Histiocytic Hyperplasia Research Articles

Clinical and Pathological Features of Pilomatrixoma in Children: A Retrospective Study

Plain Language SummaryPilomatrixoma is a benign skin neoplasm that is common in children and is often misdiagnosed. Fu et al. conducted a retrospective study at Shenzhen Baoan Women’s and Children’s Hospital. One hundred and seventy-one children with pilomatrixoma were included. There were 2 age peaks (≤1 year old, 5–11 years old) and 2 age valleys (2–4 years old, ≥12 years old). The mean disease course was 9.34 months, 69.0%, 86.5%, and 95.3% of the patients’ disease course in 6 months, 12 months, and 24 months, respectively. The mean tumor volume was 0.6 cm3, and 81.3% of patients’ tumor volume ≤1 cm3. Tumors were distributed sequentially in the head and neck (77.2%), upper limbs (12.9%), trunk (7.6%), and lower limbs (2.3%). The correct rates of clinical and ultrasonic diagnosis were 50.9% and 38.6%, respectively. The pathological features of pilomatrixoma were shadow cells (99.4%), basaloid cells (94.7%), calcification (39.8%), multinuclear giant cell aggregation (35.7%), inflammatory cell infiltration (33.9%), histiocytic hyperplasia (5.3%), and ossification (1.2%). There were no significant differences in age, disease course, or tumor volume between the male and female patients (p > 0.05). The age and tumor volume of the patients in different body parts were significantly different (P1 = 3.10E−05 and P2 = 5.60E−05, respectively). The correlation between the disease course and tumor volume was positively significant (p ≤ 0.05). There was a significant correlation between the disease course and tumor volume in patients with tumors at upper limbs (p = 0.03).

Papillary Histiocytic and Mesothelial Hyperplasia of the Ovary Related to a Huge Uterus: A Case Report

Nodular histiocytic/mesothelial hyperplasia (NHMH) is a very rare condition. It is generally thought to be associated with repeated mechanical or chemical stimulation. This study reported NHMH with papillary growth pattern in the ovary following high-intensity focused ultrasound (HIFU) treatment for uterine leiomyoma and adenomyosis. A 48-year-old female, who had a history of undergoing HIFU treatment 7 times for adenomyosis and leiomyoma of the uterus 6 months ago, was referred to the hospital. After the hysterectomy and right salpingo-oophorectomy, the patient was confirmedly diagnosed with nodular histiocytic and mesothelial hyperplasia with the papillary growth pattern of the right ovary. This benign reactive inflammatory lesion of the mesothelium mimicking malignancy must be kept in mind to avoid unnecessary treatment.

REMODELING OF THE AERO-HEMATIC LUNG BARRIER COMPONENTS UNDER HIGH ALTITUDES

The aim of the study is to examine structural and ultrastructural aero-hematic barrier (AHB) changes in rats during adaptation to high-altitude hypoxia.
 Materials and Methods. The experiments were carried out on 60 sexually mature outbred laboratory male rats weighing 140–160 g at high altitude (3200 m above sea level). The authors followed Mayer's hematoxylin and eosin staining protocol, and used transmission and scanning electron microscopy on the 7th, 15th and 30th days of the animals' life in the mountains. Statistical data processing was carried out using Statistica 6.0 (USA) and StatTech v. 2.8.4 (Russia) and Student's t-test. Differences were considered statistically significant at p<0.05.
 Results. At early stages of high-altitude adaptation, dystrophic changes in the epithelial layer of lung capillaries, hypertrophy and hyperplasia of histiocytes, fibroblasts and lipofibroblasts were noted. The authors also revealed proliferation of type II alveolocytes, thickening of the interalveolar septa (IAS) and cytoplasmic processes of endotheliocytes, destruction of type II alveolocytes (apocrine method, with the release of surfactant into the alveoli lumen), multivesicular lamellar bodies in the cytoplasm of type II alveolocytes; interstitial edema with transudate in the alveoli lumen. In later periods, surfactant system activity decreases due to a reduced release of osmiophilic lamellated corpuscles (OLC) into the alveoli lumen. The main AHB components are next to control data, while the IAS thickness exceeds the norm. In the alveoli wall, the number of fibroblasts increases, causing an increase in the number of Kohn's pores and providing collateral breathing.
 Conclusion. The study of AHD components in experimental animals at different periods of high-altitude adaptation revealed dystrophic processes of AHD in IAS, compensated by type I alveolocytes and proliferation of type II alveolocytes, confirming the adaptive mechanisms of ultrastructural alteration of all epithelial and endothelial components of the pulmonary alveoli.

