The accurate diagnosis and management of individuals with interstitial lung diseases (ILDs) poses an interesting challenge in clinical practice. A multidisciplinary team (MDT) approach is considered the gold standard. This is a single-centre retrospective review spanning a five-year period. We assessed the accuracy of prior ILD diagnosis, the methodology used to establish a correct diagnosis and how an MDT approach affected subsequent management. Our data supports an MDT approach in an experienced specialist ILD centre. We have demonstrated that diagnosis is often changed after an MDT review and that this impacts the subsequent management. Our results demonstrate that an MDT approach to diagnosis can establish a diagnosis in the majority of cases when prior diagnosis is uncertain (76%). We also show that a prior diagnosis of idiopathic pulmonary fibrosis is deemed inaccurate in over 50% of cases after MDT discussion. We have shown that during diagnostic uncertainty the considered gold standard of proceeding to a lung biopsy is not always feasible due to disease severity and comorbidities. In these circumstances, an MDT approach to diagnosis of ILDs combines clinical data with serial lung function and disease behavior, with or without responses to previous treatment trials to establish an accurate expert diagnosis.

In this case report, we describe the presentation and treatment of a patient with nasopharyngeal chondrolipoma. Lipomas are common soft tissue tumours, although their incidence in the nasopharynx is very low. A rarer variant of lipoma, chondrolipomas are benign mesenchymal tumours. They are formed by the proliferation of mature adipocytes and contain different amounts of mature cartilaginous tissue; Weiss "Enzinger and Weiss's soft tissue tumours", 4th ed: Mosby, St Louis; 2001 This represents the second reported case of a nasopharyngeal chondrolipoma. An endonasal approach to excision has not been previously described.

