A simple and durable way to create a supratarsal fold (double eyelid) in Asian patients.

BACKGROUND: Although non-incisional surgery to create a supratarsal fold (double eyelid) is preferred by Japanese patients, current procedures are either technically complex or do not produce lasting results. OBJECTIVE: We describe a new, non-incisional technique that makes use of double-armed sutures and twists to create double eyelids in Asian patients. METHODS: After everting the upper eyelid, a double-armed suture needle is passed from the conjunctival surface through the tarsal plate and then to the skin surface. The other end of the suture is advanced about 3 to 5 mm and also brought out through the tarsal plate. A second suture is used to create another U-stitch adjacent to the first suture. The upper eyelid is returned to its original position, and the sutures from the central hole are twisted around each other 4 or 5 times. They are then passed under the skin, one medially and one laterally, and the lateral and medial sutures are tied. RESULTS: The authors have performed 1108 procedures during the past 10 years with no loss of double-eyelid line in a mean follow-up time of 32 months. CONCLUSIONS: The double suture and twist technique for creating double eyelids in Asian patients is simple, reproducible, durable, and safe. (Aesthetic Surg J 2001;21:227-232.).

Unusual patterns of Histoplasma capsulatum meningitis and progressive multifocal leukoencephalopathy in a patient with the acquired immunodeficiency virus.

Disseminated histoplasmosis (DH) and progressive multifocal leukoencephalopathy occur in acquired immunodeficiency syndrome (AIDS). At autopsy, DH patients with central nervous system involvement almost always show extensive involvement of the lungs and reticuloendothelial system in addition to the brain, and progressive multifocal leukoencephalopathy is manifest as multiple demyelinating lesions in several locations in the brain. We describe an AIDS patient with a long history of aggressively treated DH who died with DH in the brain only; fungus was not found elsewhere at autopsy. In addition, there was a papovavirus infection restricted to the cerebellum with predominant involvement of the internal granular cell layer; again, demyelinating lesions were not found elsewhere in the brain. Each of these patterns of brain involvement is rare. As the incidence of AIDS increases and patients are treated aggressively, the frequency of unusual neuropathologic patterns of opportunistic infections may be expected to increase.

Human immunodeficiency virus-1 infection of the nervous system: an autopsy study of 268 adult, pediatric, and fetal brains.

The central nervous system (CNS) of 221 adults and 31 infants or children with the acquired immunodeficiency syndrome (AIDS) was examined with immunocytochemistry for infectious agents and for human immunodeficiency virus-1 (HIV-1) antigen (gp41). Since the major risk factor in this population was intravenous drug abuse, there were more female and pediatric patients than in other neuropathology autopsy series. Although children had a different spectrum of pathologic changes, including less frequent opportunistic infections, women did not differ from men in terms of types or incidence of opportunistic infections, vascular disease, neoplasia, and subacute AIDS encephalitis (SAE). Subacute AIDS encephalitis was detected in 26% of adult and 48% of pediatric brains. Immunocytochemical analysis of 100 adult and 20 pediatric brains revealed gp41 immunoreactivity in 78% and 40%, respectively. Virtually all adult brains with SAE had gp41 immunoreactivity in macrophages and microglia. Even brains with no significant pathology had frequent gp41 immunoreactivity, especially in the basal ganglia. In pediatric brains, including cases with SAE, gp41 immunoreactivity was less abundant, suggesting the possibility of latent infection or viral clearance. Spinal cords with vacuolar myelopathy or corticospinal tract degeneration had only rare gp41-positive cells. Brains from 16 aborted fetuses from HIV-1-seropositive women were all negative for gp41 immunoreactivity, but 12 brains were positive for HIV-1 by the polymerase chain reaction. These results may indicate that HIV-1 infection in fetal brains is below the limits of detection of immunocytochemistry. The differences noted between adults and children suggest that adults more often have productive CNS HIV-1 infection.

Microglia in human disease, with an emphasis on acquired immune deficiency syndrome.

