Diffuse Hyperplasia Research Articles

Diffuse dermal angiomatosis associated with calciphylaxis in a patient with end-stage renal disease

Diffuse dermal angiomatosis (DDA) represents a benign, acquired, reactive proliferation of vessels. DDA is clinically characterized by painful livedoid plaques with central ulceration, and the histopathologic hallmark is diffuse endothelial cell hyperplasia in the dermis. DDA has been rarely reported in association with calciphylaxis, a condition characterized by calcification of arterial walls with accompanying thrombosis and cutaneous necrosis. We present a case of a 72-year-old man with end-stage renal disease on peritoneal dialysis who presented with painful lesions on his legs, and was found to have DDA in the setting of calciphylaxis. The possible pathogenesis linking DDA and calciphylaxis is discussed.

Cytotoxicity and genome-wide microarray analysis of intestinal smooth muscle cells in response to hexavalent chromium induction.

Chronic ingestion of high concentrations of hexavalent chromium [Cr(VI)] in drinking water induces intestinal tumors in mice; however, information on its toxicity on intestinal smooth muscle cells is limited. The present study aimed to assess the in vitro and in vivo toxicological effects of Cr(VI) on intestinal smooth muscle cells. Human intestinal smooth muscle cells (HISM cells) were cultured with different concentrations of Cr(VI) to evaluate effects on cell proliferation ability, oxidative stress levels, and antioxidant system. Furthermore, tissue sections in Cr(VI) exposed rabbits were analyzed to evaluate toxicity on intestinal muscle cells in vivo. Gene chips were utilized to assess differential gene expression profiles at the genome-wide level in 1 μmol/L Cr(VI) treated cells. Intestinal tissue biopsy results showed that Cr(VI) increased the incidences of diffuse epithelial hyperplasia in intestinal jejunum but caused no obvious damage to the structure of the muscularis. Cell proliferation analysis revealed that high concentrations (≥64 μmol/L) but not low concentrations of Cr(VI) (≤16 μmol/L) significantly inhibited the growth of HISM cells. For oxidative stress levels, the expression of reactive oxygen species (ROS) and nitric oxide (NO) was elevated at high concentrations (≥64 μmol/L) but not at low concentrations of Cr(VI) (≤16 μmol/L). In addition, dose-dependent increases in the activity of oxidized glutathione (GSSH)/total-glutathione (T-GSH) were also observed. Gene chip screened 491 differentially expressed genes including genes associated with cell apoptosis, oxidations, and cytoskeletons. Some of these differentially expressed genes may be unique to smooth muscle cells in response to Cr(VI) induction.

Bronchiolitis: adopting a unifying definition and a comprehensive etiological classification

Bronchiolitis is an inflammatory and potentially fibrosing condition affecting mainly the intralobular conducting and transitional small airways. Secondary bronchiolitis participates in disease process of the airways and/or the surrounding lobular structures in the setting of several already defined clinical entities, mostly of known etiology, and occurs commonly. Primary or idiopathic bronchiolitis dominates and characterizes distinct clinical entities, all of unknown etiology, and occurs rarely. Secondary bronchiolitis regards infections, hypersensitivity disorders, the whole spectrum of smoking-related disorders, toxic fumes and gas inhalation, chronic aspiration, particle inhalation, drug-induced bronchiolar toxicities, sarcoidosis and neoplasms. Idiopathic or primary bronchiolitis defines clinicopathologic entities sufficiently different to be designated as separate disease entities and include cryptogenic constrictive bronchiolitis, diffuse panbronchiolitis, diffuse idiopathic pulmonary neuroendocrine cell hyperplasia, neuroendocrine hyperplasia in infants, bronchiolitis obliterans syndrome in lung and allogeneic hematopoietic cell transplantation, connective tissue disorders, inflammatory bowel disease and bronchiolitis obliterans organizing pneumonia. Most of the above are pathological descriptions used as clinical diagnosis. Acute bronchiolitis, though potentially life threatening, usually regresses. Any etiology chronic bronchiolitis contributes to morbidity and/or mortality if it persists and/or progresses to diffuse airway narrowing and distortion or complete obliteration. Bronchiolitis in specific settings leads to bronchiolectasis, resulting in bronchiectasis.