INTRODUCTION Hypercoagulability and intravascular thrombosis are well recognized but uncommon complications of inflammatory bowel disease (IBD) (1-3). Both arterial and venous thromboses have been described as early as the 1930s by Bargen and Barker (4). Intravascular thrombosis can affect various organ systems including the pelvic plexuses, lungs, central nervous system, spleen and kidneys, leading to congestion, ischemia or infarction (2-5). A few case reports on hepatic venous involvement with subsequent Budd Chiari syndrome (BCS) are found in the literature, mainly describing adult patients with ulcerative colitis (UC) (5-8). Bowel ischemia secondary to vascular thrombosis in pediatric patients with IBD has never been described before. Response of hepatic venous thrombosis to anticoagulation and colectomy has not been studied either. CASE REPORT We describe a 14-year-old girl with known UC. She was hospitalized at a local hospital with bloody diarrhea, fatigue and weight loss. She was started on methylpred-nisolone, ceftriaxone and parenteral nutrition. Her stool culture and C. difficile toxin were negative. Three days into her hospitalization, she developed progressive abdominal distension. A CT scan of the abdomen showed significant ascites and hypoechoic regions in her liver. She was then transferred to our facility for further management. Upon admission, her vital signs were stable and her physical exam revealed a soft distended abdomen without tenderness or organomegaly. There was evidence of free fluid with shifting dullness. The remainder of the exam was unremarkable. Her laboratory examinations revealed normal electrolytes and liver function tests except for mild hypokalemia and prothrombin time of 16 seconds with an INR of 1.3. Results of other tests included C reactive protein 1.5 mg/dl, hemoglobin concentration 9.2 g/dl, platelet count 289,000/mm3 and white cell count 6800/mm3 with 68% neutrophils and 25% lymphocytes. Prednisone, 5-ASA, spironolactone, metronidazole and intravenous fluids were started. Abdominal X-rays were normal. Paracentesis was performed revealing >5000 WBC/mm3. The ascitic fluid grew Enterococcus for which she was placed on antibiotics. She developed progressively worsening abdominal distension, tenderness and fever and was transferred to the pediatric intensive care unit. Radiologic studies showed intra abdominal free air. Exploratory laparotomy revealed a 5 cm circumferentially gangrenous and perforated section of the distal transverse colon. It was resected and a transverse colostomy was performed. Her resected colon sample (Fig. 1A, B) showed multiple thrombi at different stages of development with evidence of ischemia. No changes suggestive of vasculitis were found. Her hypercoagulabity workup included a fibrinogen level of 742 mg/dl, a platelet count of 426,000/mm3, a normal protein C level, antithrombin III assay and no factor V Leiden or prothrombin G20210A gene mutations. Her functional protein S level was initially low but later normalized. Protein S levels in both parents were normal. The patient was hemodynamically unstable after surgery and remained in intensive care. Post operative course was complicated by fungal sepsis and persistent ascites. Her liver function tests worsened with an ALT 70 U/L, GGT 179 U/L, total bilirubin 1.2 mg/dl and a prothrombin time of 19 seconds. As signs of hemodynamic instability were only evident around the time of perforation, we do not think her gradually worsening hepatic dysfunction was related to sepsis. The patient was started on enoxaparin subcutaneously. The medication was discontinued because of worsening rectal bleeding. Repeat paracentesis was performed revealing an elevated serum-ascitic fluid albumin gradient of 1.4 g/dl suggesting portal hypertension.FIG. 1: A, Transverse colon section showing a deep ulcer (white arrow) with surrounding hemorrhage adjacent to normal (N) colonic mucosa (H&E stain). B, Transverse colon section demon-strating thrombosed arterial vessels (white arrow) with some vessels showing signs of recanalization (black arrow) (H&E stain).A transjugular liver biopsy was performed with venography and measurement of wedged hepatic vein pressure. A free hepatic vein pressure of 6 mmHg and a wedged hepatic vein pressure of 11 mmHg were obtained. The liver biopsy showed small vessel venous occlusion with no evidence of fatty change, significant inflammation or fibrosis. A CO2 portogram was obtained, demonstrating normal appearing portal vein branches within the liver. The hepatic venograms (Fig. 2) revealed substantial narrowing of the inferior vena cava below the junction of the hepatic vein and multiple filling defects in all three hepatic veins, consistent with intravascular coagulation and Budd Chiari syndrome. Enoxaparin was re-intiated. An upper endoscopy showed superficial grade 0-1 esophageal varices and portal hypertensive gastropathy. The patient was discharged on enoxaparin, 5-ASA, prednisone and spironolactone. Two months after hospital discharge, a CT of the abdomen showed no narrowing in the inferior vena cava or hepatic veins.FIG. 2: Hepatic venogram showing pruning appearance of the hepatic venous system indicating intravascular thrombosis.One month later, the patient underwent total proctocolectomy with an ileoanal pull-through anastomosis and a diverting loop ileostomy. Her postoperative course was uneventful. Histologic sections of the colonic mucosa showed distortion of crypt architecture, cryptitis and crypt abscesses. In several foci the mucosa showed surface ischemic damage characterized by loss of upper portion of crypt with fibrin and abundant neutrophils attached to the surface. Four months after her total colectomy, she underwent ileostomy take down. Her diuretic was discontinued as there was no evidence of ascites. She continued to do well on subcutaneous enoxaparin. The patient elected to stop her anticoagulation therapy 11 months after total colectomy and has remained in stable condition with normal liver function tests and without any evidence of ascites. DISCUSSION Ischemic colitis was found on the histologic examination of the