Neuroendocrine Cell Hyperplasia Research Articles

Epidemiology of childhood interstitial lung disease in France: the RespiRare cohort

IntroductionInterstitial lung disease in children (chILD) are rare and mostly severe lung diseases. Very few epidemiological data are available in limited series of patients. The aim of this study was...

Laparoscopic total gastrectomy for multiple type І gastric neuroendocrine tumours: a case report

Background. The gastric neuroendocrine tumours (G-NETs), arising from neuroendocrine cells within the stomach. Type I lesions are associated with chronic atrophic gastritis (CAG). Multiple G-NETs are rare. Purpose – of our report is to describe a rare case of multiple Type-I G-NETs. Material and methods. During routine gastroscopy in a 44-year-old female with history of CAG and anaemia, multiple (15–20) polyps of size 2–9 mm were found. Multiple biopsies were obtained. Histopathological examination with haematoxylin and eosin staining described these lesions as undifferentiated cancer. Repeated gastroscopy was done. The three biggest polyps (5–9 mm) were removed by snare polypectomy. Repeated histopathological examination was specific for G-NET. The neoplasm presented Ki-67 proliferation index of < 3%; Cytokeratin 18, Chromogranin A, Synaptophysin, INSM1 were positive in neoplasm cells. Laparoscopic total gastrectomy was done. The operative time was 255 min, and the blood loss was 50 ml. Histopathological examination of a surgical specimen revealed multiple, Grade 1 G-NET (fig. 1–3). All lesions are limited to the mucosa and submucosa of the stomach, the longest size of the largest tumour lesion is 5 mm, what corresponds to pT1(m). No signs of lymphovascular or perineural invasion were found (L0 V0 Pn0). 18 regional lymph nodes were examined, no metastases were detected (0/18, pN0). Edges of resections of the esophagus and duodenum without signs of tumour growth (R0). Outside of tumours, there were signs of chronic inflammation of the stomach mucosa, with intestinal metaplasia and mixed glandular atrophy, there are also foci of nodular hyperplasia of neuroendocrine cells. Conclusion. We reported a rare case of multiple type-I G-NETs (pT1N0M0) with pernicious anaemia due to autoimmune CAG. Laparoscopic total gastrectomy is a method of choice in treatment of such patients.

Interstitial lung disease in the newborn.

Although relatively rare, interstitial lung diseases may present with respiratory distress in the newborn period. Most commonly these include developmental and growth disorders, disorders of surfactant synthesis and homeostasis, pulmonary interstitial glycogenosis, and neuroendocrine cell hyperplasia of infancy. Although the diagnosis of these disorders is sometimes made based on clinical presentation and imaging, due to the significant overlap between disorders and phenotypic variability, lung biopsy or, increasingly genetic testing is needed for diagnosis. These diseases may result in significant morbidity and mortality. Effective medical treatment options are in some cases limited and/or invasive. The genetic basis for some of these disorders has been identified, and with increased utilization of exome and whole genome sequencing even before lung biopsy, further insights into their genetic etiologies should become available.

Pulmonary neuroendocrine tumors : Current review

Neuroendocrine neoplasms of the lung are aheterogenous tumor group. The pathological classification comprises diffuse idiopathic pulmonary neuroendocrine cell hyperplasia, classic neuroendocrine tumors, and neuroendocrine carcinoma. Classic neuroendocrine tumors include typical and atypical carcinoid tumors. Imaging plays an important role in diagnosis and can help in identifying the tumor biology. Overall, this tumor group is rare, comprising less than 2% of all thoracic tumors. In the current review, the various tumors are presented and important aspects regarding pathological classification, imaging modalities, and treatment are described.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia in adults