Reversible gelatinous transformation of bone marrow – A rare and reversible cause of pancytopenia in tuberculosis

A 68-year-old man presented with a low-grade fever for one month. He had loss of appetite and had lost 6 kilograms of weight in the last two months. He was evaluated and found to have miliary tuberculosis with pancytopenia. The bone marrow revealed Gelatinous transformation of bone marrow and there was no evidence of other causes of pancytopenia like histiocytic hyperplasia, maturation arrest, or infiltration of the bone marrow. The pancytopenia improved with anti-tubercular treatment showing the reversible nature of the disease. To conclude, multiple mechanisms can result in pancytopenia in tuberculosis. A bone marrow study can reveal most of them including rare causes like GTBM.

Clinical Analysis of 44 Children with Subacute Necrotizing Lymphadenitis.

ObjectiveTo explore the causes, clinical features, and laboratory examination characteristics of subacute necrotizing lymphadenitis to improve the understanding of this disease, reduce misdiagnosis, and make appropriate diagnoses and treatments.MethodsThe clinical data of 44 children with subacute necrotizing lymphadenitis admitted to our hospital from January 2013 to August 2021 were collected. The clinical and laboratory examinations of the disease were systematically analyzed.ResultsAll 44 cases aged 6–13 years and averaged 10.3 ± 2.1 years, including 32 boys and 12 girls, were diagnosed with histiocytic necrotizing lymphadenitis (HNL) by lymph node biopsy. Forty-two cases had palpable superficial lymph nodes, and two showed abdominal lymph node enlargement in the imaging examination. The symptoms might be accompanied by mild hepatomegaly or splenomegaly, emaciation, night sweats, rashes, and other manifestations. Leukopenia and neutropenia occurred. The pathological features were extensive coagulative necrosis of lymph nodes with reactive hyperplasia of histiocytes as well as positive IHCl CD68. Four cases had a relapse, and the prognosis of the other cases was good.ConclusionThe case with fever and lymph node enlargement of unknown origin and no response to antibiotic treatment should undergo a pathological examination as early as possible for diagnosis and treatment. The disease has a good prognosis in most cases but may recur in a few cases.

From classical Langerhans cell histiocytosis to Erdheim-Chester disease: different sides of the same coin?

Objective. Analysis of the clinical course of classical histiocytosis (LCH) in children and clinical differences, diagnostic difficulties and a different therapeutic strategy in a child with a rare variant of LCH in the form of Erdheim-Chester syndrome (ECD). Patients and methods. Retrospective single-center analysis of the clinical course of classic LCH in 54 children who were diagnosed with the disease in the last 40 years and the differences shown in a patient with diagnosed EDC. The clinical response was assessed according to the LCH programs valid at the time for the classic form of LCH and in the child with ECD. Results. The multi-system form of LCH was diagnosed more often than the single-system form. The skull bones were the most common localization of LCH in both forms of the disease. Recurrence of the disease occurred in about 5% of patients, death in one (1.9%) patient. The course of the child with ECD was more turbulent, with rapid progression, involvement of critical organs, no response to standard chemotherapy according to the LCH 2009 protocol. After the molecular diagnosis was specified, therapy with vemurafenib, a BRAF-V600E kinase inhibitor, followed by transplantation of hematopoietic stem cells (allo-HCT) was applied. Basic disease was in remission and lasts for 12 months. Conclusions. The lack of an expected response to LCH therapy should indicate the possibility of rare forms of histiocytic hyperplasia. Molecular tests are an important element in the diagnosis of histiocytosis and allow to precisely select the most appropriate, targeted therapy. BRAF-V600E kinase inhibitors are highly safe and effective in the treatment of LCH and ECD with a confirmed BRAF-V600E mutation, however allo-HCT should be considered in selected cases.