A Novel Germline KIT Mutation (p.L576P) in a Family Presenting With Juvenile Onset of Multiple Gastrointestinal Stromal Tumors, Skin Hyperpigmentations, and Esophageal Stenosis

Familial gastrointestinal stromal tumor (GIST) syndrome is a rare autosomal dominant genetic disorder. We report on a kindred in which 3 family members carry a germline mutation (c.1727T>C, p.L576P) in exon 11 of the KIT gene. This mutation was not reported so far in familial GISTs. Apart from multiple GISTs in 2 of the mutation carriers, all of them had multiple hyperpigmented skin macules and a history of achalasia-like stenosis of the esophagus in early childhood. In the index patient >100 tumors and a diffuse Cajal cell hyperplasia of the small bowel occurred. Sequencing of DNA extracted from tumor tissue of one of his GISTs revealed the KIT mutation in exon 11 (c.1727T>C). By array comparative genomic hybridization whole chromosomal gains 3, 5, 7, 9, 12, 15, and 18 were detected. In addition, we could identify a gain on chromosome 4, spanning the KIT gene. Together with the family described here, 24 unrelated cases with proven germline mutations in KIT have been reported. In these families the diagnosis was established from the age of 30 years onwards. Because in 1 patient reported here the GIST was a coincidental finding at the age of 15 years, the tumors might occur at a very young age and remain unnoticed until they-either due to increasing size, ulceration, or malignant progression-become symptomatic. Therefore, we propose to start screening patients with known KIT mutations from a younger age.

Mesonephric adenocarcinoma with a sarcomatous component, a notable subtype of cervical carcinosarcoma: a case report and review of the literature

Carcinosarcoma of the uterine cervix is less common than its counterpart in the uterine corpus. On the other hand, mesonephric adenocarcinoma is also a rare neoplasm in the uterine cervix, and it has been reported that mesonephric adenocarcinomas are often accompanied by sarcomatous components. We present a case of mesonephric adenocarcinoma with a sarcomatous component which arose in a 63-year-old postmenopausal woman. The hysterectomy specimen grossly showed an exophytic mass measuring 1.8 cm in the uterine cervix. Histologically, diffuse mesonephric hyperplasia and adenocarcinoma with malignant spindle cell proliferation was recognized, and therefore the tumor was diagnosed as “mesonephric adenocarcinoma with a sarcomatous component.” The review of the literature of cervical carcinosarcoma and cervical mesonephric adenocarcinoma revealed that 16% of cervical carcinosarcoma is of mesonephric duct origin, and that mesonephric adenocarcinoma seems to be more likely to have sarcomatous change. We think the presence of a sarcomatous component in the cervical biopsy specimen could be helpful in the diagnosis of mesonephric duct origin.Virtual slidesThe virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1243996503911062

A microthymoma and no germinal centre in myasthenia gravis

A 43-year-old woman with a 1-year history of generalized myasthenia gravis was referred for a video-assisted thorascopic surgery thymectomy. The preoperative chest computed tomography revealed mild diffuse thymic hyperplasia. Pathology of the resected thymus gland revealed a 6-mm World Health Organization (WHO) Type AB microthymoma without thymic germinal centres. The entity of microthymoma was reviewed with a focus on examining the pathological and therapeutic differences between thymic hyperplasia and microscopic thymoma.