Diffuse Idiopathic Pulmonary NeuroEndocrine Cell Hyperplasia (DIPNECH) is an understudied rare disease that should be taken into account in the differential diagnosis of therapy-resistant bronchial obstruction combined with focal pulmonary lesions and mosaic attenuation on chest CT. The aim of this article is to discuss the aspects of clinical and morphological diagnosis, therapeutic options, prognosis assessment, and the need for follow-up using a clinical case as an example. The article describes a clinical case of DIPNECH in a 55-year-old woman, and also provides a brief review of the scientific literature on DIPNECH. DIPNECH is a rare disease that most often affects non-smoking women aged around 60 years. The most frequent clinical manifestations are cough, dyspnea, stridor, and broncho-obstructive syndrome. Only histological and immunohistochemical assays can confirm the diagnosis. DIPNECH should be considered as part of the differential diagnosis in patients with prolonged cough, dyspnea of unclear genesis and changes on chest CT in the form of pulmonary focal lesions and mosaic attenuation. Conclusion. The presented clinical case shows the challenges and importance of timely diagnosis.

A multi-lesional analysis of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia: a single-centre analysis

To conduct a multi-lesional computed tomography (CT) analysis of diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) patients to determine volumetric changes in lesions over 5 years. A retrospective case-note review was undertaken to identify 16 patients with histological and radiological features of DIPNECH between 2012-2021. Area and volume were calculated for 17 sets of lesions identified on high-resolution CT. Clinical data were extracted from electronic patient records, which included demographic data, outpatient clinic letters, histology reports, and imaging reports. One hundred and twenty-eight lesions were identified in 16 patients (one male, 15 female) and followed-up annually over a median 1,985 days (range 1,450-2,290). At year 1 follow-up, lesion area ranged from 1-48 mm2, and lesion volume ranged from 8-18,380 mm3; lesion area ranged from 1-45mm2 and lesion volume ranged from 11-17,800 mm3 and year 5. Half (8/16) of the patients had concomitant typical carcinoid tumours and one patient had an atypical carcinoid tumour. No statistically significant correlation (p<0.05) was found between lesion cross-sectional area or volume and duration of follow-up (years and days). No metastatic spread was observed at the time of analysis. No significant increase was observed in the size of over 100 lesions in patients with DIPNECH over a 5-year period and no metastasis occurred during the study period affirming the relatively indolent course of the disease.

Investigation of Clinical, Laboratory, Imaging Findings and Histopathological Features of Patients wıth Gastric Neuroendocrine Cell Hyperplasia.

Neuroendocrine cell hyperplasia is a non-neoplastic proliferation of enterochromaffin-like cells and is considered a premalignant lesion because of their potential to progress to neuroendocrine tumor. In this study, we aimed to evaluate the demographic and clinical features, laboratory, radiological and endoscopic findings, gastric biopsy histopathological features, follow-up frequency, and histopathological findings of patients diagnosed with gastric neuroendocrine cell hyperplasia as well as to investigate the factors that play a role in the development of neuroendocrine tumors on the basis of neuroendocrine cell hyperplasia. The study has been conducted in 2 centers with 282 patients that were grouped as those with and without neuroendocrine tumor. Individuals with control endoscopy were separated as those with regression of neuroendocrine cell hyperplasia and those without regression, and the determined parameters were evaluated between the groups. The most common histological subtype of neuroendocrine cell hyperplasia was linear+micronodular (50.4%). Neuroendocrine tumor developed in 4.3% (12/282) of the patients with neuroendocrine cell hyperplasia after a mean of 36 months. The presence of polyps as confirmed via endoscopy and dysplasia as confirmed via histopathological examination was significantly higher in favor of the group with neuroendocrine tumor (P = .01). In patients with neuroendocrine cell hyperplasia regressed and patients in whom it did not regress were examined, the rate of asymptomatic patients and increased sedimentation rate were found in favor of the group that did not regress (P = .02 and P = .02), but no difference was found in other parameters. Neuroendocrine tumor development rate was found to be 4.3% in the background of neuroendocrine cell hyperplasia. Two factors predicting progression from neuroendocrine cell hyperplasia to neuroendocrine tumor can be elaborated as the presence of polypoid appearance due to neuroendocrine cell hyperplasia as confirmed via endoscopy and dysplasia as confirmed via histopathological examination.