Distinctive pseudopalisaded histiocytic hyperplasia characterizes the transition of exudative to proliferative phase of diffuse alveolar damage in patients dying of COVID-19

Severe COVID-19 results in a glucocorticoid responsive form of acute respiratory distress (ARDS)/diffuse alveolar damage (DAD). Herein we compare the immunopathology of lung tissue procured at autopsy in patients dying of SARS-CoV-2 with those dying of DAD prior to the COVID-19 pandemic. Autopsy gross and microscopic features stratified by duration of illness in twelve patients who tested positive for SARS-CoV-2 viral RNA, as well as seven patients dying of DAD prior to the COVID-19 pandemic were evaluated with multiplex (5-plex: CD4, CD8, CD68, CD20, AE1/AE3) and SARS-CoV immunohistochemistry to characterize the immunopathologic stages of DAD. We observed a distinctive pseudopalisaded histiocytic hyperplasia interposed between the exudative and proliferative phase of COVID-19 associated DAD, which was most pronounced at the fourth week from symptom onset. Pulmonary macrothrombi were seen predominantly in cases with pseudopalisaded histiocytic hyperplasia and/or proliferative phase DAD. Neither pseudopalisaded histiocytic hyperplasia nor pulmonary macrothrombi was seen in non-COVID-19 DAD cases, whereas microthrombi were common in DAD regardless of etiology. The inflammatory pattern of pseudopalisaded histiocytic hyperplasia may represent the distinctive immunopathology associated with the dexamethasone responsive form of DAD seen in severe COVID-19.

Secondary haemophagocytic lymphohistiocytosis in COVID-19: correlation of the autopsy findings of bone marrow haemophagocytosis with HScore

BackgroundSecondary haemophagocytic lymphohistiocytosis (sHLH) is characterised by a hyper activation of immune system that leads to multiorgan failure. It is suggested that excessive immune response in patients with COVID-19 could...

Hiperplasia Nodular Histiocítica: Uma Manifestação Rara à Exposição ao Asbesto

A hiperplasia nodular histiocítica (HNH) consiste em uma condição rara, sem predileção por sexo ou idade, marcada por um processo proliferativo benigno, por vezes confundido com neoplasia maligna, constituído majoritariamente por histiócitos (1, 2). Inflamação crônica local e irritação mecânica estão entre as principais causas postuladas para essa entidade. Patologias malignas, por outro lado, representam os principais diagnósticos diferenciais, o que evidencia a importância clínica de seu diagnóstico assertivo sendo a imunohistoquímica uma importante ferramenta diagnóstica (3). Nesse artigo, os autores descrevem um relato de caso de hiperplasia nodular histiocítica pleuro-pulmonar em um paciente do sexo masculino, não tabagista, com história de exposição ao asbesto o qual provavelmente incitou um processo inflamatório crônico com proliferação de histiócitos. O paciente apresentava dispnéia, dor pleurítica e hemoptise além de derrame pleural hemorrágico recorrente evoluindo a óbito por exacerbação dos sintomas. Apesar da entidade ser descrita na literatura como uma proliferação celular benigna histiocitária, há raros casos relatados sobre a evolução e tratamento da doença.
 Palavras chaves: Hiperplasia nodular histiocítica, asbesto, pleura, pulmão.

Intratubal Pseudopapillary Histiocytic Hyperplasia: A New Histologic Variant in the Spectrum of Histiocytic Lesions Involving the Fallopian Tube.