Cinacalcet Upregulates Calcium-Sensing Receptors of Parathyroid Glands in Hemodialysis Patients

Background: Cinacalcet hydrochloride (cinacalcet), a calcimimetic, has been shown to upregulate calcium-sensing receptor (CaSR) expression in parathyroid glands of rats with chronic renal insufficiency. However, the effect of cinacalcet on the reduced CaSR expression in human parathyroid glands remains to be elucidated. Methods: Four normal parathyroid glands and 71 hyperplastic parathyroid glands from 18 hemodialysis patients with refractory secondary hyperparathyroidism (SHPT) treated with (n = 10; cinacalcet group) or without (n = 8; conventional group) cinacalcet were examined immunohistochemically with a specific antibody against CaSR. The expression level of CaSR was analyzed semiquantitatively. Results: Compared with normal glands, the immunohistochemical expression of CaSR was decreased significantly in both the cinacalcet and conventional groups. In the cinacalcet group, the expression of CaSR was increased significantly compared with that in the conventional group (1.83 ± 0.14 vs. 0.87 ± 0.15, p < 0.001), even though the proportion of patients using vitamin D sterols and the mean administered dose of calcitriol equivalents were not significantly different between the two groups. The expression of CaSR was significantly decreased in the larger glands (>500 mg) compared with that in the smaller glands (<500 mg) in both groups; furthermore, it was markedly decreased in areas of nodular hyperplasia compared with diffuse hyperplasia in the cinacalcet group. Conclusions: Our results indicate that cinacalcet upregulates the depressed expression of CaSR in hemodialysis patients with SHPT, and that insufficient expression of CaSR, especially in larger glands with advanced nodular hyperplasia, underlies the pathogenesis of SHPT in patients who are resistant to cinacalcet.

Histopathological Diagnosis of Primary Aldosteronism Using CYP11B2 Immunohistochemistry

Although primary aldosteronism (PA) is the most common cause of endocrine hypertension, histopathological methods to reveal the presence and sites of aldosterone overproduction remain to be established. The objective of the study was to investigate the significance of immunohistochemical staining to detect CYP11B2 and CYP11B1 in adrenal tissue of patients with PA. Thirty-two patients with PA who underwent unilateral adrenalectomy were studied. Immunohistochemical staining was performed using anti-CYP11B2 and anti-CYP11B1 antibodies on paraffin-embedded sections. We analyzed the expression of each enzyme semiquantitatively by scoring staining intensity and correlating it with clinical findings. Twenty-two patients showed positive CYP11B2 immunostaining in their tumors (aldosterone producing adenoma, APA). Four patients with CYP11B2-negative unilateral adenomas and 4 patients without tumors on computed tomography showed aldosterone-producing cell clusters (APCCs) with CYP11B2 immunostaining in the zona glomerulosa (multiple APCCs). The remaining 2 patients had unilateral multiple adrenocortical micronodules and diffuse adrenocortical hyperplasia, respectively. In APA, CYP11B2 score adjusted for tumor volume was positively correlated with plasma aldosterone and negatively correlated with serum potassium. The APA group was divided into 3 subgroups based on relative CYP11B2 and CYP11B1 immunostaining levels. The CYP11B2/CYP11B1-equivalent and CYP11B1-dominant APA groups showed significantly higher serum cortisol after 1 mg dexamethasone and larger tumor size than the CYP11B2-dominant APA group. The present study clearly demonstrates that CYP11B2 immunostaining is a powerful tool for histopathological diagnosis of aldosterone overproduction in PA and for subtype classification of APA, multiple APCCs, unilateral multiple adrenocortical micronodules, and diffuse hyperplasia.