In conclusion, there is overwhelming evidence that within the CNS the primary sites of active HIV-1 infection are microglia. CNS infection may be related to the normal repopulation of the CNS by monocytes (microglial turnover) that carry latent infection into the CNS. Activation of viral infection may depend upon microglial differentiation, soluble factors (cytokines), and/or coexistent infections. Infection of microglia may disturb the normal hemostatic balance that exists between microglia and other glia, and between microglia and neurons, processes that are only recently being explored at the molecular level. The impact that HIV infection of microglia may have on synaptic integrity is unknown. Cytokines appear to be prime candidates as mediators of some of the adverse effects of microglial infection on other CNS cells, myelin and endothelial cells.

Stroke in pediatric acquired immunodeficiency syndrome.

In a 4 1/2-year period, 4 of 68 children in a longitudinal study of neurological complications of human immunodeficiency virus (HIV) infection had clinical and/or neuroradiological evidence of stroke, yielding a clinical incidence of stroke in this population of 1.3% per year. During this period, 32 subjects died, and permission for autopsy was granted in 18 of the patients, including 3 of 4 who had clinical evidence of stroke. The prevalence of cerebrovascular pathological features in our consecutive autopsy series was higher than the clinical incidence. At autopsy cerebrovascular disease was documented in 6 (24%) of 25 children with HIV infection, including all 3 children who had clinical evidence of stroke. Four patients had intracerebral hemorrhages, 6 patients had nonhemorrhagic infarcts, and 3 had both. Hemorrhage was catastrophic in 1 child and clinically silent in 3 children, all of whom had immune thrombocytopenia. One child had an arteriopathy that affected meningocerebral arteries. In another child, the arteries of the circle of Willis were aneurysmally dilated. Two children had coexisting cardiomyopathy and subacute necrotizing encephalomyelopathy with vascular proliferation. These results suggest that stroke should be considered when children with HIV infection develop focal neurological signs.

Detection of HIV in fetal central nervous system tissue.

Neurological disease is a common finding in children with AIDS and in others without signs of disease but with evidence of congenital HIV-1 infection. To investigate the possibility that HIV-1 can infect fetal central nervous system (CNS) tissue and therefore possibly serve as the substrate for the abnormal neurodevelopment characteristic of pediatric AIDS, eight abortus CNS samples (one set of twins) from seven HIV-1-seropositive intravenous drug users (IVDUs) and eight control abortus CNS samples from eight HIV-1-seronegative IVDUs were analyzed for HIV-1 infection. HIV-1 nucleic acid was detected only after the use of polymerase chain reaction (PCR) in three of eight CNS samples from HIV-seropositive IVDUs but not in samples from seronegative subjects. In situ hybridization confirmed that HIV-1 DNA sequences were in cells in the CNS parenchyma of two of the three positive samples. This study demonstrates that HIV-1 can infect human fetal CNS tissue in vivo, but that the use of PCR may be necessary for its detection.

Appendiceal infection by Entamoeba histolytica and Strongyloides stercoralis presenting like acute appendicitis.

A 58-year-old male from Puerto Rico who was taking orally administered cortisone analogs for chronic obstructive pulmonary disease presented with fever, absolute eosinophilia, right lower quadrant pain, and rebound tenderness associated with Strongyloides stercoralis infection of the appendix. A 37-year-old alcoholic male developed fever, right lower quadrant abdominal pain, and rebound tenderness because of infection of the appendix with Entamoeba histolytica. These are the seventh reported case of isolated amebic appendicitis and the ninth reported case of appendiceal involvement with Strongyloides. In all these cases the diagnosis was made only after surgery. Patients with unexplained right lower quadrant pain, particularly if immunosuppressed or with an appropriate travel history, should have stool examinations for ova and parasites. Early diagnosis and treatment may prevent life-threatening complications such as perforation and peritonitis.

Cellular localization of an HIV-1 antigen in subacute AIDS encephalitis using an improved double-labeling immunohistochemical method.