Although histiocytic lesions of the fallopian tube are relatively rare compared to their epithelial counterparts, there exists a spectrum of histiocytic lesions involving the fallopian tube that are described under different terminologies dependent on the involved compartment of the fallopian tube. A common histologic denominator of all the hitherto reported tubal histiocytic lesions is the presence of sheets and clusters of histiocytes without any supportive connective tissue. The current study describes three cases of a heretofore-undescribed papillary histiocytic lesion in the lumen of the fallopian tube. All 3 lesions were characterized by avascular, hyaline collagenous papillary cores surrounded by a monotonous population of epithelioid cells, morphologically resembling mesothelial cell hyperplasia, but displaying a histiocytic immunophenotype with diffuse immunopositivity for CD68. Since the papillary cores did not harbor any vasculature, the term intratubal pseudopapillary histiocytic hyperplasia was proposed for this histiocytic proliferation which expands the spectrum of histiocytic lesions of the fallopian tube. Although probably of no clinical significance, practicing pathologists should be aware of this peculiar histiocytic lesion of the fallopian tube to avoid misdiagnosis and unnecessary immunohistochemical testing.

Pathological findings in the postmortem liver of patients with coronavirus disease 2019 (COVID-19)

Although coronavirus disease 2019 (COVID-19) is transmitted via respiratory droplets, there are multiple gastrointestinal and hepatic manifestations of the disease, including abnormal liver-associated enzymes. However, there are not many published articles on the pathological findings in the liver of patients with COVID-19. We collected the clinical data from 17 autopsy cases of patients with COVID-19 including age, sex, Body mass index (BMI), liver function test (alanine aminotransaminase (ALT), aspartate aminotransaminase (AST), alkaline phosphatase (ALP), direct bilirubin, and total bilirubin), D-dimer, and anticoagulation treatment. We examined histopathologic findings in postmortem hepatic tissue, immunohistochemical (IHC) staining with antibody against COVID-19 spike protein, CD68 and CD61, and electron microscopy. We counted the number of megakaryocytes in liver sections from these COVID-19–positive cases. Abnormal liver-associated enzymes were observed in 12 of 17 cases of COVID-19 infection. With the exception of three cases that had not been tested for D-dimer, all 14 patients’ D-dimer levels were increased, including the cases that received varied doses of anticoagulation treatment. Microscopically, the major findings were widespread platelet-fibrin microthrombi, steatosis, histiocytic hyperplasia in the portal tract, mild lobular inflammation, ischemic-type hepatic necrosis, and zone 3 hemorrhage. Rare megakaryocytes were found in sinusoids. COVID-19 IHC demonstrates positive staining of the histiocytes in the portal tract. Under electron microscopy, histiocyte proliferation is present in the portal tract containing lipid droplets, lysosomes, dilated ribosomal endoplasmic reticulum, microvesicular bodies, and coronavirus. The characteristic findings in the liver of patients with COVID-19 include numerous amounts of platelet-fibrin microthrombi, as well as various degrees of steatosis and histiocytic hyperplasia in the portal tract. Possible mechanisms are also discussed.

Histiocytic hyperplasia with hemophagocytosis and acute alveolar damage in COVID-19 infection

The spectrum of COVID-19 infection includes acute respiratory distress syndrome (ARDS) and macrophage activation syndrome (MAS), although the histological basis for these disorders has not been thoroughly explored. Post-mortem pulmonary and bone marrow biopsies were performed in 33 patients. Samples were studied with a combination of morphological and immunohistochemical techniques. Bone marrow studies were also performed in three living patients. Bone marrow post-mortem studies showed striking lesions of histiocytic hyperplasia with hemophagocytosis (HHH) in most (16/17) cases. This was also observed in three alive patients, where it mimicked the changes observed in hemophagocytic histiocytosis. Pulmonary changes included a combination of diffuse alveolar damage with fibrinous microthrombi predominantly involving small vessels, in particular the alveolar capillary. These findings were associated with the analytical and clinical symptoms, which helps us understand the respiratory insufficiency and reveal the histological substrate for the macrophage activation syndrome-like exhibited by these patients. Our results confirm that COVID-19 infection triggers a systemic immune-inflammatory disease and allow specific therapies to be proposed.