Precursor lesions of endocrine system neoplasms

The concept of precursor lesions of endocrine neoplasms is a new and interesting topic in endocrine pathology. A variety of clinicopathological conditions are associated with a sequence of cellular changes from hyperplasia to neoplasia; dysplasia is, in contrast, quite rare. The majority of precursor lesions is associated with familial genetic syndromes. These include C-cell hyperplasia in thyroid that is associated with familial medullary thyroid carcinoma, adrenal medullary hyperplasia as a precursor of phaeochromocytomas in MEN2 syndrome, rare pituitary adenohypophyseal cell hyperplasia in familial syndromes associated with pituitary adenomas, MEN1-related precursor gastric enterochromaffin-like cell (ECL) hyperplasia, and duodenal gastrin producing (G) and/or somatostatin producing (D) cell hyperplasia that give rise to type II gastric neuroendocrine tumours (NETs) and duodenal NETs, respectively, and MEN1- or VHL-related islet hyperplasia, islet dysplasia and ductulo-insular complexes that are associated with pancreatic NETs. Other hyperplasias are not thought to be associated with genetic predisposition. Some are attributed to inflammation; autoimmune chronic atrophic gastritis-related ECL hyperplasia can progress to type I gastric NETs, and EC (enterochromaffin) cell or L cell hyperplasia associated with inflammatory bowel diseases can progress to colorectal NETs. In the lung, diffuse idiopathic pulmonary neuroendocrine cell hyperplasia can give rise to peripherally-located low grade pulmonary NETs and tumourlets (neuroendocrine microtumours <5 mm). Rarely, secondary hyperplasias develop into autonomous neoplasms, as in tertiary hyperparathyroidism or pituitary thyrotroph adenomas in primary hypothyroidism. While some precursor lesions, such as thyroid C cell hyperplasia, represent frankly premalignant conditions, others may represent a sequence of proliferative changes from hyperplasia to benign neoplasia that may also progress to malignancy.

Facts and fiction: premalignant lesions of lung tissues

Lung cancer is now the leading cause of death from cancer in Australia. Most patients are diagnosed with late-stage disease. Although diagnosis at pre-invasive stages could theoretically improve outcomes, mooted precursor lesions are often asymptomatic and often undetectable by non-invasive investigations. Nonetheless, they merit study to identify early and essential molecular steps involved in lung carcinoma pathogenesis, with the aim of developing therapies targeted against one or more such steps. Some lung cancers appear to develop via a series of progressive morphological changes with correlating molecular alterations, but others seem to arise in histologically normal epithelium, and these differences may reflect anatomically and functionally distinct epithelial compartments of the respiratory tract. Pre-invasive precursor lesions recognised by the World Health Organization (WHO) include squamous metaplasia with dysplasia and carcinoma in situ, atypical adenomatous hyperplasia, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia. Other lesions that likely represent pre-invasive lesions, but which are not currently WHO-listed, include human papillomavirus (HPV)-related respiratory papillomatosis and mesothelioma in situ. No single cancer stem cell marker has been identified. Field cancerisation plays an important role in lung cancer development, and includes the spread of pre-invasive clones along the respiratory epithelium or the occurrence of multiple separate foci of pre-invasive abnormalities such as squamous dysplasia and carcinoma in situ.In addition to well-characterised step-wise progression in squamous cell carcinomas and some adenocarcinomas, alternative pathways exist, and are currently being investigated. In addition, molecular techniques, including miRNA screening on blood samples or cytology samples--such as sputum samples--may become clinically relevant and more accurate in predicting lung cancer progression.

A misleading cause of pseudo-thymic tumor in ectopic Cushing’s syndrome

A 27-year-old man was referred with typical features of severe Cushing's syndrome. A bilateral adrenalectomy was performed. Three months later, a triangular nodular mediastinal enlargement, evocative of a right anterior thymic tumor, was discovered. Thymectomy was undertaken. Histological examination revealed diffuse thymic hyperplasia with negative immunostaining for adrenocorticotropic hormone. Five years later, a right endobronchial tumor corresponding to a carcinoid tumor was removed.

