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Biomedical subjects

G O Rosenwasser

Publications and source records attributed to G O Rosenwasser.

At least 19 recordsLinked to original sources
PubMed1997

Herpes simplex blepharoconjunctivitis presenting as complete acquired ankyloblepharon.

PURPOSE: A 90-year-old woman was referred to us with a 1-month history of progressively worsening blepharoconjunctivitis. She had a complete acquired ankyloblepharon of the right lids, which resulted in the appearance of a right upper lid abscess on computed tomography. METHODS: Blepharotomy with separation and debridement of the lid margins was performed. RESULTS: Cultures were positive only for herpes simplex virus, type II. CONCLUSIONS: Herpes simplex blepharoconjunctivitis may take many clinical forms. Our patient's severe manifestations led to the clinical and radiologic appearance of preseptal cellulitis with a right upper lid abscess.

Aged↗
PubMed1996

Comparison of ciprofloxacin ophthalmic solution 0.3% to fortified tobramycin-cefazolin in treating bacterial corneal ulcers. Ciprofloxacin Bacterial Keratitis Study Group.

PURPOSE: The purpose of the study is to compare the clinical efficacy and safety of ciprofloxacin ophthalmic solution 0.3% (Ciloxan) with a standard therapy regimen (fortified tobramycin, 1.3%-cefazolin, 5.0%) for treating bacterial corneal ulcers. METHODS: This randomized, parallel group, double-masked, multicenter study was conducted in 324 patients at 28 centers in the United States, Europe, and India. Patients were randomized into 2 treatment groups: 160 to ciprofloxacin and 164 to fortified tobramycin-cefazolin. Positive microbiologic cultures were obtained in 188 (58%) of 324 patients. Of these, 176 patients met protocol criteria and were evaluated for treatment efficacy: 82 in the ciprofloxacin group and 94 in the standard therapy group. The dosing schedule for both treatment groups was 1 to 2 drops of the first study medication (ciprofloxacin or fortified tobramycin) every 30 minutes for 6 hours, then hourly for the remainder of day 1; 1 to 2 drops every hour on days 2 and 3; 1 to 2 drops every 2 hours on days 4 and 5, followed by 1 to 2 drops every 4 hours on days 6 to 14. The second medication (ciprofloxacin or cefazolin) was instilled 5 to 15 minutes after the first drug, following the same dosing frequency. Physician's judgment of clinical success, cure rate, changes in ocular sings, and symptoms and the rate of treatment failures were the primary efficacy criteria. RESULTS: Topical ciprofloxacin monotherapy is equivalent clinically and statistically to the standard therapy regimen of fortified antibiotics. No statistically significant treatment differences were found between ciprofloxacin (91.5%) and standard therapy (86.2%) in terms of overall clinical efficacy (P = 0.34). Similarly, no differences were noted in resolution of the clinical signs and symptoms (P > 0.08) or the time to cure (P = 0.55). The incidence of treatment failures was less in the ciprofloxacin group (8.5%) compared with the standard therapy group (13.8%). Significantly fewer patients treated with ciprofloxacin reported discomfort than did patients treated with the standard therapy regimen (P = 0.01). CONCLUSION: Ciprofloxacin ophthalmic solution 0.3% monotherapy is equivalent clinically and statistically to standard therapy (fortified tobramycin-cefazolin) for the treatment of bacterial corneal ulcers and produces significantly less discomfort.

Adolescent↗
PubMed1994

Three autosomal dominant corneal dystrophies map to chromosome 5q.

The two most common autosomal dominant dystrophies of the corneal stroma are lattice corneal dystrophy type I and granular dystrophy. A third autosomal dominant stromal dystrophy (Avellino) has also been recognized. Chromosome linkage analysis of four families with Avellino dystrophy mapped the disease-causing gene to chromosome 5q. Subsequent linkage analysis of two families with typical lattice dystrophy and two with typical granular dystrophy also revealed significant linkage with the same markers. Thus, each of three clinically and histopathologically distinct phenotypes is independently linked to 5q. The maximum combined lod score using all 114 affected patients was 28.6 with marker D5S393. None of the 14 known human amyloid-associated genes map to chromosome 5.

