DOCSLIB.ORG

Role of Epithelial Hyperplasia in Regression Following Photorefractive Keratectomy Br J Ophthalmol: First Published As 10.1136/Bjo.80.6.545 on 1 June 1996

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Role of Epithelial Hyperplasia in Regression Following Photorefractive Keratectomy Br J Ophthalmol: First Published As 10.1136/Bjo.80.6.545 on 1 June 1996 British Journal of Ophthalmology 1996;80:545-548 545 Role of epithelial hyperplasia in regression following photorefractive keratectomy Br J Ophthalmol: first published as 10.1136/bjo.80.6.545 on 1 June 1996. Downloaded from Charline A Gauthier, Brien A Holden, Daniel Epstein, Bj6rn Tengroth, Per Fagerholm, Helene Hamberg-Nystr6m Abstract Materials and methods Aim-To determine the relation between SUBJECTS epithelial hyperplasia and regression of We examined subjects who had previously had effect after photorefractive keratectomy PRK performed on one eye for correction of (PRK). myopia (Table 1). Out of approximately 800 Methods-Seventy unilaterally treated pa- patients treated at our clinic with the Excimed tients with PRK were examined. All eyes UV200LA excimer laser (Summit Technology, had been treated with the Summit exci- Waltham, MA, USA), 216 were unilateral at mer laser 27 (SD 7) months previously the time the study was conducted. Study with zone diameters of 4.1 to 5.0 mm. The subjects were asked to participate by letter or in untreated fellow eyes served as controls. person in advance or when they presented to Epithelial thickness was measured cen- the clinic for their regularly scheduled follow trally with a thin slit optical pachometer up, and 70 were able to participate. The and manifest subjective refraction was reasons why the participating subjects re- performed. mained unilaterally treated are given in Table Results-The epithelium was 21% thicker 2. All eyes were free of any obvious ocular in the treated eye (p<0.0001). The relation disease. Informed consent was obtained from between refractive regression and epithe- all subjects. lial hyperplasia was significant (r=0.41; The unoperated eye was used as the control p<0.OOl). in all cases. Subjects were asked to remove Conclusions-Epithelial hyperplasia after their contact lens from the untreated eye at PRK correlated with the myopic shift least 1 night before the study visit. Five (including hyperopia reduction) after subjects presented to the clinic wearing soft treatment with the Summit laser. A model lenses in their control eye and the lenses were http://bjo.bmj.com/ is proposed suggesting that both subepi- removed immediately. Although contact lens thelial and epithelial layers contribute to induced hypoxia may cause stromal swelling, Cooperative Research regression in the Summit treated eyes O'Leary et alF have shown that the corneal epi- Centre for Eye with 18 gm of epithelial hyperplasia con- thelium does not swell even after 6 hours of Research and tributing each dioptre ofregression. anoxia. Therefore contact lens induced Technology, (BrJ7 Ophthalmol 1996;80:545-548) oedema would not be expected to have affected and Cornea and on September 28, 2021 by guest. Protected copyright. Contact Lens Research the epithelial thickness and these subjects were Unit, School of included in the study. Optometry, Despite the growing popularity ofphotorefrac- University ofNew tive keratectomy (PRK) and the relatively high SURGICAL PROCEDURES South Wales, Sydney, patient satisfaction with the results,' the prob- All patients had PRK performed for myopia by Australia C A Gauthier lems of individual predictability and long term one of four surgeons (BT, DE, PF, HHN). All B A Holden stability of refraction remain. The aetiology surgeries were performed in Stockholm, Sweden. of myopic regression is still unclear.2' It Surgical factors are summarised in Table 1. Department of has been widely suggested that there is a The surgical procedure was preceded by Ophthalmology, relation between regression and epithelial topical anaesthesia with amethocaine (tetra- University Hospital, hyperplasia and/or stromal remodelling.2 4-8 caine) 0.5%, and marking of the treatment Uppsala, Sweden