patients resected bowel. This is extremely rare in the pediatric population with IBD. A 13-year-old patient with Crohn disease was reported by Talbot et al., with necrosis of the ileum, cecum and ascending colon and who later died of sepsis (2). This has been noted in very few adult patients. It is theoretically possible that such a process can possibly affect any part of the arterial system, including the mesenteric vessels. Therefore, ischemic colitis should be included on the growing list of complications of UC. Patients with IBD can develop thromboembolic complications. A hypercoagulable state has been postulated and hemostatic abnormalities have been sometimes identified. These include elevated platelet counts and coagulation factors such as fibrinogen, factor V and factor VIII. Others include decreased blood clotting activation inhibitors such as antithrombin III, protein S and protein C and decreased fibrinolytic activity (1,5,7-11). Thrombophilic mutations such as factor V Leiden, prothrombin or methylene tetrahydrofolate reductase have also been implicated (12). Coagulation abnormalities have been observed in 60% in a series of 7,199 adult patients with UC and Crohn disease (2,13). Hemostatic abnormalities are not found in all patients who develop thrombosis. Conversely, hemostatic abnor-malities have been described with IBD patients with no obvious thromboembolic phenomenon. Thromboembolic complications have been described in only 1.3 to 6.4% of cases of IBD patients in several series (2,9,14). Thus, it is difficult to accurately relate coagulation abnormalities to the occurrence of thromboembolism. There are possibly other factors that contribute to the risk of thromboembolism in such patients, including dehydration, immobilization, infection and surgery. In our patient, fibrinogen rose to a peak of 742 mg/dl (normal 160-340 mg/dl) and the platelet count increased to 426,000. She tested negative for factor V Leiden and Prothrombin G20210A gene mutations. Functional protein C level was 71% (normal, 64-116%) and anti-thrombin III assay measured 101% (normal, 80-137%). Functional protein S level was initially low at 28% (normal, 63-136%) but gradually normalized 11 months after proctocolectomy. The initially low level was ascribed to a consumptive state. Thus our case did not have any identifiable cause of hypercoagualtion other than having active UC. Antiphospholipid antibodies, which are a heterogeneous group of polyclonal immunoglobulins, are also thought to play a role in hypercoagulability in a small percentage of this patient population. Antiphospholipid syndrome includes a wide variety of clinical entities including arterial or venous thrombosis, strokes, recurrent abortion and thrombocytopenia (1,3,14). This consideration was ruled out in our case as she tested negative for such antibodies. The most common sites for venous thrombosis in IBD patients are the pulmonary vasculature, the pelvis and the deep veins of the legs (5,9,15). Involvement of the splenic, portal, renal and central nervous systems have been described. Hepatic vein thrombosis has rarely been reported. Risk factors for thrombosis include polycythemia, malignancies, myeloprolifrative disorders, homocystinuria, inherited deficiency of antithrombin III, protein C or protein S and medication intake such as oral contraceptives and L-Asparaginase (9,10,14). Our patient did not have any such risk factors. She was, however, initially dehydrated, and probably had low grade sepsis with an intra abdominal infection. This would have placed her at a higher risk for a thromboembolic event. Arterial thrombosis is a known but infrequent complication in patients with IBD. Thrombosis within the renal arteries with subsequent ischemia and partial or complete kidney infarction has been reported. Similar mechanisms have led to pulmonary, retinal and central nervous system infarctions (9,10,13). Peripheral arterial thromboembolic complications have developed, resulting in ischemic finger tips, lower extremity claudication, limb loss, and infarction of the glans penis (2). Such events have been associated in the adult population with pancolonic disease and poorer prognosis in UC patients (13). Young adults with active UC have developed myocardial ischemia and infarction in rare cases (16). Osteonecrosis has been described with IBD patients, however such a population is commonly on steroids and that might be the predisposing factor. Well recognized hepatic complications of UC include fatty liver changes, pericholangitis, sclerosing cholangitis, chronic active hepatitis and rarely cirrhosis and hepatic failure (5-8). Hepatic vein thrombosis or BCS has been described in very few case reports as a rare complication of IBD. Most such cases are adults with UC. Classically, BCS presents with hepatomegaly, ascites and right upper quadrant abdominal pain. BCS can present acutely or insidiously over months or years. Other causes of BCS in children include ventriculoatrial shunt, sickle cell disease, systemic lupus erythrematosus, antiphos-pholipid antibody syndrome, toxins, webbed inferior vena cava and malignancies (6,7). None of these were present in our patient. BCS is usually progressive with rare spontaneous resolution. Definitive treatment with side to side portocaval shunt, mesocaval shunts or hepatic transplantation may be needed (7,8). Our patient is the youngest described in the literature with BCS as a complication of UC. She is also unique in her complete recovery after anticoagulation and total colectomy. CONCLUSION Intravascular thrombosis can involve multiple organ systems in UC patients even in the pediatric population. It is rare to see BCS in such an age group as a complication of UC in the absence of other predisposing factors. Such a complication can often be managed successfully by medical therapy alone. In this case, anticoagulation was safe and effective. Other possible etiologies of intravascular thrombosis should be investigated and ruled out as that can affect the duration of anticoagulation therapy. Colectomy may be helpful in some cases especially those refractory to medical treatment.