Classification of gastric neuroendocrine tumors and associations with survival.

597 Background: The World Health Organization (WHO) classification of gastric body neuroendocrine tumors (GNETs) includes type 1 tumors characterized by hypergastrinemia and arising in a background of atrophic gastritis, type 2 tumors associated with gastrinomas, and type 3 tumors with low serum gastrin level and no background mucosal pathology. However, certain tumors remain unclassified, and the prognostic significance of these tumors is currently unknown. The purpose of this study was to better characterize GNET types and to determine associations with distant metastasis and disease-specific survival (DSS). Methods: Patients diagnosed with GNET (1986-2021) were retrospectively identified and tumors classified as type 1, 2, or 3. Unclassified tumors were reviewed for background gastric mucosal changes associated with chronic proton pump inhibitor (PPI) use. Tumors were categorized as PPI-associated if there were prominent parietal and neuroendocrine cell hyperplasia in the background mucosa, in the absence of a gastrinoma and a positive history of chronic PPI use. WHO grade was determined using mitotic index or Ki-67 proliferative index when available. Characteristics by tumor type, associations with distant metastasis at initial diagnosis, and DSS were determined using standard statistical methods. Results: Of 246 patients, 164 (66.7%) had type 1, 5 (2.0%) had type 2, 52 (21.1%) had type 3, 18 (7.3%) were PPI-associated, and 7 (2.8%) remained unclassified. Multifocal disease was more common for types 1 (56.1%) and 2 (40.0%) than type 3 (13.5%) and PPI-associated tumors (27.8%, P&lt;0.001). Patients with type 3 GNET were also less likely to have WHO grade 1 tumors (26.9%) compared to other GNETs (type 1 37.2%, type 2 40.0%, PPI-associated 50.0%, P&lt;0.001). Additionally, distant metastases at presentation occurred more frequently with type 3 (38.5%) than type 1 (1.2%), type 2 (20.0%), and PPI-associated tumors (11.1%, P&lt;0.001). GNET type (type 1 vs 3, odds ratio [OR] 0.005 [95% confidence interval [CI] 0.001-0.050; PPI-associated vs type 3, OR 0.040 [95% CI 0.004-0.45]), race (non-white vs white, OR 0.17 [95% CI 0.040-0.73]), and WHO grade (2/3 vs 1, OR 10.5 [95% CI 1.93-57.2]) were associated with distant metastasis at presentation. Five-year DSS rates were 100.0% for type 1, 59.7% (95% CI 42.7-73.2%) for type 3, and 90.9% (95% CI 50.8-98.7%) for PPI-associated (log-rank P&lt;0.001). By multivariable analysis, multifocality of primary tumors (hazard ratio [HR] 0.070 [95% CI 0.010-0.46]) and distant metastasis at diagnosis (HR 44.9, 95% CI 6.21-324.8) were independently associated with DSS, while tumor type was not (type 1 vs 3, HR 0.18 [95% CI 0.010-2.44); PPI-associated vs type 3, HR 0.13 [95% CI 0.010-1.33]). Conclusions: PPI-associated tumors may represent a distinct GNET type with intermediate outcomes compared to type 1 and type 3 tumors. However, factors other than tumor type must be considered in determining survival.

Congenital Pulmonary Airway Malformation Type 1 with Pulmonary Neuroendocrine Cell Hyperplasia in an Adult Male: a Rare Case Report