Alleles↗
PubMed1994

Phototherapeutic keratectomy in the treatment of Avellino dystrophy.

Avellino corneal dystrophy has rarely been reported in literature. It consists of a combination of granular and lattice dystrophy. Patients may complain of glare and decreased night vision with or without decreased visual acuity, depending on the degree of corneal involvement. Current treatment for this dystrophy includes bandage contact lenses for the erosions or corneal transplant in the case of decreased visual acuity. We describe the first patient with Avellino corneal dystrophy to have been treated with phototherapeutic keratectomy.

Aged↗
PubMed1993

Phenotypic variation in combined granular-lattice (Avellino) corneal dystrophy.

OBJECTIVE: To describe the phenotypic variation exhibited by members of families with combined granular-lattice (Avellino) corneal dystrophy. SETTING: We examined 40 patients (age range, 12 to 85 years) from six unrelated families with Avellino corneal dystrophy. This included the first individuals to ever be examined near the presumed site of origin in Italy. In addition, one family was the first to trace its origins to Germany rather than to Italy. We studied the phenotypic expression of the disease in the cornea, visual acuities, subjective complaints, complications, treatment, and histologic condition of these individuals. RESULTS: The granular stromal lesions reach their mature quantity and size early in life, and appear as either gray and crumb-shaped deposits or superficial with an annular and planar distribution. The lattice component appears gradually, beginning and maturing later in life. The phenotypic variation within families was found to be substantial. Widely variable proportions of lattice and granular changes were found within single sibships. Visual acuities ranged from 20/20 to 20/400. Recurrent corneal erosions were present but infrequent. Subjective complaints included glare and decreased night vision. Penetrating keratoplasty was required in one individual to restore vision. Histopathologic examination revealed typical amyloid and granular deposits. Granular deposits were found replacing Bowman's membrane and extending to the corneal surface. These deposits probably represent the cause of recurrent erosions. CONCLUSIONS: Combined granular and lattice corneal dystrophy may present with substantial phenotypic variation. The disease can be found in individuals who trace their ancestry to both Italy and Germany, a wider geographic distribution than previously proposed.

Adolescent↗
PubMed1990

Topical anesthetic abuse.

Topical ocular anesthetic abuse is a serious disorder causing keratitis and persistent epithelial defects. It may be the result of either prescription by the patient's eye care practitioner, theft from the practitioner's office, or occult additives in therapeutic medications. The authors report observations of six individuals suffering from this disorder which suggest that persistent epithelial defects, corneal stromal ring infiltrates, disproportionate pain, and prescription or nonprescription substance abuse may be factors involved. Penetrating keratoplasty was required to treat corneal perforation in two patients, and permanent corneal structural damage was noted in two eyes. Two eyes had a relentless downhill course culminating in enucleation. Because five of the six patients were diagnosed and treated as having presumed Acanthamoeba keratitis during the course of their disease, topical ocular anesthetic use should be included in the differential diagnosis of chronic keratitis and may masquerade as Acanthamoeba keratitis. The authors believe that practitioners should not prescribe or dispense topical anesthetics and should avoid clinical settings which provide an opportunity for the theft of topical ocular anesthetics.

Acanthamoeba Keratitis↗
PubMed1990

Presumed choroidal metastasis of Merkel cell carcinoma.

Merkel cell carcinoma is a rare skin tumor of neural crest origin and is part of the amine precursor uptake and decarboxylase system. It typically occurs on the face of elderly people. Distant metastasis is almost uniformly fatal. Choroidal metastasis, to our knowledge, has not been described. We report a patient with Merkel cell carcinoma who had a synchronous solid choroidal tumor and a biopsy-proven brain metastasis. Our 56-year-old patient presented with a rapidly growing, violaceous preauricular skin tumor. Computed tomography of the head disclosed incidental brain and choroidal tumors. Light and electron microscopy of biopsy specimens of both the skin and the brain lesions showed Merkel cell carcinoma. Ophthalmoscopy, fluorescein angiography, and A and B echography revealed a solid choroidal mass. The brain and skin tumors responded well to irradiation. A radioactive episcleral plaque was applied subsequently to the choroidal tumor. All tumors regressed, and the patient was doing well 28 months later. To our knowledge this is the first case of presumed choroidal metastasis of Merkel cell carcinoma.

