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Performing injections with a bulking agent consisting of nonanimal stabilized hyaluronic acid and dextranomer is a well-tolerated and efficacious treatment for mild to moderate fecal incontinence. Here, we discuss a case of a patient with a history of a bulking procedure for fecal incontinence who presented to the obstetrics/gynecology clinic for evaluation of a new vaginal "cyst," which was excised. Histopathologic examination revealed migrated bulking agent within the excised specimen., Competing Interests: The authors declare no conflict of interest., (Copyright © 2021 by the International Society of Gynecological Pathologists.)

We describe a 53-year-old man in good general health who presented with an 8-month history of progressive gray hyperpigmentation of the face. He denied using any prescription medications; however, he admitted to taking a herbal supplement. Clinically, the differential diagnosis included hemochromatosis, Wilson's disease and hyperpigmentation secondary to supplement use. Punch biopsies from the left forehead and preauricular region showed heavily sun-damaged skin with a minimal inflammatory infiltrate. Closer inspection, however, revealed minute scattered black/brown particles distributed in the basement membrane zone of eccrine and sebaceous glands. Similar particles were also present in hair follicles, blood vessels and arrector pili muscles. The particles did not stain with Gomori methenamine silver, Fontana-Masson or iron stains. Electron microscopy with energy-dispersive x-ray analysis showed numerous particles, less than 1 µm in greatest dimension, which showed peaks for silver and sulfur. This analytical result confirmed the impression of argyria. Further history revealed that the patient had indeed been taking a silver supplement for several months under the premise that it would boost his immune system. This case is unique in that the patient's hyperpigmentation developed in a short period of time as compared with other reports in the medical literature., (Published 2011. This is a US Government work and is in the public domain in the USA.)

Background: Tens of thousands of Persian Gulf War veterans (GWVs) have presented with medical symptoms since Operation Desert Shield and Operation Desert Storm. The Kuwait Registry at the Armed Forces Institute of Pathology was established to act as a repository for surgical pathology, cytopathology, and autopsy material from GWVs., Objective: To identify conditions known to be endemic to the theater of operations in our cohort of GWVs., Methods: The Kuwait Registry database was searched by computer for listed conditions endemic to the Persian Gulf region included in the registry through December 31, 1997., Results: Of the 2582 patients in this cohort, 1 patient with hepatitis B and 15 patients with hepatitis C were identified. Other known endemic conditions of the Persian Gulf region were not found., Conclusions: Viral hepatitis (B and C), which is prevalent in the US population, was the only listed endemic condition identified in surgical pathology or cytopathology specimens in our cohort of GWVs.

Multinucleated giant cells (MNGCs) expressing the human immunodeficiency virus (HIV) are characteristically found in hyperplastic tonsils and adenoids, acquired immunodeficiency syndrome encephalitis, vacuolar myelopathy, and lymph nodes coinfected with opportunistic pathogens. We identified similar polykaryons in the hyperplastic gut-associated immune system of an HIV-infected patient. Colonic biopsy specimens from this patient with heme-positive stools were studied by light and transmission electron microscopy (TEM), immunohistochemistry, and in situ hybridization for HIV-specific RNA. No bleeding source was identified by endoscopic or light microscopic examination of the biopsied tissues. There was diffuse and nodular lymphoid hyperplasia with germinal centers. HIV RNA-positive and p24 gag-positive Langhans'-type MNGCs and mononuclear cells (MNCs) were present within the lamina propria The MNGCs and MNCs were identified as macrophages on the basis of TEM and expression of CD68, HAM56, and lysozyme markers. They also expressed S100 protein, a marker of dendritic/Langerhans' cells, but they lacked Birbeck granules by TEM. In situ hybridization demonstrated RNA expression by MNGCs, MNCs, and follicular dendritic cells. TEM revealed budding and mature HIV particles on the plasma membranes of MNGCs, MNCs, and follicular dendritic cells. We conclude, therefore, that hyperplastic gut-associated immune systems can contain HIV-positive MNGCs and MNCs of the type seen in tonsils and adenoids and opportunistic pathogen-infected lymph nodes. Associated with immune activation, macrophages can express markers of dendritic/Langerhans' cells, cell types derived from the same CD34-positive bone marrow progenitor.

Infection with the human immunodeficiency virus (HIV) and the subsequent derangement of host immunity place affected patients at risk for secondary infections. Some of the secondary pathogens occur with such frequency or are so rare in the non-immunosuppressed population that they have become part of the Centers for Disease Control and Prevention (CDC) classification for HIV/acquired immune deficiency syndrome (AIDS). Other infectious agents not yet included in the CDC definition are being reported in the HIV-infected population with increased frequency. General observations of the degree of immunosuppression associated with specific secondary infections have been useful in developing classification systems for HIV disease such as that of the CDC. However, the specific alterations in host immunity that promote infection with specific secondary pathogens are generally unknown. Geographic differences in the types and frequency of secondary infections also have been reported. Variation in strains of HIV, effect of malnutrition, lack of appropriate medical treatment, prevalence of virulent infectious diseases, and epidemiologic differences are possible contributing factors. Some infections that seemed likely to be closely associated with HIV infection have not occurred more frequently in HIV-infected patients. This review summarizes the histopathology of infectious conditions in the current CDC classification and highlights some conditions seen in HIV-infected individuals that are not currently HIV/AIDS-defining infections, yet may be seen by practicing pathologists.