Toxic Multinodular Goiter

To the Editor: Toxic multinodular goiter (TMNG) is one of the hyperthyroidism disorders. It is as a result of diffuse hyperplasia of follicular cells whose functional capacity is independent of thyroid-stimulating hormone. The cardiopulmonary symptoms may predominate in the elderly. We report a case of TMNG with right pleural effusion and normal cardiac evaluation. She underwent thyroidectomy that led to resolution of the pleural effusion suggesting TMNG as the cause of the fluid. A 63-year-old woman with a past medical history of hypertension, hyperlipidemia, and TMNG presented with 1-week history of shortness of breath. She was receiving pravastatin 40 mg, ramipril 10 mg, methimazole 10 mg, and zoloft 50 mg/d. She had 5-pack-year smoking history, having quit 30 years ago. Coronary angiogram performed 7 years ago was unremarkable. Her physical examination revealed a large thyroid goiter and decreased breath sound over the right lung base. Her chest x-ray and computed tomography of the chest revealed large right pleural effusion with mediastinal shift to the left (Fig. 1). She underwent a right thoracocentesis. One liter of pleural fluid was removed. The results revealed exudative pleural effusion. White blood cell count was 137 cells/mm3 with 53% neutrophils, 29% macrophages, and 28% lymphocytes. Red blood cell count was 1057 cells/mm3. Lactic dehydrogenase level was 275 mg/dL, protein 4.5 gm/dL, glucose 94 mg/dL, and pH was 7.42. Cultures for bacteria, mycobacteria, and fungi were negative. Her thyroid-stimulating hormone was <0.006 µIU/mL. Free T3 level was 3.8 pg/mL (2.3 to 4.2 pg/mL) and free T4 level was 0.91 ng/mL (0.82 to 1.77 ng/mL). Ultrasound of the thyroid gland revealed a bilateral heterogenous multinodular goiter. Her echocardiogram was unremarkable. She subsequently underwent a right pleuroscopy with parietal pleura biopsy. Examination revealed chronic inflammation with adhesions around the right middle lobe. The pleural fluid was negative for malignancy and infections. Pleural pathology revealed chronic inflammation (Fig. 2). She continued to have recurrent and persistent right pleural effusion with unclear etiology. Fine needle aspiration of her thyroid gland revealed Hurthle cells favoring benign inflammation. She underwent an uneventful thyroidectomy. Pathology revealed chronic follicular thyroiditis. After thyroidectomy, a repeated chest radiograph revealed spontaneously resolved pleural effusion.FIGURE 1: Chest radiograph revealed large right pleural effusion with mediastinal shift to the left.FIGURE 2: Pleural pathology revealing chronic inflammation.We believe this patient represents a case of pleural effusion induced by hyperthyroidism from TMNG. Hyperthyroidism is a rare cause of pleural effusion. Mechanism of effusion in hyperthyroidism includes thyroid cardiomyopathy, which usually presents as a transudative effusion. Constrictive pericarditis from hyperthyroidism can also produce transudative effusion.1 Propylthiouracil, medication used for hyperthyroidism, is known to cause eosinophillic pleural effusion.2 On rare occasion, hyperthyroidism may present with chyrothorax and malnutrition.3 In 1 study, thyroid hormone and thyroid antibodies including thyroglobulin antibody and thyroperoxidase antibody were detected in pleural fluid from patients with Graves disease.4 This finding suggested that the immunologic effects may contribute to pathogenesis of pleural effusion. Our patient had a long-standing history of hyperthyroidism and was treated with methimazole. She had a normal echocardiogram and no signs of heart failure or malnutrition. She underwent thoracocentesis, which showed exudative pleural effusion. Microbiology and cytology were negative for infection and malignancy. Pleuroscopy revealed chronic inflammation but no malignancy or infection was identified on pleural biopsy. Her pleural effusion resolved after thyroidectomy. Patients with hyperthyroidism-induced pleural effusion usually present with dyspnea. Pleuritic chest pain is a common manifestation. Pleural fluid is exudative with lymphocytic predominance. The presence of erythrocytes is consistent with serositis. Serositis can present with hemorrhage or without hemorrhage like in our case. Treatment consists of controlling hyperthyroidism.5 Our patient responded well after her thyroidectomy. If present, hyperthyroidism should be included in the diagnosis of pleural effusion. The case emphasizes on early diagnosis and an appropriate treatment of hyperthyroidism to prevent pleural effusion. Thitiwat Sriprasart, MD* Sadia Benzaquen, MD† Mitchelle Kirshner, NP† *UCSF Fresno MEP, Internal Medicine Fresno, CA †University of Cincinnati, Pulmonary, Critical Care and Sleep Medicine, Cincinnati, OH