D Epstein Epithelial hyperplasia has been reported zone. With the patient fixating an internal fixa- histologically9"4 and clinically.25 However, the tion target within the laser, a 5.0 mm radial St Erik's Eye Hospital, relation between epithelial hyperplasia and keratotomy marker with cross hairs was Karolinska Institutet, refractive changes has not been investigated. centred on the entrance pupil and pressed on Stockholm, Sweden Epstein et al'6 have questioned the stromal the cornea to delineate the treatment zone. B Tengroth remodelling hypothesis with their report of the Removal of the central corneal epithelium was P Fagerholm H presence of the original pattern of laser performed manually with a Beaver blade Hamberg-Nystrom ablation rings below the epithelium as long as 2 (Becton Dickinson, AcuteCare, Franklin Correspondence to: years after surgery. We have yet to understand Lakes, NJ, USA). With the patient again fixat- Charline Gauthier, PhD, the ways in which different components of the ing the same target, PRK was performed with Cooperative Research Centre for Eye Research and corneal wound healing process contribute to the Summit argon fluoride laser with spectral Technology, University of the postoperative refractive outcome. emission at 193 nm and pulse frequency fixed New SouthWales, Sydney, The aim of this study was to determine if at 10 Hz. The pulse energy resulted in a radiant NSW 2052, Australia. there is a relation between epithelial hyper- exposure of 180 mJ/cm'. The number of pulses Accepted for publication plasia and refractive regression (myopic shift) was computed by a proprietary algorithm. All 11 March 1996 after PRK. subjects had less than 1 D of astigmatism and 546 Gauthier, Holden, Epstein, Tengroth, Fagerholm, Hamberg-Nystrom Table 1 Subject details and laser variables (600 000 lux), higher magnification (32x), thinner slit width (12 jm), and wider angle Sample size 70 between observation and illumination systems Br J Ophthalmol: first published as 10.1136/bjo.80.6.545 on 1 June 1996. Downloaded from Males:females (%) 56:44 Right eyes treated 51 (730) than those used in conventional optical Age at time of study (years): pachometry. It has an accuracy of 4-7 Mean (SD) 34 (9) gm Minimum 21 depending on the experience of the user. The Maximum 55 pachometer was fitted with a precision potenti- Follow up time (months): ometer to monitor electronically the position of Mean (SD) 27 (7) Minimum 13 the rotatable pachometer plate to an accuracy Maximum 37 of 3 minutes of arc. The voltage output gener- Attempted correction (D): ated by the potentiometer is input directly into Mean (SD) -4.1 (1.5) Minimum -1.8 a personal computer which is programmed to Maximum -8.0 convert voltage readings to thickness values Pulse frequency (Hz) 10 and store readings for each subject. This data Pulse energy (mJ/cm2) 180 Ablation zone diameter (mm): storage system guards against examiner bias by Mean (SD) 4.6 (0.2) automatically storing the thickness values in Minimum 4.1 Maximum 5.0 the computer without the examiner being Ablation depth (pm): aware of the results during measurement. The Mean (SD) 36 (13) corneal measurement location is maintained Minimum 15 Maximum 74 vertically and horizontally by two small align- ment light emitting diodes (LEDs). These lights also ensure normality of the incident were treated with spherical ablations. Em- light with the corneal surface. The pachometer metropia was the desired outcome in all eyes. system was calibrated using a series of hard Patients received an ablation with a diameter of contact lenses of known thickness. 4.1 (n=2), 4.3 (n=6), 4.5 (n=47), or 5.0 mm Epithelial thickness was measured at a (n=15). central corneal position located by having the Postoperative treatment consisted of subject fixate the light used for vertical cinchocaine-bibrocathol ointment (a combina- alignment. Ten measurements of epithelial tion of a topical anaesthetic and an antiseptic thickness were made for each of the averaged component in a paraffin/Vaseline base) for 1 recorded values. The average standard devia- day and patching overnight. Topical steroid tion of the 10 measurements was 3 gm. The (dexamethasone 1 mg/ml) therapy was started difference between the two eyes was taken as on the first postoperative day. Patients were the PRK treated eye value minus the control either treated for 3 months (five times daily for eye value. 