English

The leaves of Piper guineense Schum. and Thonn (Piperaceae) are used in ethnomedicine for the management/treatment of various diseases. The objective of this study was to establish the pharmacognostic and toxicological profiles of P. guineense to help practitioners in making choices, and to assist scientists involved in the research of the Piper genus. The fresh leaves were examined for their macroscopic and microscopic properties. Numerical (quantitative analysis) and phytochemical evaluations were carried out using standard methods. Acute toxicity profile of the plant, including LD 50 was investigated using mice while sub-acute toxicity to determine effects of the plant leaf extract on some major organs was investigated for 30 days in rats. The macroscopic, microscopic and numerical features observed in the leaves of P. guineense could aid in sample identification. Glycosides, alkaloids and phenolics were among the secondary plant metabolites present. Oral doses ≤ 8000 mg/kg did not lead to death of the animals. Sub-acute toxicological evaluations at the doses of 250 and 500 mg/kg showed mild congestion in all the target organs, except spleen, where at 500 mg/kg, in addition to mild stromal oedema, there was mild follicular activation and moderate hyperplasia of sinus histiocytes. These results could aid researchers and practitioners in the investigations and consumption of the leaves of P. guineense. Its overall safety profile needs to be further evaluated and care should be taken on prolonged usage. Key words: Piper guineense, Piperaceae, pharmacognostic standardization, toxicological.

Pathology of the outbreak of subgenotype 2.5 classical swine fever virus in northern Vietnam

Classical swine fever (CSF) is an endemic disease in southeastern Asia and is one of the most important swine diseases in Vietnam. This study was conducted to characterize the pathology of natural cases of CSF in northern Vietnam in 2018 and their genetic prevalence. A total of 10 representative pigs were collected from four provinces (Hung Yen, Ha Noi, Quang Ninh and Thai Binh) during five outbreaks and examined pathologically. The gross and histopathological findings showed the disease was expressed as the acute or the subacute to chronic form of CSF, depending on the age of the animals. The most consistently observed lesions associated with infection by the classical swine fever virus (CSFV) included lymphoid depletions in tonsils, lymph node and spleen; histiocytic hyperplasia in spleen; cerebral haemorrhage; perivascular cuffing in the brain; renal erythrodiapedesis; urothelial vacuolation and degeneration and interstitial pneumonia. The immunohistochemical findings showed a ubiquitous CSFV antigen mainly in the monocytes/macrophages and in the epithelial and endothelial cells in various organs. CSFV neurotropism was also found in the small neurons of the cerebrum and the ganglia of the myenteric plexus. Analysis of the full‐length envelope protein (E2) genome sequence showed that all strains were genetically clustered into subgenotype 2.5, sharing a nucleotide identity of 94.0%–100.00%. Based on the results of this study, the strain was categorized as a moderately virulent CSFV.

Nodular histiocytic hyperplasia: A rare incidental finding that can be potentially misdiagnosed as malignancy

Introduction: Nodular histiocytic hyperplasia is a rare benign condition that occur most commonly in body cavities such pleura, peritoneum, pericardium and in hernial sacs. Morphologically, it comprises nodular florid proliferation of histiocytes which can mimic malignant neoplasms such as metastatic carcinoma and mesothelioma. Therefore, it is essential to recognize this entity to prevent a potential diagnostic pitfall.Aim: To familiarize pathologists with a rare entity to prevent a potential diagnostic pitfall. Material and Methods: A case of inguinal hernia sac with incidental nodular histiocytic hyperplasia was studied for detailed histopathological examination and expression of immunohistochemical markers. Results: Running a wide panel of immunohistochemical stains revealed that the proliferative cells are positive for the histiocytic markers CD68 and CD163 but negative for epithelial and mesothelial markers. Conclusion: Nodular histiocytic hyperplasia is a benign condition characterized by proliferation of histiocytes that were believed previously to be of mesothelial origin. It is essential to recognize this entity as it can be potentially misdiagnosed as a malignant neoplasm.