Both Head and Neck Surgeons and General Surgeons are frequently referred patients with cervical lymphadenopathy. An uncommon but important cause is histiocytic necrotising lymphadenitis. This is a benign self-limiting disease that has been confused with malignant lymphomas. Some patients may also experience distressing and debilitating symptoms which can last for months. We describe four cases to illustrate the varied clinical presentation of this disease and present new signs seen in association with it. A remarkable therapeutic response to a short course of oral corticosteroids was observed in one case.

Journal of Pediatric Gastroenterology and NutritionVolume 39, Issue S1 p. S489-S490 ABSTRACTS: Poster Session Abstracts P1139 A NOVEL METHOD FOR DIRECT ENDOSCOPIC PLACEMENT OF GASTROJEJUNAL FEEDING TUBES D. E. DiMeo, D. E. DiMeo Pediatrics, University of Iowa, Iowa City, United StatesSearch for more papers by this authorW. P. Bishop, W. P. Bishop Pediatrics, University of Iowa, Iowa City, United StatesSearch for more papers by this author D. E. DiMeo, D. E. DiMeo Pediatrics, University of Iowa, Iowa City, United StatesSearch for more papers by this authorW. P. Bishop, W. P. Bishop Pediatrics, University of Iowa, Iowa City, United StatesSearch for more papers by this author First published: 01 June 2004 https://doi.org/10.1002/j.1536-4801.2004.tb13569.x Submitted by: [email protected] Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume39, IssueS1June 2004Pages S489-S490 RelatedInformation

The treatment of constipation and encopresis in children seems to be changing. Increasingly, gastroenterologists and other physicians in the United States are abandoning long-used therapies, such as ingestion of mineral oil and milk of magnesia, in favor of a “new” and apparently highly effective stool softener–electrolyte-free polyethylene glycol (PEG). Electrolyte-free PEG, with an average molecular weight of 3,350, is being marketed in the United States under the brand name MiraLax (Braintree Laboratories, Braintree, MA). This product has no detectable taste and can be mixed with any clear liquid beverage. Patient compliance is much better using this solution versus the bad-tasting alternatives. Should we all be switching to this new therapy? As with all new treatments, prudent physicians are raising questions about safety and effectiveness. What is known about the use of a PEG in treating constipation? Are there safety concerns? Polyethylene glycol, similar to milk of magnesia, is an osmotic laxative. Taking PEG orally results in a net increase in fecal water content (Gastroenterology 1988; 94:933–41). All gastroenterologists are familiar with PEG in balanced salt solutions used for intestinal lavage before colonoscopy and surgery (Gastroenterology 1980; 78:991–995). Unfortunately, the unpleasantly salty taste of these products limits their usefulness in young children. Although added electrolytes may be necessary for the safe use of PEG in a large-volume intestinal lavage, these are not required for small-volume PEG administration. When given daily over 2 weeks to constipated adult patients, no change in serum electrolytes or other blood chemistries was observed (Am J Gastroenterol 2000; 95:446–50). Longer-term therapy in adults has also been evaluated. Electrolyte-containing PEG given in small daily doses over 20 weeks to constipated adult patients resulted in no side effects and was effective in alleviating symptoms (Gut 2000; 46:522–6). How toxic is MiraLax compared with other laxatives? Its active ingredient, PEG, is approved by the Food and Drug Administration (FDA) for use as a food additive, and it is commonly used by the food industry as a coating, binding, and texture-improving agent. Polyethylene glycol 3350 is absorbed in barely detectable amounts from the intestines when taken orally and when absorbed is excreted unchanged in the urine (Gastroenterology 1986; 90:1914–8). The toxicity of PEG is directly related to molecular weight; larger polymers that are solids at room temperature, such as MiraLax, have minimal toxicity. The median lethal dose (LD 50 ) of PEG 4000 in rats is greater than 50 g/kg (Patty's Industrial Hygeine and Toxicology, 4th edition. New York: Wiley; 1994; vol. 2F). The safety of our “old friends” is perhaps more questionable. Excessive absorption of salts from saline osmotic agents, such as milk of magnesia, magnesium citrate, and phosphate agents, is well described, even in patients with normal renal function (Ann Pharmacother 1998; 32:312–5). Mineral oil administration may result in pulmonary injury if aspirated (Pediatrics 1999; 103:E19) and may interfere with fat-soluble vitamin absorption. Use of nonabsorbable disaccharides, such as lactulose and sorbitol, can commonly cause excessive colonic gas production as a result of fermentation, resulting in cramps and flatulence (J Pediatr Gastroenterol Nutr 1999; 29:612–26). The information available to us therefore suggests that MiraLax and related products are at least as safe as the older therapies for chronic constipation and perhaps causes fewer side effects. At the University of Iowa, we began using MiraLax soon after it was marketed, initially for patients who were noncompliant with other therapies. Our success with PEG was much better than with the older drugs, and it has rapidly become our first-line therapy. Caregivers are instructed to prepare a roughly isosmotic solution of MiraLax by dissolving 1 measuring capful (17 g) in 8 ounces (240 mL) of clear liquid beverage. We use a starting dose of 10 to 14 mL of this solution per kilogram of body weight per day (0.7 to 1 g · kg −1 · d −1 PEG) divided into two doses. Parents are told to increase or decrease the volume administered, in small increments, until the child is having two or three soft to runny stools per day. Compliance with this regimen is uniformly excellent, and the results have been equally satisfying. The most common side effect, seen in a minority of patients, has been flatulence or cramping when fruit juices are used to mix the PEG. This probably results from fermentation of carbohydrates and can be avoided by using an artificially sweetened beverage instead of fruit juice. Our initial success with PEG led to a Braintree Laboratories–funded study of MiraLax for constipation in children, which has been completed and submitted for publication. When this and results of other peer-reviewed studies in children are published and as additional experience with PEG therapy accumulates, I predict that electrolyte-free PEG will rapidly become the standard therapy for functional constipation in children.