1 month, three times daily for 1 month, and once daily for 1 month) or for 5 weeks (five http://bjo.bmj.com/ times daily for the first week, with a subsequent Manifest subjective refraction reduction of dose by one drop per week). Two Manifest refractive error was determined using subjects were not prescribed corticosteroid standard subjective techniques without treatment immediately after surgery. Topical cycloplegia. Refraction was performed by a dexamethasone was reinstituted in 26% of trained ophthalmic technician at the 1 month Summit subjects for regression to a myopia of visit and by the operating surgeons at the 3, 6, at least 0.50 D. One subject was using topical 9, 12, 18, 24, 30, and 36 month visits. One on September 28, 2021 by guest. Protected copyright. dexamethasone once daily at the time of the independent observer (CAG) performed the study. refraction during the study visit at which epithelial thickness was measured. STUDY PROCEDURES For the purposes of this paper, the total Epithelial thickness amount of refractive regression was calculated Epithelial thickness measurements were per- as the change in refraction from the first post- formed by one unmasked observer (CAG). operative visit (1 month) until the study visit. The Payor-Holden micropachometer, a Haag- Therefore, total regression includes hyperopia Streit optical pachometer adapted to a Roden- reduction as well as any additional regression stock Model 2000 slit-lamp, was used to mea- from emmetropia to a myopic state. Refractive sure epithelial thickness.28 29 The instrument error is expressed as the spherical equivalent in allows epithelial thickness measurements to be all analyses. made by utilising a higher illumination level STATISTICAL ANALYSIS Table 2 Reasons why subjects remained unilaterally Pearson's product moment regression analysis treated was used to determine relations between two sets of data.
Load more

Recommended publications
  • Lung, Epithelium, Alveolus – Hyperplasia
    Lung, Epithelium, Alveolus – Hyperplasia 1 Lung, Epithelium, Alveolus – Hyperplasia Figure Legend: Figure 1 Lung, Epithelium, Alveolus - Hyperplasia in a male B6C3F1/N mouse from a chronic study. There is a small proliferation of alveolar epithelial cells with no inflammation. Figure 2 Lung, Epithelium, Alveolus - Hyperplasia in a male F344/N rat from a chronic study. There is no change in the normal alveolar architecture in this focus of alveolar epithelial hyperplasia. Figure 3 Lung, Epithelium, Alveolus - Hyperplasia in a male F344/N rat from a chronic study (higher magnification of Figure 2). The hyperplastic epithelial cells are cuboidal. Figure 4 Lung, Epithelium, Alveolus - Hyperplasia in a male B6C3F1/N mouse from a chronic study. The hyperplastic epithelial cells line slightly thickened alveolar septa. Figure 5 Lung, Epithelium, Alveolus - Hyperplasia in a male F344/N rat from a subchronic study. Alveolar epithelial hyperplasia secondary to inflammation is associated with numerous alveolar macrophages and minimal hemorrhage. Figure 6 Lung, Epithelium, Alveolus - Hyperplasia, Atypical from a male F344/N rat in a chronic study. Atypical cells (arrows) are enlarged with enlarged nuclei. Comment: Alveolar epithelial hyperplasia is a proliferation of type II pneumocytes and may be primary (Figure 1, Figure 2, Figure 3, and Figure 4) or secondary to type I pneumocyte injury or inflammation (Figure 5). Type II pneumocytes are thought to be the progenitors of type I cells. Type I pneumocytes are especially vulnerable to oxidant injury, and proliferation of type II pneumocytes is often seen following injury and loss of type I cells. When alveolar epithelial hyperplasia is secondary to type I pneumocyte damage, it is usually associated with inflammation, as opposed to primary alveolar epithelial hyperplasia, which is typically not associated with inflammation.