Biopsy↗
PubMed1989

Merkel cell carcinoma. Long term survival in a patient with proven brain metastasis and presumed choroid metastasis.

Merkel cell carcinoma (Trabecular carcinoma) is a rare malignant tumor of the skin. Because these tumors tend to spread locally via the lymphatic system, very few papers have dealt with the treatment of distant metastasis. Systemic disease is uncommon and usually fatal. In this paper, we report a case of Merkel cell carcinoma with proven brain metastasis and a solid choroidal tumor. The patient responded well to radiation and chemotherapy and is alive and neurologically intact three years after diagnosis. All previous patients with metastatic Merkel cell carcinoma to the brain died within two months of the diagnosis. We use this case to discuss possible routes of metastatic dissemination and to review the treatment options in patients with distant metastatic disease. To our knowledge, this is the first reported case of presumed choroidal metastasis of Merkel cell carcinoma and the longest documented survival in a patient with brain involvement.

Brain Neoplasms↗
PubMed1989

Genetic linkage mapping of chromosome 17 markers and neurofibromatosis type I.

The von Recklinghausen neurofibromatosis (NF1) gene has been localized to the pericentromeric region of chromosome 17. We have screened six multigenerational families with multiple, tightly linked markers to aid in mapping this region of the chromosome. More than 150 members in six families were typed with probes including HHH202, D17Z1, EW203, EW206, EW207, EW301, pA10-41, D17S37, and D17S36. Two-point lod scores for NF1 versus all markers were calculated. HHH202 demonstrated the tightest linkage to NF1 with theta = .0, z = 3.86 (95% confidence limits [CL] of theta = .0-.13), suggesting that HHH202 be considered as a potential candidate marker for use in carrier detection and prenatal diagnosis. Pairwise marker-to-marker lod scores were used in examining the most likely order of subsets of the markers. Of those tested, the most likely order was (pter)-pA10-41-EW301-D17Z1-HHH202-NF1-E W206-EW207-EW203-(qter). In addition, we have ascertained an NF1 x NF1 half-cousin mating in which there are four affected family members who are potentially homozygous for the disease gene. Two of these four individuals have been sampled and typed for marker loci. When their D17Z1 genotypes are considered, the probability that both these individuals are heterozygous is 85%.

Chromosome Mapping↗
PubMed1987

Genetic linkage studies of chromosome 17 RFLPs in von Recklinghausen neurofibromatosis (NF1).

Recent localization of the gene for von Recklinghausen neurofibromatosis (NF1) to chromosome 17 has led to studies to identify additional tightly linked probes that can be used in defining the primary genetic defect in NF1. We have examined and obtained blood for DNA linkage studies on over 250 individuals from 10 multigeneration neurofibromatosis families. We have analyzed 130 members in 7 families with the available chromosome 17 NF1 linked probes, pE51, D17S71, and D17Z1, as well as two probes generated from our own chromosome 17/19 enriched library (LDR92, LDR152A). Tight linkage was found between NF1 and the centromeric probe D17Z1 (theta = 0.04) and between NF1 and D17S71 (theta = 0.08). A definite recombinant was seen for the D17Z1 marker, which previously had not exhibited crossingover. Chromosome 17 DNA markers pE51, LDR92, and LDR152A gave slightly positive scores, which were not statistically significant.

Chromosomes, Human, Pair 17↗
PubMed1986

Isolated anterior chamber relapse in acute monoblastic leukemia.

A case of acute monoblastic leukemia relapsing in the anterior chamber of the eye is described. Despite rigorous evaluation, no systemic or central nervous system involvement was detected. All previously reported cases of anterior chamber infiltrates in AML have had coexistent systemic or central nervous system disease.

Acute Disease↗