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Biomedical subjects

J D Gass

Publications and source records attributed to J D Gass.

At least 91 records · Page 5Linked to original sources
PubMed1991

Acquired pigmentation simulating Peutz-Jeghers syndrome: initial manifestation of diffuse uveal melanocytic proliferation.

A 74-year-old man with an occult carcinoma of the colon developed pigmentation of the mouth and penis typical of the Peutz-Jeghers syndrome as the first manifestation of bilateral diffuse uveal melanocytic proliferation. The simultaneous appearance of extraocular pigmented lesion and those in the uveal tract of both eyes of this patient provides further evidence that bilateral diffuse uveal melanocytic proliferation may be caused by activation of occult melanocytic naevus cells in response to either a hormone-producing carcinoma or to some other common oncogenic stimulus.

Adenocarcinoma↗
PubMed1990

Observations concerning patients with suspected impending macular holes.

Between September 1987 and April 1989, 18 patients (21 eyes) with suspected impending Stage 1 macular holes were referred to the Bascom Palmer Eye Institute. Only one patient had a Stage 1 hole. The others had an aborted stage of macular hole formation (eight eyes), Stage 2 holes (four eyes), a Stage 3 hole (one eye), or other lesions unrelated to hole formation. We believed that most of the apparently incorrect referring diagnoses were the product of incorrect interpretation of the biomicroscopic and fluorescein angiographic findings, and were not caused by changes occurring before our examination.

Fluorescein Angiography↗
PubMed1990

Bilateral diffuse uveal melanocytic proliferation in patients with occult carcinoma.

The development of multiple, round or oval, subtle, red patches at the level of the pigment epithelium in the posterior ocular fundus and their striking early hyperfluorescence angiographically are characteristic features of the bilateral diffuse uveal melanocytic proliferation syndrome. They may be accompanied by severe visual loss and may antedate the appearance of multiple melanocytic tumors, retinal detachment, and cataract in these patients with occult systemic carcinomas. These hyperfluorescent patches are caused by focal damage to the pigment epithelium overlying an intact choriocapillaris and diffuse benign nonpigmented uveal melanocytic infiltration of the outer choroid. We suggest that outer retinal damage may not be primarily caused by melanocytic proliferation, but rather by toxic and immune factors generated by interaction between a systemic carcinoma and congenital melanocytosis of the uveal tract. We report the longest survivor of this disorder to date (102 months).

Aged↗
PubMed1990

Purtscher's-like retinopathy after childbirth.

Severe bilateral visual loss attributable to multiple retinal arteriolar occlusions occurred in four young women within 24 hours after childbirth. In two patients, labor was complicated by preeclampsia requiring cesarean section. One patient was suffering from pancreatitis. None had connective tissue disease or antecedent trauma. Ophthalmoscopy and fluorescein angiography revealed evidence of multiple superficial peripapillary and macular patches of ischemic retinal whitening simulating Purtscher's retinopathy. By 8 weeks, the white patches were resolving in all eyes and visual acuity had significantly improved in three of the four patients. The pathogenesis of this disorder is unknown but may involve arteriolar obstruction by complement-induced leukoemboli formed during parturition.

Adolescent↗
PubMed1990

Acute syphilitic posterior placoid chorioretinitis.

Six patients with evidence of secondary syphilis presented with visual loss in both eyes caused by large, placoid, yellowish lesions with faded centers at the level of the pigment epithelium in the macula and juxtapapillary areas. All eyes had vitreitis. All of the lesions showed a similar fluorescein angiographic pattern of early hypofluorescence and late staining. Five patients had mucocutaneous lesions typical of secondary syphilis. All five patients treated with antibiotics had prompt improvement in visual function and resolution of the fundus lesions. The ophthalmoscopic and angiographic appearance of these posterior fundus lesions was sufficiently characteristic to suggest a diagnosis of secondary syphilis. Modification of the host response to syphilis by human immune deficiency virus (HIV) infection may be partly responsible for this peculiar fundus picture. Three of the four patients tested positive for HIV.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Surgical management of the idiopathic uveal effusion syndrome.

Twenty-three eyes of 20 patients with idiopathic ciliochoroidal effusion underwent quadrantic partial-thickness sclerectomies without decompression of the vortex veins. The mean postoperative follow-up interval was 41 months (range, 6-86 months). Resolution of subretinal and/or supraciliochoroidal fluid occurred within 6 months in 19 eyes (83%) after one procedure and in 22 eyes (96%) after one or two procedures. The mean interval to reattachment for the 19 successfully treated eyes with nonrhegmatogenous retinal detachment (RD) was 2.4 months compared with an average preoperative detachment duration of 18.5 months (P = 0.0005). Recurrences were seen in 23% of eyes; all resolved spontaneously or with a single reoperation. Final visual acuity was improved by two or more lines in 13 eyes (56%), stable in 8 (35%), and worse in 2 (9%). The efficacy of this surgical technique supports the hypothesis that an abnormality of transscleral protein transport plays a primary pathophysiologic role in this disorder.

Adult↗
PubMed1989

Choroidal neovascular membrane and other chorioretinal complications of acquired syphilis.