    [Show full text]
  • Villous Atrophy with Crypt Hyperplasia in Malignant Histiocytosis of the Nose
    J Clin Pathol: first published as 10.1136/jcp.35.6.606 on 1 June 1982. Downloaded from J Cliii Pathol 1982;35:606-610 Villous atrophy with crypt hyperplasia in malignant histiocytosis of the nose K AOZASA Fronm Osaka University, Faculty oJ Medicine, Departmentt of Pathology, Osaka, Japanl SUMMARY Intestinal changes, mainly in the jejunum, were investigated in 13 cases of malignant histiocytosis at necropsy and who had presented as lethal midline granuloma.Villous atrophy with crypt hyperplasia was observed in all cases, and a proliferation of atypical histiocytes was observed in seven cases. In the remaining cases, histiocytes with normal morphology increased in number. These findings showed that a prolonged abnormal proliferation of histiocytes was present in the smnall intestine of these cases concurrently with the nasal lesions. The term malignant histiocytosis was introduced by from the jejunum were available in all cases. In one Rappaport, for "a systemic, progressive, and case, material from the jejunum was also obtained invasive proliferation of morphologically atypical at operation. Adequate clinical data were available histiocytes and their precursors".' Malignant histio- in II cases. cytosis of the intestine has been described in con- nection with malabsorption and ulcerative jejunitis.2 Results In these cases, peroral jejunal biopsy and surgical resection specimens showed villous atrophy with CLINICAL FINDtNGS crypt hyperplasia even in the jejunum remote from The 13 cases showed progressive and destructive areas of ulceration or frank lymphoma. Villous lesions in the nose and adjacent structures, which atrophy with crypt hyperplasia was suggested as a presented as clinical lethal midline granuloma. Nasal http://jcp.bmj.com/ prolonged cryptic phase of malignant histiocytosis.
    [Show full text]
  • Clinicopathological Characteristics and KRAS Mutation Status of Endometrial Mucinous Metaplasia and Carcinoma JI-YOUN SUNG 1, YOON YANG JUNG 2 and HYUN-SOO KIM 3
    ANTICANCER RESEARCH 38 : 2779-2786 (2018) doi:10.21873/anticanres.12521 Clinicopathological Characteristics and KRAS Mutation Status of Endometrial Mucinous Metaplasia and Carcinoma JI-YOUN SUNG 1, YOON YANG JUNG 2 and HYUN-SOO KIM 3 1Department of Pathology, Kyung Hee University School of Medicine, Seoul, Republic of Korea; 2Department of Pathology, Myongji Hospital, Goyang, Republic of Korea; 3Department of Pathology, Severance Hospital, Yonsei University College of Medicine, Seoul, Republic of Korea Abstract. Background/Aim: Mucinous metaplasia of the papillary mucinous metaplasia suggests that papillary endometrium occurs as a spectrum of epithelial alterations mucinous metaplasia may be a precancerous lesion of a ranging from the formation of simple, tubular glands to certain subset of mucinous carcinomas of the endometrium. architecturally complex glandular proliferation with intraglandular papillary projection and cellular tufts. Endometrial metaplasia is defined as epithelial differentiation Endometrial mucinous metaplasia often presents a diagnostic that differs from the conventional morphological appearance challenge in endometrial curettage. Materials and Methods: of the endometrial glandular epithelium (1). Endometrial We analyzed the clinicopathological characteristics and the mucinous metaplasia is particularly relevant as it is mutation status for V-Ki-ras2 Kirsten rat sarcoma viral frequently encountered in endometrial curettage specimens oncogene homolog (KRAS) of 11 cases of endometrial obtained from peri-menopausal or postmenopausal women mucinous metaplasia. Electronic medical record review and (2). Mucinous epithelial lesions of the endometrium present histopathological examination were performed. KRAS a frequent disparity between cytological atypia and mutation status was analyzed using a pyrosequencing architectural alteration, and often present significant technique. Results: Cases were classified histopathologically diagnostic challenges to pathologists.