Among 102 brains obtained from patients with acquired immune deficiency syndrome (AIDS), 34 cases with subacute AIDS encephalitis were characterized by immunohistochemistry using an antibody that binds to a human immunodeficiency virus-1 (HIV-1) envelope glycoprotein, gp41. This glycoprotein was detected in mononucleated and/or multinucleated cells in 90% of adult and 50% of pediatric brains with subacute AIDS encephalitis. In addition, many gp41-positive cells with bipolar or multipolar processes were found in 10 cases, and these cells occurred most frequently in the basal ganglia and internal capsule. The phenotype of the gp41-positive cells was determined using an improved double-labeling immunohistochemical technique that employed beta-galactosidase and peroxidase conjugated reagents. Cell-type specific markers for double-labeling included: Ricinus communis agglutinin-1 (RCA-1) for macrophages and microglia; Ulex europaeus agglutinin-1 for endothelium; anti-glial fibrillary acidic protein (GFAP) for astrocytes; anti-amyloid precursor protein for neurons; and anti-leukocyte common antigen for leukocytes. Results of double-immunostaining revealed that gp41-positive cells of all morphologic types, including cells with bipolar or multipolar processes, were double-labeled with RCA-1, but not with markers for astrocytes, neurons, or endothelia. These findings support the contention that HIV-1 infection of the CNS is predominantly restricted to cells of the macrophage/microglia lineage.

Morphology and distribution of HIV-1 gp41-positive microglia in subacute AIDS encephalitis. Pattern of involvement resembling a multisystem degeneration.

Among 100 brains from patients with acquired immunodeficiency syndrome (AIDS), 33 brains (21 adults and 12 children) with histological evidence of subacute AIDS encephalitis were immunostained with one of the most sensitive antibodies to HIV-1 antigen, anti-gp41. Twenty-six (20/21 adults, 6/12 children) of the 33 brains showed pg41 positivity. Brains from children had fewer gp41-positive cells than brains from adults. The distribution of gp41-positive cells was characteristic. They were frequently detected and most numerous in the globus pallidus (medial greater than lateral). Although gp41-positive cells were prevalent, fewer were detected in the corpus striatum and thalamus. Of infratentorial areas involved, the ventral midbrain, especially the substantia nigra, and the dentate nucleus contained many positive cells. Lower levels of infections, often patchy, were noted in the cerebral and cerebellar white matter and pontine base. Gp41-positive cells were rarely seen in the cerebral cortex, medulla, spinal cord, leptomeninges, choroid plexus, ependyma, subependymal areas and endothelia. Besides immunoreactive macrophages and multinucleated cells, gp41-positive microglia with various morphological alterations were abundant in the deep cerebral gray matter, ventral midbrain and dentate nucleus. Most of these microglia were undetectable with conventional histological methods. We discuss the significance of the distribution of HIV-1-infected cells, especially microglia, with respect to cellular tropism and involvement of deep gray matter nuclei in a pattern reminiscent of a multisystem atrophy.

[Role of attached gingiva in the extension of gingival inflammation. An experimental study in monkeys].

The purpose of this study was to evaluate the inflammatory response in dento-gingival units with or without attached gingiva in monkeys. Two different types of dento-gingival units with or without attached gingiva were established in premolar and first molar areas of three monkeys. In the experimental group, a part of the keratinized gingiva was removed with periodontal scissors following mucoperiosteal flap procedure, while in the control group, sham surgery was performed. After the surgery, plaque control was performed by mechanical tooth cleaning procedures three times a week for 3 months. As baseline examinations, width of the keratinized gingiva, probing pocket depth, position of the gingival margin, and the clinical attachment level were recorded and oral photographs were taken. Following these examinations silk ligatures were placed around the neck of the teeth to induce gingival inflammation in both the experimental and control groups. A soft diet which allowed plaque accumulation on the teeth was given during the experimental periods. The clinical examinations were carried out at 0, 1, 2, 3, 5 and 12 weeks and all monkeys were sacrificed for histological examination. The results obtained were as follows: 1. The use of silk ligature and a soft diet produced moderate to severe gingival inflammation in the monkeys. 2. The degree of gingival inflammation was greater in the experimental group which was characterized by the absence of the attached gingiva. 3. Marked marginal tissue recession with an apical shift of the attachment level was found in the gingival units of the experimental group at 12 weeks. 4. Histologically, a distance between the level of notch on the root surface and the most apical position of epithelial cell was greater in the experimental groups at 5 and 12 weeks, compared with the pre-experimental level. 5. The degree of alveolar bone resorption was higher in the experimental group at 5 and 12 weeks. These results suggest that an attached gingival tissue plays a certain role as a barrier against the extension of gingival inflammation.