Neonatal Langerhans cell histiocytosis: a case report

We reported a case of neonatal Langerhans cell histiocytosis (LCH) with his clinical manifestations, examinations, diagnosis and treatment. This infant was hospitalized due to the rash and poor response. He was diagnosed as LCH after admission by imaging, skin biopsy and immunohistochemistry. The infant died because his parents refused all possible treatments. At the moment, no effective treatment is available for LCH patients, while the main managements are infection control and necessary supportive care. Pulmonary infections often contribute to the death of LCH patient and can aggravate the situation by stimulating histiocytic hyperplasia. Key words: Histiocytosis, langerhans-cell; Infant, newborn; Case reports

RUNX1 associated Familial Platelet Disorder with Myeloid Malignancy (FPD-MM) in Children: A Novel New Phenotype with Juvenile and Chronic Myelomonocytic Leukemia (JMML/CMML) Characteristics

Introduction:RUNX1 (aka AML1; 21q22.12) is indispensable in the establishment of definitive hematopoiesis in humans. Activating RUNX1 mutations are associated with both Acute Myeloid and Lymphoblastic Leukemias (AML, ALL). On the other hand, hypofunctioning RUNX1 mutations cause dominantly inherited Familial Platelet Disorder (FPD). RUNX1 FPD has a high risk for progression to pancytopenia, myeloproliferative disorders (MPD) or AML, hence the new WHO category FPD with myeloid malignancy (FPD-MM). Those with MM carry mutations in other genes seen in AML, MDS. It is a relatively rare disorder with ~75 affected kindreds reported worldwide (Sood, et al. Blood 2017). Detailed reviews of pediatric cases are few.Case Histories: We encountered two children with RUNX1 associated thrombocytopenia; the mutations are novel. The first family is that of 14 yr old AAF, presenting with fainting- blood counts are shown in Table 1; fetal hemoglobin (HbF) was elevated; bone marrow was hypercellular with 6% type 1 blasts, extreme paucity of megakaryocytes, erythroid hyperplasia and large numbers of sea blue histiocytes. The high HbF suggested JMML while the monocyte CD16;14 profile (95.6% CD14+ cells) was similar to that seen in the adult type Chronic Myelomonocytic Leukemia (CMML). Her mother has pancytopenia without excess blasts in the marrow. The second case presented with neonatal thrombocytopenia; father has history of excessive bruising.Results: Blood counts and values for HbF are listed in Table 1.Molecular testing:Case1: A Myeloid gene panel showed RUNX1 - NM_001754.4:c.501delT, p.Ser167Argfs*9; PHF6 - NM_032458.2:c.902dupA, p.Tyr301*; CUX1- NM_001202543.1:c.2378delC, p.Pro793Argfs*26. No mutations were noted in PTPN11, CBL or RAS genes, the latter confirmed by JMML panel done at University of California, San Francisco. UCSF panel identified a mutation in SH2B3, a gene linked to erythrocytosis not caused by JAK2 mutations. Her mother has the same RUNX1 mutation, thus identifying a germline mutation of RUNX1 in her and her child but not the PHF6, CUX1 or the SH2B3 mutations seen in her daughter. A half sibling is unaffected and is a potential transplant donor for the mother.Case2: No coding sequence mutations were detected in genes associated with familial thrombocytopenia including ETV6, GATA1 and RUNX1. Array Comparative Genomic Hybridization studies (Prevention Genetics) identified a heterozygous deletion of the entire exon 5 of RUNX1.To understand the complex findings in family 1 additional studies were done- DRAQ5, CD71, Fetal Hb staining showed that NRBC in Case 1 contained predominantly high HBF cells. LIN28B was markedly elevated in the proband but not the mother (HbF- normal); LIN28B expression was normal in Case 2.Treatment/Outcome: In Case 1, low dose decitabine therapy resulted in the control of MPD features with good Hb recovery and normalization of the monocyte CD16;14 profiles. There was no platelet response to decitabine nor to a course of valproic acid. The child died of fulminant acute graft vs host disease affecting the liver following a 4/6 cord mismatch transplantation. Mother continues to show moderately severe pancytopenia requiring frequent transfusion support. The second child is symptom free with mild thrombocytopenia.Discussion: The hybrid JMML/CMML features in the index child are likely caused by the concurrent CUX1/PHF6/SH2B3 mutations. We are unable to establish if these are true de novo mutations as the father was not available for study; she had no full siblings. Neither high HbF nor high LIN28B are known feature of FPD by itself nor CMML or Polycythemia Vera (p Vera). Recently, the high HbF in JMML has been linked to high expression of LIN28B. SH2B3 mutation may have contributed to the high erythroid proliferation observed in our case. Induced CUX1 haploinsufficiency in mice causes MPD akin to CMML and megakaryocytic (Meg) proliferation (An N, et al. Blood 2018). The virtual absence of Megs in our case indicates that the CUX1 mutation was unable to overcome the Meg ploidization defect caused by the RUNX1 mutation. PHF6 mutations occur in T-ALL and AML but have not been linked to high HbF.Conclusions: Normal HbF and normal LIN28B expression in the mother of Case1 and in Case2 indicate that increased LIN28B is linked to the high HbF in Case 1 and that high LIN28B itself is a consequence of the malignant transformation caused by the concurrent CUX1/PHF6/SH2B3 mutations. DisclosuresChitlur:Baxter, Bayer, Biogen Idec, and Pfizer: Honoraria; Novo Nordisk Inc: Consultancy. Ravindranath:AGIOS: Other: Site Investigator for Pyruvate Kinase Deficiency.

