injury. Crystalline iron deposition was found in 0.9% of upper gastrointestinal endoscopic examinations (12 of 1,300), and iron medication-associated erosive mucosal injury was present in 0.7% (9 of 1,300). These results indicate that crystalline iron deposition in the upper gastrointestinal tract is not uncommon. It can induce or exacerbate a distinctive histologic pattern of erosive mucosal injury, especially in patients with associated upper gastrointestinal disorders. Recognition of this pattern by pathologists and its communication to clinicians may aid in optimizing therapy.