Abstract Introduction/Objective Congenital pulmonary airway malformations (CPAM) is rare, usually diagnosed in the pediatric population, and may occur in adults. Pulmonary neuroendocrine cell hyperplasia (PNECH) mimicking diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) associated with CPAM has not been described previously. We report a case of CPAM Type 1 with PNECH. Methods/Case Report A 33-year-old male, with past medical history of latent tuberculosis (TB) by Quantiferon blood testing, recurrent pneumonia, recurrent lung abscesses, and lung cavitary lesion for three years, presented with fever, cough with hemoptysis, shortness of breath, and left-sided chest pain. Computerized tomography of chest displayed a 10.8 cm cavitary lesion in the left lower lobe of the lung. The patient underwent left lower lobectomy of the lung. Grossly, the lobectomy specimen revealed a 10.5 cm irregular cavity communicating to the superior segmental bronchus of the left lower lobe. Microscopically, the dominant large cyst was surrounded by lung parenchyma and small cystically dilated spaces resembling bronchioles under the fibrotic pleura. The large cyst was lined by respiratory epithelium with rare pathognomonic mucous cells in clusters. Cyst walls contained smooth muscle, small islands of cartilage, and focal intense acute and chronic inflammatory cell infiltrates with hemorrhage. There were multiple foci of proliferation of pulmonary neuroendocrine cells centered around bronchioles surrounding the large cyst. The neuroendocrine cells were arranged from individual cells and cellular aggregates to larger tumorlets, highlighted by Synaptophysin and Chromogranin immunostains. No granuloma or necrosis was present. No acid-fast bacilli or fungal microorganisms were identified by special stains. The findings are consistent with CPAM type 1, with PNECH. Results (if a Case Study enter NA) NA Conclusion Our study demonstrates a histologically diagnosed adult congenital pulmonary airway malformations type 1 with an incidental pulmonary neuroendocrine cell hyperplasia, which mimics diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. To the best of our knowledge, this is the first report of such an association.

Radiological–pathological correlation in diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH): imaging and histopathology

To review histologically confirmed diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) cases and carry out a detailed pathological-radiological correlation to see if computed tomography (CT) can be used to confidently identify DIPNECH. Twenty-three histologically confirmed DIPNECH patients in the shared database of two NHS Trusts were reviewed. CT images were reviewed by two independent radiologists, each of them with >10 years of experience in thoracic imaging. All histological specimens were reviewed by a single pathologist with >25 years of experience. The diagnosis of DIPNECH was made according to the current World Health Organization (WHO) definition included in the WHO 2015 classification of pulmonary tumours. The results on histology were compared to the presence of nodules and air trapping on CT. Demographic information and, when available, molecular imaging studies and pulmonary function tests were also considered. There are prototypal clinical and radiological findings reflecting the presence of underlying histological DIPNECH: middle-aged women with multiple small and scattered nodules due to the clustering and proliferation of neuroendocrine cells. At least one larger, dominant, lung nodule reflecting a carcinoid tumour is very common and mosaic attenuation/air trapping is seen approximately in 50% of cases in inspiratory scans. Airflow obstruction is rarely associated with histological bronchial or peribronchial fibrosis, which suggests other mechanisms must be involved in its development. CT can be used to predict pathological DIPNECH in the appropriate clinical setting. It is important to consider DIPNECH to avoid overdiagnosis of more sinister conditions such as lung cancer or metastases.

Precursor lesions of lung tumors

Lung cancer is the leading cause of cancer deaths globally with many new cases diagnosed each year. Recent studies have shown that an accumulation of various genetic abnormalities results in progressive morphologic changes in bronchial epithelium. Such changes are part of the continuum from precursor lesions to invasive lung cancers. Improvement in diagnostic modalities has made the detection of such preneoplastic lesions possible and resection at this stage confer excellent prognosis. The World Health Organization (WHO) has recognized atypical adenomatous hyperplasia/ adenocarcinoma in situ, squamous dysplasia/ squamous cell carcinoma in situ, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia as the precursor lesions of adenocarcinoma, squamous cell carcinoma, and carcinoid tumors respectively. This review summarizes the key features of these preneoplastic lesions based on the current understanding and knowledge.