Chorionic Histiocytic Hyperplasia is Associated With Chronic Inflammatory Lesions in the Placenta.

Background Chorionic histiocytic hyperplasia (CHH) is a cellular proliferation at the base of the chorion that was identified by the authors in examining placentas for chronic chorioamnionitis (CC). This study is a retrospective review of cases diagnosed with CHH, describing its incidence alone and with associated lesions, and the immunophenotype of lesional cells. Design In this retrospective study, a laboratory information system search over a 34-month period using the key phrase "chorionic stromal" was performed. Cases identified were reviewed for presence of the following: CC, chronic villitis (CV), chronic deciduitis (CD), maternal (MIR), and fetal (FIR) acute inflammatory responses, meconium deposition; and whether CD3 immunostaining was performed. Incidences were tabulated and compared with known prevalences in our population. Select cases were stained with various immunostains to identify cell lineage and X and Y fluorescent probes to identify fetal or maternal cell origin in cases with male infants. Results Eighty cases of CHH were identified during the study period. Incidences of inflammatory lesions associated with CHH were: CV (54/80, 68%), CD (32/80, 40%), CC (25/80, 31%), MIR (39/80, 49%), and FIR (9/80, 11%). Only chronic inflammatory lesions had a significant correlation with the co-incidence of CHH. CC was identified alongside CHH in 12 of 22 cases in which a CD3 immunostain was performed. The cell population in CHH was vimentin+, CD68+, CD3-, CD45-, CD56-, hPL-, SMA-, OCT 3/4- and, in some cases, variably mixed with CD3+ lymphocytes. The cells had a male genotype by fluorescent in situ hybridization analysis. Conclusion The association of CHH with acute and chronic inflammatory conditions and its immunophenotype suggest that it may be a reactive process. CD3 immunostaining is helpful to identify concurrent CC.

Extracavitary primary effusion lymphoma associated with hemophagocytic lymphohistiocytosis.

Extracavitary primary effusion lymphoma associated with hemophagocytic lymphohistiocytosis.

Pelvic Nodular Histiocytic and Mesothelial Hyperplasia in a Patient with Endometriosis and Uterine Leiomyoma.

Nodular histiocytic and mesothelial hyperplasia (NHMH) is a rare and benign proliferative lesion composed of histiocytes with scattered mesothelial cells which was first reported in hernia sac by Rosai and Dehner in 1975 [1]. They described NHMH as a “benign reactive condition simulating a neoplastic process [1].” Since then, several cases have been reported in lung, pleura, inguinal region, urinary bladder, and pelvic cavity [2-9]. We report a case of incidentally detected NHMH, presenting as a pelvic nodule during laparoscopic surgery for uterine myoma and endometriosis.