    [Show full text]
  • Repair, Regeneration, and Fibrosis Gregory C
    91731_ch03 12/8/06 7:33 PM Page 71 3 Repair, Regeneration, and Fibrosis Gregory C. Sephel Stephen C. Woodward The Basic Processes of Healing Regeneration Migration of Cells Stem cells Extracellular Matrix Cell Proliferation Remodeling Conditions That Modify Repair Cell Proliferation Local Factors Repair Repair Patterns Repair and Regeneration Suboptimal Wound Repair Wound Healing bservations regarding the repair of wounds (i.e., wound architecture are unaltered. Thus, wounds that do not heal may re- healing) date to physicians in ancient Egypt and battle flect excess proteinase activity, decreased matrix accumulation, Osurgeons in classic Greece. The liver’s ability to regenerate or altered matrix assembly. Conversely, fibrosis and scarring forms the basis of the Greek myth involving Prometheus. The may result from reduced proteinase activity or increased matrix clotting of blood to prevent exsanguination was recognized as accumulation. Whereas the formation of new collagen during the first necessary event in wound healing. At the time of the repair is required for increased strength of the healing site, American Civil War, the development of “laudable pus” in chronic fibrosis is a major component of diseases that involve wounds was thought to be necessary, and its emergence was not chronic injury. appreciated as a symptom of infection but considered a positive sign in the healing process. Later studies of wound infection led The Basic Processes of Healing to the discovery that inflammatory cells are primary actors in the repair process. Although scurvy (see Chapter 8) was described in Many of the basic cellular and molecular mechanisms necessary the 16th century by the British navy, it was not until the 20th for wound healing are found in other processes involving dynamic century that vitamin C (ascorbic acid) was found to be necessary tissue changes, such as development and tumor growth.
    [Show full text]
  • Hyperplasia (Growth Factors
    Adaptations Robbins Basic Pathology Robbins Basic Pathology Robbins Basic Pathology Coagulation Robbins Basic Pathology Robbins Basic Pathology Homeostasis • Maintenance of a steady state Adaptations • Reversible functional and structural responses to physiologic stress and some pathogenic stimuli • New altered “steady state” is achieved Adaptive responses • Hypertrophy • Altered demand (muscle . hyper = above, more activity) . trophe = nourishment, food • Altered stimulation • Hyperplasia (growth factors, . plastein = (v.) to form, to shape; hormones) (n.) growth, development • Altered nutrition • Dysplasia (including gas exchange) . dys = bad or disordered • Metaplasia . meta = change or beyond • Hypoplasia . hypo = below, less • Atrophy, Aplasia, Agenesis . a = without . nourishment, form, begining Robbins Basic Pathology Cell death, the end result of progressive cell injury, is one of the most crucial events in the evolution of disease in any tissue or organ. It results from diverse causes, including ischemia (reduced blood flow), infection, and toxins. Cell death is also a normal and essential process in embryogenesis, the development of organs, and the maintenance of homeostasis. Two principal pathways of cell death, necrosis and apoptosis. Nutrient deprivation triggers an adaptive cellular response called autophagy that may also culminate in cell death. Adaptations • Hypertrophy • Hyperplasia • Atrophy • Metaplasia HYPERTROPHY Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ No new cells, just larger cells. The increased size of the cells is due to the synthesis of more structural components of the cells usually proteins. Cells capable of division may respond to stress by undergoing both hyperrtophy and hyperplasia Non-dividing cell increased tissue mass is due to hypertrophy.