Diagnostic anatomic pathologists play a crucial role in the battle against acquired immunodeficiency syndrome (AIDS). Not only are they intimately involved in the treatment of individual patients with human immunodeficiency virus (HIV) infection, but also they make important observations that result in the expansion of the scientific understanding of its pathogenesis. Pathologists studying tissue from patients with HIV infection should be familiar with the conditions to which these patients are susceptible. Although opportunistic infections are important causes of morbidity and mortality, noninfectious conditions frequently make substantial contributions to the disease course. Patients with HIV infection may be at increased risk for neoplastic disease. They do not, however, have an increased incidence of the most common tumors affecting the general population, such as breast, colon, and prostate carcinoma. Immunodeficiency results in increased susceptibility to malignant neoplasms, both by decreased immunologic response to abnormal cells and increased susceptibility to infection by viruses. All of the malignant neoplastic diseases that are Centers for Disease Control and Prevention (CDC) AIDS indicator conditions have been shown to have an association with a virus: Kaposi sarcoma (KS) with herpes hominis virus 8 (HHV-8), malignant lymphoma with Epstein-Barr virus (EBV), and cervical carcinoma with human papilloma virus (HPV). Patients with HIV infection also can develop reactive processes that are attributable to direct effects of HIV or immune system alterations. Such conditions include salivary gland cystic lymphoepithelial lesion, lymphadenopathy, lymphocytic interstitial pneumonitis, encephalopathy, enteropathy, nephropathy, hepatic conditions, dermatologic conditions and anemia.

Retinoids produce facial defects in chicken embryos. Outgrowth of the frontonasal mass with accompanying cartilage differentiation and pattern formation is inhibited. In contrast, the development of the mandibular primordia that give rise to the lower beak proceeds normally. To investigate whether the upper beak defect is based on the inhibition of cartilage differentiation specifically in the frontonasal mass, the effects of retinoids on chondrogenesis in micromass (high density) cultures of cells from facial primordia have been studied. When either 10(-6) M retinoic acid or 10(-8) M (E)-4-[2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-napthalenyl-1- propenyl]benzoic acid (TTNPB; a stable retinoid) is added to the culture medium, cartilage differentiation is inhibited. Both frontonasal mass and mandible cultures are equally affected. The concentration of TTNPB found in both facial primordia in vivo, after a treatment that produces the defect, is also about 10(-8) M. This rules out preferential accumulation of the retinoid by the frontonasal mass as an explanation for the defect. In fact, the concentration of retinoid found in vivo, should, from the culture studies, be sufficient to markedly inhibit chondrogenesis in both the frontonasal mass and mandibles. The effects of exposure to retinoids in the intact face appear to be different to those in culture. Furthermore, when cells from retinoid-treated facial primordia are cultured in micromass, the extent and pattern of chondrogenesis in frontonasal mass cultures is identical to that of cells from untreated primordia. Cartilage differentiation in mandible cultures is slightly affected. These findings suggest that retinoids do not produce the specific facial defect by directly interfering with cartilage differentiation.

Chondrogenesis of mesenchymal cells from the frontonasal mass, mandibles and maxillae of stage-24 chick embryos has been investigated in micromass (high-density) cultures. Distinct differences in the amount and pattern of cartilage differentiation are found. In cultures of frontonasal mass cells, a central sheet of cartilage develops; in cultures of mandible cells, less cartilage differentiates and nodules form; while in cultures of maxillae cells, virtually no chondrogenesis takes place. The same patterns of cartilage are found in cultures established from stage-20 embryos. At stage 28, frontonasal mass cultures form cartilage nodules and the number of nodules in mandible cultures is markedly decreased. There are striking parallels between the chondrogenic patterns of cells from the face and limb buds in micromass culture. The frontonasal mass cell cultures of stage-20 and -24 chick embryos resemble those established from the progress zone of limb buds. The progress zone is an undifferentiated region of the limb in which positional cues operate. Cultures established from the frontonasal mass of stage-28 chick embryos and from the mandibles of all stages resemble cultures of whole limb buds. These contain a mixture of committed and uncommitted cells. Ectoderm from facial primordia locally inhibits chondrogenesis in micromass cultures and this could provide a positional cue. The differences in chondrogenic potential of cells from facial primordia may underlie the specific retinoid effects on the frontonasal mass.