Parathyroid carcinoma in tertiary hyperparathyroidism

Parathyroid carcinoma is a rare disease of unknown etiology. This study presents a case of parathyroid carcinoma in a patient with tertiary hyperparathyroidism. Despite a successful kidney transplantation, the intact parathyroid hormone (iPTH) level of the patient was elevated consistently and could not be controlled by medical therapy. Due to the development of tertiary hyperparathyroidism with bone pain and osteoporosis, subtotal parathyroidectomy was performed 4 months after the kidney transplantation. Histological evaluation revealed that one of four parathyroid lesions was a parathyroid carcinoma, while the others were diffuse hyperplasia. Postoperative laboratory studies indicated a decreased level of iPTH. A positron emission tomography-computed tomography performed 6 months after the operation revealed no evidence of local recurrence or distant metastasis.

Immunomodulating Effect of Chitosan Extracted from &lt;em&gt;Aspergillus niger&lt;/em&gt;

This study was conducted to extract chitosan from Aspergillus niger mycelia using hot alkaline followed by acid treatment and after 12 days of fermentation in sabouro dextrose broth containing 8% glucose, 1.246 g/L of chitosan was obtained. Five male albino Swiss mice were injected intraperitoneally with constant dose of chitosan (1 mg/mL) twice during two weeks and then blood picture, microscopic examination and double diffusion test were carried out. Chitosan was reported to increase the number of cells which were 530, 250 and 1237%, for Lymphocyte, Granulocytes and monocyte respectively when compared with control group. Also mice organs were crossly examined and they showed hypertrophy of liver and spleen, while microscopic examination reveled that spleen diffuse hyperplasia and infiltrate of mononuclear cells and megakaryocte. Moreover no antibody was detected in the serum of treated animals against chitosan.

Calcium-sensing receptor and apoptosis in parathyroid hyperplasia of patients with secondary hyperparathyroidism

This retrospective study investigated the characteristics of secondary hyperparathyroidism (SHPT) by examining the presence of the calcium-sensing receptor (CaSR) and the rate of cell proliferation and apoptosis in parathyroid glands. Eighteen diffuse and 57 nodular hyperplastic parathyroid glands from 24 patients with SHPT were compared with 14 primary adenomas and 33 normal parathyroid glands using immunohistochemical staining of CaSR and a marker of proliferative activity (Ki67 antigen). Apoptosis was measured using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling assay. The mean ± SE labelling index (LI) of CaSR (12.8% ± 1.5%) in nodular hyperplasia was significantly lower than that in normal parathyroid glands (26.8% ± 0.8%), whereas the mean ± SE LI of CaSR in diffuse hyperplasia was similar to that in normal parathyroid glands (23.3% ± 1.8%). The mean ± SE LI of Ki67 antigen was significantly higher in primary adenoma and nodular hyperplasia than in normal parathyroid glands. These results indicate that downregulation of CaSR, and a higher rate of proliferation over apoptosis, could contribute to the pathological progression of SHPT.

Malatya’da yapılan tiroidektomilerde tiroid kanseri sıklığı

Objective: Thyroid cancers are the most common malignancy of the endocrine organs. It accounts for 1% of all cancer. Environmental, genetic and hormonal factors play an important role in its etiology. The aim of this study is to investigate the incidence of thyroid cancer and types at thyroidectomy materials in the city of Malatya. Methods: The pathology reports of thyroid surgical materials, which were sent to Inonu University Medical Faculty Pathology Department retrospectively from the archives between the years January 2007 and May 2013. Postoperative histopathologic examinations of 543 cases were evaluated for 6 years period. Results: 128 (23.5%) of 543 cases male and 415 (76.5%) were female. The youngest patient was 10, the oldest patient was 89 years-old, and the average age is 48.1p15.2. Histopathological examination of 346 (64%) cases of nodular hyperplasia, 20 (4%) cases of diffuse hyperplasia, 13 (2.4%) cases of lymphocytic thyroiditis, 164 (30.2%) patient had thyroid tumors. The 164 tumors on the 57 (35%) cases benign, 107 (65%) cases were malign. As a type of cancer 88 (53.6%) cases papillary carcinoma, 10 (6%) cases follicular carcinoma, 1 (0.6%) case medullary carcinoma, 3 (1.8%) cases were anaplastic carcinoma. Conclusion: Thyroid cancer incidence is 19.7% at thyroidectomy materials in the city of Malatya and most cancers is seen as a type of thyroid papillary carcinoma.