    [Show full text]
  • Studies on Wound Healing, with Special Reference to Epithelial Hyperplasia and Its Role in the Process
    STUDIES ON WOUND HEALING, WITH SPECIAL REFERENCE TO EPITHELIAL HYPERPLASIA AND ITS ROLE IN THE PROCESS T,OUIS H. JORSTAII (Fro))&the Iieaearch Lahorntoria of thc Brrr7iaid Free XhirL and Cancer Hospifol, Sciin t Lowis, Missouri) We have been interested in the healing of simple cutaneous wounds for a considerable period of time. Burrows has studied the nature of the healing process in sterile wounds of this type in the tissue culture (1). He and others in the laboratory have studied a large series of simple wounds in the laboratory animal. In some of these experiments precautions were taken in keeping the wound clean or sterile. The great majority of these wounds were made by marking the surface of the skin on the dorsal or ventral surf:tce of the animal by means of a cork borer of one centimeter or less in diameter and removing the skin with sharp curved scissors. Depending upon the nature of the skin folds arid its relation to stress and strain the wound would remain round in contour or become somewhat eliptical in outline after the animal became active following the operative procedure. All of these wounds were made with the animal under anaes- thesia. In addition to observations and measurements of these wounds in the gross, from day to day, many of them were sectioned and studied microscopically. In the tissue culture studies Burrows noted that epithelial cells do not separate from each other in the culture while the con- nective tissue cells separate and disperse. Epithelial membranes appear only from firmly anchored fragments of skin in these cultures.
    [Show full text]
  • The Effects of Postoperative Astaxanthin Administration On
    Journal of Clinical Medicine Article The Effects of Postoperative Astaxanthin Administration on Nasal Mucosa Wound Healing 1, 2 3 1 Lavinia-Gianina Manciula *, Cristian Berce , Flaviu Tabaran , Veronica Trombitas, and Silviu Albu 1 1 2nd Department of Otolaryngology, Iuliu Hatieganu University of Medicine and Pharmacy, 8 Victor Babes Street, 400012 Cluj-Napoca, Romania; [email protected] (V.T.); [email protected] (S.A.) 2 Department of Experimental Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 8 Victor Babes Street, 400012 Cluj-Napoca, Romania; [email protected] 3 Pathology Department, University of Agricultural Sciences and Veterinary Medicine, 400372 Cluj-Napoca, Romania; fl[email protected] * Correspondence: [email protected]; Fax: 0040-264-598278 Received: 22 August 2019; Accepted: 8 November 2019; Published: 11 November 2019 Abstract: Background: Wound healing of the nasal mucosa after endoscopic sinus surgery (ESS) is frequently complicated by scaring and consequently recurrences are encountered. Methods of optimizing results have been sought. In the present study we evaluated the effects of a powerful antioxidant, astaxanthin, on nasal mucosa healing after surgery, comparing it to the extensively studied properties of dexamethasone. Materials and Methods: 63 Wistar rats were used. The nasal mucosa from one side was damaged employing the brushing method. They were randomly divided into three experimental groups, one treated with astaxanthin, the second treated with dexamethasone and the third one acted as the control and was given normal saline. The rats were killed on days 5, 14 and 28 following injury. We observed the temporal evolution of the wound healing process and quantified the results by assessing four parameters: the epithelial thickness index (ETI), the subepithelial thickness index (STI), the goblet cell count and the subepithelial fibrosis index (SFI).
    [Show full text]
  • Sacrococcygeal Teratoma and Normal Alphafetoprotein Concentration on September 26, 2021 by Guest
    J Med Genet: first published as 10.1136/jmg.22.5.405 on 1 October 1985. Downloaded from Case reports 405 Lymphocyte studies revealed the mother's band has been incorporated into another breakpoint chromosomes to be normal. The father was unavail- site. The smallness of the deleted segment may able for study. explain her minimal dysmorphogenetic features; however, there is a lack of clinical similarity Discussion between our patient and the other two cases of interstitial 2p deletions. For example, our patient The clinical features of patients with deletions of 2p had premature closure of her fontanelles, whereas are summarised in the table. The patient of three other patients, including one with a deleted Ferguson-Smith et at2 is not included in the tabula- segment incorporating band 2p14,4 had delayed tion because he was also partially trisomic for the closure of their fontanelles. It is possible that our distal four bands of Sq and so was not a pure case of patient's physical and mental stigmata are the partial 2p monosomy. The patient reported by consequence of a disruption in one or more gene's Zachai et at5 is identical to case 2 of Emanuel et al. 1 nucleotide sequence resulting from this child's Given the paucity of reported cases, only the most numerous chromosome breaks. Given the uncer- tentative statements can be made regarding the tainty of our patient's karyotype and the limited clinical picture associated with deletions of 2p. The number of 2p deletion cases, it is evident that more Iwo cases presented by Emanuel et all have nearly cases of 2p deletions are required before a clear cut identical deleted segments and share the following 2p deletion syndrome, or syndromes, emerges.