STUDY OBJECTIVE:Low bone mineral density is a common complication of cystic fibrosis (CF), and recent studies have implicated vitamin D insufficiency as a significant etiologic factor. The aim of this study was to establish whether there was bone biopsy evidence of vitamin D deficiency osteomalacia in patients with CF and to document the general histomorphometric characteristics of CF bone.PATIENTS AND METHODS:A retrospective descriptive and histomorphometric study of postmortem L2/L3 vertebral bone biopsy specimens was undertaken on tissue from 11 posttransplant CF patients and 4 nontransplanted CF patients. Control data were derived from postmortem bone specimens from 15 young adults.RESULTS:Bone from all CF patients was characterized by severe osteopenia in both trabecular and cortical bone. At the cellular level, there was decreased osteoblastic and increased osteoclastic activity. The reduction in osteoblastic activity was due to both a decrease in osteoblast number and a decrease in the biosynthetic potential of osteoblasts. The osteoclastic changes were due to an increase in the number of osteoclasts. The increase in osteoclasis and the uncoupling of osteoblastic and osteoclastic activity resulted in an increase in resorptive surfaces. Although there were few significant differences between the transplanted and nontransplanted CF groups, both cortical and trabecular bone mass tended to be lower after transplantation. None of the CF undecalcified biopsy specimens showed osteoid parameters characteristic of vitamin D deficiency osteomalacia.CONCLUSIONS:CF patients have an unusual and complex pattern of cellular changes within bone that are not typical of vitamin D deficiency osteomalacia.

Aim: After a misdiagnosis of pulmonary adenocarcinoma as desquamative interstitial pneumonia (DIP), we investigated whether immunohistochemical markers could differentiate these conditions.Methods and results: Three cases of DIP and one pulmonary adenocarcinoma masquerading as DIP were studied by light and electron microscopy, All cases were mucin-negative. The cases of DTP were CD68 positive but cytokeratin-negative. The adenocarcinoma was cytokeratin-positive (AE1/3 and CAM5.2), as well as showing some CD68-positive cells. Markers for carcinoma (CEA, Ber-EP4, and Leu M1) were negative in all cases. Ultrastructurally the adenocarcinoma appeared to be derived from Type II pneumocytes.Conclusion: Before a diagnosis of DIP is made, cytokeratin markers should be used.

Journal of Pediatric Gastroenterology and NutritionVolume 25, Issue 2 p. 245-246 Selected Summary Breath Hydrogen Testing for Small Bowel Bacterial Overgrowth-A Lot of Hot Air? Warren P. Bishop, Warren P. Bishop Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorCharles Bijleveld M.D., Charles Bijleveld M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorHans Buller M.D., Hans Buller M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorJan Taminiau M.D., Jan Taminiau M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorAdrian Thomas M.D., Adrian Thomas M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorSteven N. Lichtman M.D., Steven N. Lichtman M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorBenjamin L. Shneider M.D., Benjamin L. Shneider M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorWarren P. Bishop M.D., Warren P. Bishop M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorBarbara Anne Haber M.D., Barbara Anne Haber M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this author Warren P. Bishop, Warren P. Bishop Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorCharles Bijleveld M.D., Charles Bijleveld M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorHans Buller M.D., Hans Buller M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorJan Taminiau M.D., Jan Taminiau M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorAdrian Thomas M.D., Adrian Thomas M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorSteven N. Lichtman M.D., Steven N. Lichtman M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorBenjamin L. Shneider M.D., Benjamin L. Shneider M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorWarren P. Bishop M.D., Warren P. Bishop M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this authorBarbara Anne Haber M.D., Barbara Anne Haber M.D. Department of Pediatrics, University of Iowa, Iowa City, Iowa, U.S.A.Search for more papers by this author First published: 01 August 1997 https://doi.org/10.1002/j.1536-4801.1997.tb00695.xRead the full textAbout ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume25, Issue2August 1997Pages 245-246 RelatedInformation