Mesonephric adenocarcinoma (endometrioid type) of endocervix with diffuse mesonephric hyperplasia involving cervical wall and myometrium: An unusual case report

Malignant mesonephric tumors are rare variants of cervical adenocarcinoma, derived from remnants of mesonephric ducts and are associated with mesonephric remnants and/or mesonephric hyperplasia. Few cases have been described in literature. We report an unusual case of cervical mesonephric adenocarcinoma of endometrioid type with squamous morules in association with diffuse mesonephric hyperplasia involving the cervical walls and extending into the myometrium.

Clinicopathological study of endometrium in IUCD users

Background and Aims: Use of intrauterine contraceptive device (IUCD) is now a common practice. The present study was taken up to study the clinicopathological changes in endometrium following use of IUCD. Methods: Endometrium obtained from 65 cases who had IUCD of varying duration, presenting with different symptoms were studied by Hematoxylin and Eosin stained slides. Results: Patients presented with various menstrual irregularities and pelvic inflammatory disease. Duration of IUCD use ranged from 4 months to 10 years. The spectrum of endometrial changes were interstitial edema 22(33.8%), hemorrhage 36(55.3%), focal hyperplasia 18(27.6%), diffuse hyperplasia 2(3%), cystoglandular hyperplasia 4(6.1%), predecidual changes 5(7.6%), inflammatory cell infiltrate 9(13.8%), lymphoid follicles 2(3%), vascular changes 2(3%), metaplasia 1(1.5%). Conclusion: The present study tries to focus on the spectrum of endometrial changes associated with IUCD use, their clinical symptomatology and possible pathogenetic mechanisms. The endometrial changes were possibly due to inflammation, hyperplasia and metaplasia induced by IUCD.

The Role of IL-17, Metaphase Reactants on Patients with Early Rheumatoid Arthritis disease Activity and Trace Elements

Rheumatoid arthritis (RA) represents the most common form of chronic inflammatory joint disease leading to cartilage and bone destruction, It affects approximately 1-2 % of world's population. The inflammatory process causes diffuse thickening and hyperplasia of the joint Interleukin (IL)-17 is a pleiotropic pro-inflammatory cytokine produced from Th17 cells. IL-17A is the prototypic member belonging to a family of 6 ranging from IL-17A to IL-17F. IL-17A mediates its biological effects through binding to a receptor complex consisting of IL-17RCA and IL-17RCC subunits. Objective. To assess the role of IL-17 on the disease process of Rheumatoid arthritis and the effects on the trace elements such as Zinc, copper , Magnesium. Subjects and method: A total of 60 patients with early Rheumatoid Arthritis were studied. Their ages ranged from 20-52 years with a mean age of ( 39.3 ± 9.01)years. , while the range was between (20-51) years and the mean was (37.5 ± 8.6) years for healthy control non significant difference P > 0.4 with no complaint of other chronic or systemic diseases were considered as control. the samples were collected during period from ( December 2012 - july 2013 ). the mean disease duration of RA was (3.27±1.2) month. Blood samples were collected from patients and controls to assess Erythrocyte Sedimentation Rate (ESR) and serum levels of White blood cells ( WBC), Hemoglobin (Hb), Interleukin-17A and were estimated by agglutination test, and IL-17A was estimated by (ELIZA).

Diffuse Intrapulmonary Neuroendocrine Cell Hyperplasia

Diffuse intrapulmonary neuroendocrine cell hyperplasia is a rare, potential precursor lesion to typical pulmonary carcinoid tumours. Fewer than 50 cases have been reported in the literature. Their pathogenesis, clinical significance and management is controversial. A patient who presented with diffuse intrapulmonary neuroendocrine cell hyperplasia associated with a primary typical carcinoid tumour of the lung is reported.