    [Show full text]
  • Non-Cancerous Breast Conditions Fibrosis and Simple Cysts in The
    cancer.org | 1.800.227.2345 Non-cancerous Breast Conditions ● Fibrosis and Simple Cysts ● Ductal or Lobular Hyperplasia ● Lobular Carcinoma in Situ (LCIS) ● Adenosis ● Fibroadenomas ● Phyllodes Tumors ● Intraductal Papillomas ● Granular Cell Tumors ● Fat Necrosis and Oil Cysts ● Mastitis ● Duct Ectasia ● Other Non-cancerous Breast Conditions Fibrosis and Simple Cysts in the Breast Many breast lumps turn out to be caused by fibrosis and/or cysts, which are non- cancerous (benign) changes in breast tissue that many women get at some time in their lives. These changes are sometimes called fibrocystic changes, and used to be called fibrocystic disease. 1 ____________________________________________________________________________________American Cancer Society cancer.org | 1.800.227.2345 Fibrosis and cysts are most common in women of child-bearing age, but they can affect women of any age. They may be found in different parts of the breast and in both breasts at the same time. Fibrosis Fibrosis refers to a large amount of fibrous tissue, the same tissue that ligaments and scar tissue are made of. Areas of fibrosis feel rubbery, firm, or hard to the touch. Cysts Cysts are fluid-filled, round or oval sacs within the breasts. They are often felt as a round, movable lump, which might also be tender to the touch. They are most often found in women in their 40s, but they can occur in women of any age. Monthly hormone changes often cause cysts to get bigger and become painful and sometimes more noticeable just before the menstrual period. Cysts begin when fluid starts to build up inside the breast glands. Microcysts (tiny, microscopic cysts) are too small to feel and are found only when tissue is looked at under a microscope.
    [Show full text]
  • Cutaneous Lymphoid Hyperplasia Associated with Leishmania Panamensis Infection
    418 Letters to the Editor Cutaneous Lymphoid Hyperplasia Associated with Leishmania panamensis Infection Sebastiano Recalcati1, Pamela Vezzoli1*, Valentina Girgenti1, Luigia Venegoni1, Stefano Veraldi1 and Emilio Berti2 1UO Dermatologia, Fondazione IRCCS Ca’ Granda – Ospedale Maggiore Policlinico, Dipartimento di Anestesiologia, Terapia Intensiva e Scienze Dermatologiche, Università degli Studi di Milano, via Pace 9, IT-20122 Milan, and 2Università degli studi di Milano-Bicocca, Milan, Italy. *E-mail: [email protected], [email protected] Accepted March 16, 2010. Cutaneous leishmaniasis (CL) is an infection caused by protozoa from the genus Leishmania. The disease is transmitted by sandflies. Reservoirs are dogs, mice, wild rodents and, more rarely, humans. CL is clinically characterized by a single, polymorphous lesion, usually localized on the face or limbs. Nowadays, CL is more frequently seen among travellers returning from tropical and subtropical countries (1). Cutaneous lymphoid hyperplasia (CLH), also known as pseudolymphoma, is a reactive proliferation, proba- bly secondary to persistent antigenic stimulation. We present here a case of CLH associated with L. panamensis infection. CASE REPORT In May 2005 a 66-year-old Ecuadorian woman present- ed with a 15-month history of 3 brownish, crusted nodu- les on her right arm (Fig. 1a), left leg and forehead (Fig. 1b). Clinical history and general physical examination were unremarkable. Histopathological examinations of specimens from both the forehead and the arm revealed a prominent dermal infiltrate of small-to-medium- size lymphocytes, plasmocytes, blasts and histiocytes, with a nodular pattern and reactive germinal centres (Fig. 2a and b). The infiltrate was predominantly of B lymphocytes CD20+, CD79a+ and several plasmocytes CD138+.