Clinical and Morphological Features of Dysplasia and Early Gastric Cancer in the Patients with Autoimmune Gastritis

Аim: to analyze a series of cases of dysplasia and early gastric cancer developed in patients with autoimmune gastritis (AIG), and to identify their clinical and morphological features.Materials and methods. The study included six cases of detection of early gastric cancer on the background of AIG. Four out of six patients underwent endoscopic treatment, and in three out of six cases patients underwent endoscopic mucosectomy with dissection in the submucosal layer. One patient underwent endoscopic surgery in 2017, he continues annual dynamic follow-up without signs of tumour recurrence. A female patient with type 1 neuroendocrine tumour and mild dysplasia is awaiting treatment.Results. In five out of six patients with AIG, the localization of lesions prevailed in the stomach body, while all detected tumours were early ones, and according to the immunophenotype — of a gastric type. The presented cases of tumours were not accompanied by hyperplasia of neuroendocrine cells directly in the area of the tumour itself, but only in the surrounding gastric mucosa. Additionally, several cases of early gastrointestinal stromal tumours were found, which were characterized by low proliferative activity and had small sizes.Conclusion. The predominance of pseudopyloric metaplasia in the surrounding mucosa allows us to consider pseudopyloric metaplasia as a potentially significant change in the gastric mucosa of patients with AIG that may precede the development of gastric cancer.

The USnational registry for childhood interstitial and diffuse lung disease: Report of study design and initial enrollment cohort.

Childhood interstitial and diffuse lung disease (chILD) encompasses a broad spectrum of rare disorders. The Children's Interstitial and Diffuse Lung Disease Research Network (chILDRN) established a prospective registry to advance knowledge regarding etiology, phenotype, natural history, and management of these disorders. This longitudinal, observational, multicenter registry utilizes single-IRB reliance agreements, with participation from 25 chILDRN centers across the U.S. Clinical data are collected and managed using the Research Electronic Data Capture (REDCap) electronic data platform. We report the study design and selected elements of the initial Registry enrollment cohort, which includes 683 subjects with a broad range of chILD diagnoses. The most common diagnosis reported was neuroendocrine cell hyperplasia of infancy, with 155 (23%) subjects. Components of underlying disease biology were identified by enrolling sites, with cohorts of interstitial fibrosis, immune dysregulation, and airway disease being most commonly reported. Prominent morbidities affecting enrolled children included home supplemental oxygen use (63%) and failure to thrive (46%). This Registry is the largest longitudinal chILD cohort in the United States to date, providing a powerful framework for collaborating centers committed to improving the understanding and treatment of these rare disorders.

Children’s interstitial lung disease: Multidetector computed tomography patterns and correlations between imaging and histopathology

PurposeChildhood interstitial lung disease (chILD) is an umbrella concept covering a wide range of rare lung diseases, many of which are unique to childhood. The diagnosis is based on clinical presentation, multidetector computed tomography (MDCT), genetic testing, lung-function testing, and lung biopsy. Because knowledge of the usefulness of MDCT pattern recognition in ChILD is at present limited, we examined the occurrence of MDCT patterns in children with histologically confirmed interstitial lung disease. MethodWe searched the biopsy, MDCT, and clinical information database of a single national paediatric referral hospital for 2004–2020. Data were from affected children under age 18. MDCT images we reanalysed while blinded to the identity and referral information. ResultsWe included 90 patients, of whom 63 (70 %) were male. The median age at biopsy was 1.3 years (interquartile range 0.1–16.8). Biopsy findings fell into 26 histological classes covering all nine chILD classification categories. We recognized six distinct MDCT patterns: neuroendocrine cell hyperplasia of infancy (23), organizing pneumonia (5), non-specific interstitial pneumonia (4), bronchiolitis obliterans (3), pulmonary alveolar proteinosis (2), and bronchopulmonary dysplasia (n = 2). Of the total 90, in 51 (57 %) children, none of these six MDCT patterns appeared. Of those 39 children with a recognizable MDCT pattern, in 34 (87 %), that pattern predicted their final diagnosis. ConclusionsAmong cases of chILD, we identified a specific predefined MDCT pattern in only 43 %. However, when such a recognizable pattern occurred, it was predictive of the final chILD diagnosis.