Immunohistochemical localization of an HIV epitope in cerebral aneurysmal arteriopathy in pediatric acquired immunodeficiency syndrome (AIDS).

A 6-year-old boy with acquired immunodeficiency syndrome (AIDS) developed aphasia and quadriplegia 3 months before his death. Cerebral vascular ectasia and multiple cerebral infarcts were noted on premortem radiological studies. Postmortem evaluation revealed diffuse aneurysmal dilatation of the circle of Willis associated with fresh and organizing thrombi, destruction of the elastic lamina, and marked intimal fibroplasia. Multiple cerebral infarcts and subacute AIDS encephalitis with basal ganglia calcification were also present. Immunohistochemistry with a monoclonal antibody (anti-gp41) to human immunodeficiency virus (HIV) demonstrated positively stained cells in the arterial wall of the circle of Willis and in the cerebral parenchyma. Double immunostaining demonstrated that gp41-positive cells in the circle of Willis were also positive for a macrophage marker or leukocyte-common antigen, but not with an endothelial marker. Some macrophages or microglia in the cerebrum were also colabeled with anti-gp41. These results suggest that HIV may be directly involved in vascular pathology associated with pediatric AIDS.

Solitary midbrain toxoplasmosis and olivary hypertrophy in a patient with acquired immunodeficiency syndrome.

Toxoplasmosis, one of the most common central nervous system lesions in patients with the acquired immunodeficiency syndrome (AIDS), has not been reported as a solitary lesion in the brainstem. This report describes a patient with AIDS that presented with third cranial nerve palsy and contralateral cerebellar signs, who at autopsy had a necrotic midbrain lesion due to toxoplasma. Inferior olivary hypertrophy, due to interruption of olivary afferent fibers by the lesion, in addition to subacute encephalitis and vacuolar myelopathy were other CNS findings.

Central nervous system pathology in pediatric AIDS: an autopsy study.

The neuropathologic findings of brains and spinal cords removed at autopsy from 26 infants and children with AIDS is described; in two cases, only the spinal cords were available. The most common finding in the brains was dystrophic calcification of blood vessels of all calibers in the basal ganglia and deep cerebral white matter (21 og 24 cases). The next most frequent finding was subacute encephalitis (SE) (15 of 24 cases) with microglial nodules and multinulceated giant cells. Immunocytochemical and in situ hybridization studies showed HIV antigen or genetic sequences only in the brains of cases with SE. Multinucleated giants cells (MGC) were the most frequent cells with reaction products. MGC were labeled with ricinus lectin (RCA), but not with leukocyte common antigen (LCA) or glial fibrillary acidic protein. Many cells in microglial nodules were labeled with RCA, but not LCA; cells in the perivascular compartment were labeled with LCA, but not RCA. Corticospinal tract degeneration was noted in 15 of 20 spinal cords. In six cases tract degeneration was consistent with delayed myelination, and the remaining cases had axonal injury consistent with Wallerian degeneration. Opportunistic infections were rare (three cases). Central nervous system lymphoma occurred in three children and was the most common mass lesion. In two cases lymphoma occurred in the setting of a systemic polyclonal immunoproliferation possibly related to Epstein-Barr virus infection. Cerebrovascular accidents were noted in seven cases. Two cases had hemorrhage associated with immune thrombocytopenia; one hemorrhage was catastrophic. Two children had large vessel arteriopathy with multiple encephalomalacias. Two children had a necrotizing encephalopathy with encephalomalacia and vascular changes suggestive of a mitochondrial cytopathy.(ABSTRACT TRUNCATED AT 250 WORDS)