    [Show full text]
  • Role of Liver Atrophy, Hepaticresection Andhepatocyte Hyperplasia In
    Gut: first published as 10.1136/gut.28.8.1022 on 1 August 1987. Downloaded from Gut, 1987, 28, 1022-1028 Liver and biliary Role of liver atrophy, hepatic resection and hepatocyte hyperplasia in the development ofportal hypertension in biliary disease N S HADJIS AND L H BLUMGART From the Hepatobiliary Surgical Unit, Royal Postgraduate Medical School, Hammersmith Hospital, London SUMMARY Portal fibrosis is considered to be pivotal in the pathogenesis of portal hypertension associated with extrahepatic biliary obstruction. The histological features, however, include diffuse hepatocyte hyperplasia as well as portal fibrosis, but not cirrhosis, and it is possible that the contribution of hepatocyte hyperplasia in the initiation of portal hypertension is equally important. If so, we hypothesised that patients with biliary obstruction and a coincident condition such as liver atrophy, or hepatic resection, with the potential of accelerating the hepatocyte proliferation caused by biliary obstruction itself, might be expected to develop portal hypertension earlier than patients with biliary obstruction alone. To examine this concept we studied 10 patients with post- cholecystectomy bile duct stricture, portal hypertension and liver atrophy, or hepatic resection (group I) and compared them with nine patients with postcholecystectomy stricture and portal hypertension, but no atrophy or resection (group II). Portal hypertension was diagnosed a mean 28 months (range 18-48 months) after cholecystectomy in group I compared with 62 months (range http://gut.bmj.com/ 36-100 months) for patients in group II (p<O0OO5 Mann-Whitney test). Thus hepatocyte hyperplasia may be an important part of the mechanism underlying the development of portal hypertension in chronic biliary disease.
    [Show full text]
  • Endometrial Hyperplasia
    AQ The American College of Obstetricians and Gynecologists FREQUENTLY ASKED QUESTIONS FAQ147 GYNECOLOGIC PROBLEMS Endometrial Hyperplasia • What is endometrial hyperplasia? • How does the endometrium normally change throughoutf the menstrual cycle? • What causes endometrial hyperplasia? • When does endometrial hyperplasia occur? • What risk factors are associated with endometrial hyperplasia? • What are the types of endometrial hyperplasia? • What are signs and symptoms of endometrial hyperplasia? • How is endometrial hyperplasia diagnosed? • What treatments are available for endometrial hyperplasia? • What can I do to help prevent endometrial hyperplasia? • Glossary What is endometrial hyperplasia? Endometrial hyperplasia occurs when the endometrium, the lining of the uterus, becomes too thick. It is not cancer, but in some cases, it can lead to cancer of the uterus. How does the endometrium normally change throughout the menstrual cycle? The endometrium changes throughout the menstrual cycle in response to hormones. During the first part of the cycle, the hormone estrogen is made by the ovaries. Estrogen causes the lining to grow and thicken to prepare the uterus for pregnancy. In the middle of the cycle, an egg is released from one of the ovaries (ovulation). Following ovulation, levels of another hormone called progesterone begin to increase. Progesterone prepares the endometrium to receive and nourish a fertilized egg. If pregnancy does not occur, estrogen and progesterone levels decrease. The decrease in progesterone triggers menstruation, or shedding of the lining. Once the lining is completely shed, a new menstrual cycle begins. What causes endometrial hyperplasia? Endometrial hyperplasia most often is caused by excess estrogen without progesterone. If ovulation does not occur, progesterone is not made, and the lining is not shed.
    [Show full text]