(857) Bilateral Lung Transplant with Recognition of Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) of rhe Donor Lungs in the Immediate Postoperative Period

(857) Bilateral Lung Transplant with Recognition of Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia (DIPNECH) of rhe Donor Lungs in the Immediate Postoperative Period

Distinct roles for SOX2 and SOX21 in differentiation, distribution and maturation of pulmonary neuroendocrine cells

Pulmonary neuroendocrine (NE) cells represent a small population in the airway epithelium, but despite this, hyperplasia of NE cells is associated with several lung diseases, such as congenital diaphragmatic hernia and bronchopulmonary dysplasia. The molecular mechanisms causing the development of NE cell hyperplasia remains poorly understood. Previously, we showed that the SOX21 modulates the SOX2-initiated differentiation of epithelial cells in the airways. Here, we show that precursor NE cells start to develop in the SOX2 + SOX21 + airway region and that SOX21 suppresses the differentiation of airway progenitors to precursor NE cells. During development, clusters of NE cells start to form and NE cells mature by expressing neuropeptide proteins, such as CGRP. Deficiency in SOX2 resulted in decreased clustering, while deficiency in SOX21 increased both the numbers of NE ASCL1 + precursor cells early in development, and the number of mature cell clusters at E18.5. In addition, at the end of gestation (E18.5), a number of NE cells in Sox2 heterozygous mice, did not yet express CGRP suggesting a delay in maturation. In conclusion, SOX2 and SOX21 function in the initiation, migration and maturation of NE cells.

РЕЗУЛЬТАТЫ КАТАМНЕСТИЧЕСКОГО НАБЛЮДЕНИЯ И ОСОБЕННОСТИ ТЕЧЕНИЯ COVID-19 У ПАЦИЕНТОВ С НЕЙРОЭНДОКРИННОЙ КЛЕТОЧНОЙ ГИПЕРПЛАЗИЕЙ МЛАДЕНЦЕВ

Neuroendocrine cell hyperplasia of infancy (NEHI) is a rare interstitial lung disease in children. The clinical features of the disease are characterized by tachypnea, moist rales/crepitus, retraction of compliant chest areas and delayed weight gain. The disease is diagnosed using the NEHI clinical scale coupled with the computed tomography of the chest organs. The clinical manifestations of NEHI regress as the child grows, but may persist up to the age of 10 y/o. The purpose of the research was to characterize the course of NEHI including the features of COVID-19 and the impact of passive smoking in children below the age of 8 y/o. Materials and methods: a single-center longitudinal study with follow-up observation of 29 patients with NEHI in January 2012 - December 2022 aged 8 months to 8 years old, 21 of which had COVID-19. Results: 20 of 29 patients with a known follow-up have undergone the long-term oxygen therapy (LTOT) at home lasting from 2 weeks up to 5.5 years (Me 1 year and 2 months; IQR 6 months - 4.5 years). Bronchial asthma was diagnosed in 2. 8 (28%) were diagnosed with atopic dermatitis, 6 (21%) with mental retardation, 3 (10%) with acute urticaria, and 2 (7%) with allergic rhinitis. Gastroesophageal reflux disease (GERD) was diagnosed in 7, all requiring LTOT. The frequency of episodes of respiratory infection was maximum in the first 2 years of life, amounting to 16 episodes per 2 years (Me 7; IQR 4 to 10), and the maximum frequency of hospitalizations during this age period was 5 (Me 2; IQR 1 to 2). Children-passive smokers were diagnosed with malnutrition more often (75%, p=0.449) and required LTOT more often (75%, p=0.694), were more often hospitalized (42%, p=0.422). Despite the possible need for LTOT patients with NEHI had COVID-19 in the form of nasopharyngitis in the majority of cases (89%). Only 8 out of 14 patients had symptoms of NEHI after 5 years of age, and only 1 out of 5 after 7 years. Malnutrition (body mass index for the age&lt;-2) in the first year of life was diagnosed in 13 (45%) children. Malnutrition persisted in 9 out of 24 (37%) by the second year of life, in 5 out of 19 (26%) by the third year, and in 2 out of 14 (14%) by the fourth year of life. Not a single child died. Conclusion: the course of NEHI is characterized by the absence of lethal outcomes, frequent respiratory infections that led to hospitalizations in the first 2 years of life, mild course of COVID-19, regression of clinical symptoms and malnutrition as the child grows, comorbidity with atopic diseases and GERD. The priority should be given to the prevention of passive smoking in children with NEHI.