We reviewed ten patients who had posterior segment complications of acquired syphilis. Five of these patients had a neovascular membrane of the choroid associated with secondary or tertiary syphilis. Vision was stabilized after laser photocoagulation in one patient who had a choroidal neovascular membrane. Five additional patients had ocular manifestations including uveitis, optic neuritis, neuroretinitis, chorioretinitis, retinal hemorrhages, arterial and venous occlusion, vasculitis, and retinitis. Treatment of chorioretinal complications of syphilis with intravenous penicillin, if initiated early in the course of the disease, may result in excellent visual recovery.

Adult↗
PubMed1989

Acute macular neuroretinopathy and multiple evanescent white dot syndrome occurring in the same patients.

A young woman developed acute macular neuroretinopathy in one eye and five years later developed the multiple evanescent white dot syndrome in the same eye. Another young woman developed unilateral multiple evanescent white dot syndrome and central macular lesions typical of acute macular neuroretinopathy that appeared soon after the peripheral macular and juxtapapillary white lesions resolved. The findings in these two patients suggest that these two relatively rare syndromes may have pathogenetic and etiologic features in common.

Adult↗
PubMed1989

Protracted enlargement of the blind spot in multiple evanescent white dot syndrome.

Two patients had protracted blind spot enlargement, photopsia, and no optic disc edema. Both had fundus and fluorescein angiographic findings typical of multiple evanescent white dot syndrome that resolved within several weeks, leaving a persistent enlarged blind spot and photopsia. These clinical findings and an analysis of the literature data suggest that acute idiopathic blind spot enlargement without optic disc edema may be a subset of multiple evanescent white dot syndrome.

Adolescent↗
PubMed1989

Focal congenital anomalies of the retinal pigment epithelium.

The terms, 'hamartoma', 'choristoma', 'phacoma' (mother-spot), and 'naevus', are used to describe benign developmental tumours or placoid lesions. Stedman's Medical Dictionary defines a hamartoma as: 'A focal malformation that resembles a neoplasm grossly and even microscopically, but results from faulty development in an organ; it is composed of an abnormal mixture of tissue elements, or an abnormal proportion of a single element, normally present in that site, which develop and grow at virtually the same rate as normal components, and are not likely to result in compression of the adjacent tissue (in contrast to neoplastic tissue).' A choristoma is defined as 'a mass formed by maldevelopment of tissue of a type not normally found at that site.' Phacoma is defined as, 'a hamartoma found in phacomatosis,' a group of hereditary diseases characterised by hamartomas of multiple tissues. A naevus is a, 'birthmark; a circumscribed malformation of the skin, especially if coloured by hyperpigmentation or increased vascularity; it may be predominantly epidermal, adnexal, melanocytic, vascular, or mesodermal, or a localised overgrowth of melanin-forming cells arising in the skin early in life.' Ophthalmologists have adopted the term to refer to developmental melanocytic lesions of the uveal tract, but heretofore have not used it to describe developmental melanocytic, glial, or vascular lesions of the retina. The purpose of this report is to summarise the author's observations and concepts concerning focal lesions that probably are developmental tumours and placoid lesions composed of either entirely or in part retinal pigment epithelium (RPE). Two of the lesions are tumefactions and may properly be termed 'hamartomas'. Four of the lesions are placoid and might better be described as naevi. Two are composed of hypertrophied RPE cells engorged with melanin granules, one is presumed to be hypertrophied RPE cells filled with a white pigment of unknown nature and one is composed of RPE cells containing no pigment. Three are widely recognised, three others are not.

Adolescent↗
PubMed1988

Idiopathic senile macular hole. Its early stages and pathogenesis.

Evidence is presented that idiopathic senile macular hole is caused by focal shrinkage of the vitreous cortex in the foveal area. The most reliable biomicroscopic signs of impending hole formation (stage 1) are the development of a yellow spot or ring in the center of the fovea, loss of the foveal depression, and no evidence of separation of the vitreous from the foveal retina. Although in a majority of eyes with stage 1 changes there is a progression to hole formation, spontaneous separation of the vitreous without hole formation may occur in some cases (44%) and cause characteristic biomicroscopic changes, including foveal reattachment, disappearance of the yellow spot or ring, and, in some cases, a pseudo-operculum, with one or more lamellar holes or facets. A prospective collaborative study is recommended to confirm these findings and to test the clinical value of surgical peeling of the vitreous cortex in eyes with stage 1 changes as a means of preventing hole formation.

Aged↗
PubMed1988

Idiopathic macular holes. Observations, stages of formation, and implications for surgical intervention.

The authors have reviewed 158 eyes with evolving or completed idiopathic macular holes. Observations of these patients suggest that prefoveal vitreous cortex contraction is probably the cause of idiopathic macular holes. The earliest sign of an impending macular hole (stage 1) appears to be the development of a yellow spot or halo associated with loss of the normal anatomic foveal depression. No vitreous separation is present. This may resolve or progress to a small, early macular hole (stage 2). This hole gradually enlarged to a diameter of approximately 485 micron. The vitreous usually remained attached or a vitreofoveal separation developed (stage 3). Some eyes had complete posterior vitreous separation (stage 4). The implications for surgical intervention are discussed. A prospective study should be undertaken to confirm these findings and to investigate the feasibility of vitrectomy intervention to peel the prefoveal vitreous cortex in eyes with a stage 1 lesion.

Adult↗