AIMS:We describe the cutaneous pseudoneoplastic lesions in two patients with nodular erythema elevatum diutinum, a rare chronic disorder in which polymorph nuclear fragmentation (leukocytoclasis) is present within dermal nodules showing spindle cells and fibrosis. In both cases diagnostic difficulty was encountered clinically and pathologically and various benign and malignant neoplasms were considered in the differential diagnosis. METHODS AND RESULTS:Immunohistochemically the spindle cells were negative for CAM5.2, AE1/3, S100 protein and desmin (D33). They were positive for vimentin and focally positive for CD34 and alpha-smooth muscle actin. Some of the spindle cells were positive for Mac 387 and KP1(CD68). By electron microscopy, the lesions were shown to consist of fibroblasts/myofibroblasts and fusiform macrophages. CONCLUSIONS:Increased awareness of the features described will help to avoid misdiagnosis as a neoplastic process.

HistopathologyVolume 24, Issue 1 p. 101-102 The bone marrow trephine biopsy P.W. Bishop, P.W. Bishop Wythenshawe Hospital, University of Manchester School of Medicine, Southmoor Road, Manchester M23 9LT, UKSearch for more papers by this author P.W. Bishop, P.W. Bishop Wythenshawe Hospital, University of Manchester School of Medicine, Southmoor Road, Manchester M23 9LT, UKSearch for more papers by this author First published: January 1994 https://doi.org/10.1111/j.1365-2559.1994.tb01284.xAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume24, Issue1January 1994Pages 101-102 RelatedInformation

An immunophenotypic study of 17 cases of diffuse lymphocyte predominance Hodgkin's disease and 20 cases of nodular lymphocyte predominance Hodgkin's disease, along with eight of mixed cellularity and five of nodular sclerosing Hodgkin's disease, is reported. The atypical cells in nodular lymphocyte predominance Hodgkin's disease showed only minor differences from the published consensus. However, the atypical cells in diffuse lymphocyte predominance Hodgkin's disease showed an immunophenotype which was commonly B-cell positive (59%), but in a minority of cases LeuM1 (24%) or epithelial membrane antigen (12%) positive; none of the cases was Ber-H2 positive. These results do not differ greatly from our findings in nodular lymphocyte predominance Hodgkin's disease, but do diverge from the published consensus for diffuse lymphocyte predominance Hodgkin's disease. The question as to whether morphology or immunophenotype should form the primary diagnostic criterion for the definition of lymphocyte predominance Hodgkin's disease is discussed.

Acute hydrops of the gallbladder is a well-recognized complication of Kawasaki syndrome. We report a case of a child with this syndrome whose gallbladder hydrops slowly resolved after intravenous gamma-globulin therapy. However, he continued to experience postprandial right upper quadrant abdominal pain. Hepatobiliary scintigraphy revealed normal filling of the gallbladder but marked impairment of meal-stimulated gallbladder emptying. Endoscopy with biopsy of the esophagus, stomach, and duodenum was normal, ruling out peptic complications of his aspirin therapy. This child's discomfort improved slowly over several months, finally ending approximately 6 months after the onset of his illness. A repeat gallbladder emptying study done ultrasonographically at that time revealed near-normal meal-stimulated gallbladder emptying. We conclude that poor emptying of the gallbladder may be associated with prolonged abdominal pain in Kawasaki syndrome. Meal-stimulated gallbladder emptying can be assessed by a simple ultrasonographic technique and should be considered in any patient with Kawasaki syndrome and abdominal pain.

Sarcoid granulomata were found incidentally in the mammary lobules adjacent to an excised fibroadenoma in a case of sarcoidosis of the breast. The diagnosis of sarcoidosis was established by the radiological finding of bilateral hilar lymphadenopathy, raised concentrations of serum angiotensin converting enzyme and lysozyme, and, finally, by a positive Kveim test.