A 10-month-old infant with respiratory distress and hypoxemia

A 10-month-old infant with Prader-Willi Syndrome presented with a 7 month history of increased work of breathing, wheeze, inspiratory crepitations, and mild hypoxemia. Subsequent investigations including chest CT suggested the diagnosis to be neuroendocrine cell hyperplasia of infancy (NEHI). NEHI is a rare cause of children’s interstitial lung disease. Childhood interstitial lung disease should be considered in an infant with persistent tachypnea, crepitations, and hypoxemia.

Comparative morphological characteristics of helicobacter pylori and autoimmune gastritis

Objective: to conduct a comparative morphological analysis of helicobacter pylori (H. pylori) and autoimmune gastritis and to determine the significant morphological criteria for differential diagnosis.Materials and methods. 30 cases of chronic atrophic helicobacter gastritis and 30 cases of chronic atrophic autoimmune gastritis were retrospectively selected for the study. In all cases of helicobacter gastritis, the presence of H. pylori was confirmed by morphological diagnostic methods using Giemsa staining or additionally using immunohistochemistry. All cases of autoimmune gastritis were additionally confirmed by clinical and laboratory diagnostic methods, some patients had a long history of follow-up and biopsy material was taken from them repeatedly. A prerequisite was taking at least 5 biopsies according to the Sydney Protocol.Results. The main differential diagnostic feature in our study was the detection of H. pylori, as well as the localization of the lesion in the stomach body characteristic of autoimmune gastritis and in the antrum in helicobacter gastritis. The study groups differed by gender (the predominance of females in the group of autoimmune gastritis), the prevalence and activity of inflammation (all cases of helicobacter gastritis had signs of inflammation activity). When studying the content of neuroendocrine cells in cases of helicobacter gastritis in the stomach body, simple hyperplasia of neuroendocrine cells was noted, in cases of autoimmune gastritis, the appearance of chains and nodules was noted, which corresponded to linear and nodular hyperplasia of neuroendocrine cells.Conclusion. The morphological criteria obtained in the study make it possible to make a differential diagnosis between helicobacter and autoimmune gastritis. This is extremely important because of the differences in treatment approaches and dynamic monitoring tactics in these variants of chronic gastritis.

Pulmonary Function Tests as a Biomarker in Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia Patients Treated With Somatostatin Analogues.

Diffuse idiopathic pulmonary neuroendocrine cell hyperplasia (DIPNECH) describes an indolent, under-recognised and poorly understood pulmonary condition with fewer than 200 reported cases across the literature. Currently, cases are diagnosed following a biopsy of the primary lesion, with treatment options centring on symptomatic benefit as opposed to targeting the underlying aetiology. Classically, DIPNECH lesions have been described as slow growing and benign, but with growing awareness of the condition, reports of metastatic disease with significant symptomatic burden have been reported. However, effectively addressing the subset of DIPNECH patients with greater metastatic potential remains an unmet clinical need. Due to the similarities between DIPNECH and carcinoid patients, several centres have considered using somatostatin analogues to not only help symptomatically but also to initiate tumour regression. However, to date, there are limited biomarkers to help evaluate the benefit of such options. In this review, we consider the use of pulmonary function tests (PFTs) to help quantify the benefit of somatostatin analogues. Although much of the evidence stems from small single-centre studies, the use of PFTs within the treatment pathway for both localised and metastatic DIPNECH represents a meaningful improvement from subjective monitoring of disease.