Corneal Densitometry and In Vivo Confocal Microscopy in Patients with Monoclonal Gammopathy—Analysis of 130 Eyes of 65 Subjects

Background: Corneal imaging may support an early diagnosis of monoclonal gammopathy. The goal of our study was to analyze corneal stromal properties using Pentacam and in vivo confocal cornea microscopy (IVCM) in subjects with monoclonal gammopathy. Patients and methods: In our cross-sectional study, patients with monoclonal gammopathy (130 eyes of 65 patients (40.0% males; age 67.65 ± 9.74 years)) and randomly selected individuals of the same age group, without hematological disease (100 eyes of 50 control subjects (40.0% males; age 60.67 ± 15.06 years)) were included. Using Pentacam (Pentacam HR; Oculus GmbH, Wetzlar, Germany), corneal stromal light scattering values were obtained (1) centrally 0–2 mm zone; (2) 2–6 mm zone; (3) 6–10 mm zone; (4) 10–12 mm zone. Using IVCM with Heidelberg Retina Tomograph with Rostock Cornea Module (Heidelberg Engineering, Heidelberg, Germany), the density of hyperreflective keratocytes and the number of hyperreflective spikes per image were manually analyzed, in the stroma. Results: In the first, second and third annular zone, light scattering was significantly higher in subjects with monoclonal gammopathy, than in controls (p ≤ 0.04). The number of hyperreflective keratocytes and hyperreflective spikes per image was significantly higher in stroma of subjects with monoclonal gammopathy (p ≤ 0.012). Conclusions: Our study confirms that increased corneal light scattering in the central 10 mm annular zone and increased keratocyte hyperreflectivity may give rise to suspicion of monoclonal gammopathy. As corneal light scattering is not increased at the limbal 10–12 mm annular zone in monoclonal gammopathy subjects, our spatial analysis provides evidence against the limbal origin of corneal paraprotein deposition. Using IVCM, stromal hyperreflective spikes may represent specific signs of monoclonal gammopathy

Fusarium és Sarocladium okozta fertőzések szemészeti vonatkozásai és azok kezelése

Absztrakt: A Fusarium-, Acremonium- és Sarocladium-gombafajok nevezéktana 2017-ben megváltozott. A morfológiailag homogén, de filogenetikailag heterogén fajokat, illetve fajkomplexeket ma már nukleinsav-összetételük szerint a MALDI–TOF MS-vizsgálat segítségével el lehet különíteni. Ez indokolta a taxonómiai besorolás módosítását. Közleményünkben a Fusarium- és Sarocladium-fajok okozta szaruhártya-gyulladás (keratitis) klinikai lefolyását ismertetjük, összefoglaljuk a diagnosztikus és kezelési lehetőségeket. Mindezek jelentős kihívást jelentenek a szemorvos számára. Súlyos szövődményekhez vezet a késői felismerés és kezelés, a folyamat gyors progressziója, a kórokozó átjutása a Descemet-membránon, a gombaellenes terápia korlátozott hozzáférhetősége és penetrációja, valamint a gyakori terápiarezisztencia. A diagnózis felállításához az anamnézisben szereplő trauma vagy kontaktlencse-viselés, PCR és MALDI–TOF MS-vizsgálat, konfokális mikroszkópia, a minta mikrobiológiai tenyésztése és a gyulladás területéből vett citológiai minta mikroszkópos vizsgálata vezet. A primeren választandó konzervatív terápia a lokálisan alkalmazott 5%-os natamicin, illetve esetenként érzékenység meghatározását követően az 1%-os vorikonazol vagy 0,15–0,25%-os amfotericin B szemcsepp, ezenkívül a 0,02%-os polihexametilén-biguanid (PHMB) szemcsepp használatának sikeréről is beszámoltak. Fusarium okozta keratitisben napi 2 × 200 mg vorikonazol tabletta adása is javasolt lehet. Terápiarezisztens esetekben korai, széles átmérőjű perforáló keratoplasztika (PKP) végzendő, épben történő trepanációval. Megkésett diagnózis és specifikus kezelés esetén a gombafonalaknak a Descemet-membránon történt átjutásával az esetek mintegy negyedében a látás elvesztése és a szemgolyó eltávolítása következik be. Jelen közleményünk öt, Fusarium- és Sarocladium-fajok okozta keratitis klinikai lefolyásának változatosságát is bemutatja. Orv Hetil. 2019; 160(1): 2–11. | Abstract: Since 2017, the nomenclature of Fusarium, Acremonium and Sarocladium species have changed, as these morphologically homogeneous, but phylogenetically heterogeneous species and species complexes may be differentiated using MALDI–TOF MS examination, analyzing nucleotic sequences. This resulted in taxonomical changes. We summarize the clinical course, diagnostic and therapeutic options of keratitis caused by Fusarium and Sarocladium. The challenge of Fusarium and Sarocladium keratitis management for an ophthalmologist lies in delayed diagnosis and therapy, fulminant progression and penetration of the Descemet’s membrane, restricted availability, poor penetration of antifungal agents and therapy resistance. The diagnosis is based on the clinical history of corneal trauma or contact lens wear, PCR and MALDI–TOF MS, confocal microscopic examination, microbiological culture and light-microscopic analysis of corneal scrapings. As primary conservative treatment, 5% natamycin eye drops have to be used and with results of an antimycogram, topical 1% voriconazole or 0.15–0.25% amphotericin B, in some cases 0.02% polyhexamethylene-biguanide (PHMB) may be applied. Fusarium keratitis may benefit from additional 2 × 200 mg oral voriconazole treatment, daily. In therapy resistant cases, early, large diameter penetrating keratoplasty (PKP) has to be performed, with complete removal of the infected area. With late diagnosis, delayed specific treatment and surgery, mycotic hyphae may penetrate the Descemet’s membrane, leading to the loss of vision and enucleation in about every fourth patient. In our paper, we also present the heterogeneous clinical history of five Fusarium and Sarocladium keratitis cases. Orv Hetil. 2019; 160(1): 2–11

Corneal Densitometry and In Vivo Confocal Microscopy in Patients with Monoclonal Gammopathy—Analysis of 130 Eyes of 65 Subjects

Background: Corneal imaging may support an early diagnosis of monoclonal gammopathy. The goal of our study was to analyze corneal stromal properties using Pentacam and in vivo confocal cornea microscopy (IVCM) in subjects with monoclonal gammopathy. Patients and methods: In our cross-sectional study, patients with monoclonal gammopathy (130 eyes of 65 patients (40.0% males; age 67.65 ± 9.74 years)) and randomly selected individuals of the same age group, without hematological disease (100 eyes of 50 control subjects (40.0% males; age 60.67 ± 15.06 years)) were included. Using Pentacam (Pentacam HR; Oculus GmbH, Wetzlar, Germany), corneal stromal light scattering values were obtained (1) centrally 0–2 mm zone; (2) 2–6 mm zone; (3) 6–10 mm zone; (4) 10–12 mm zone. Using IVCM with Heidelberg Retina Tomograph with Rostock Cornea Module (Heidelberg Engineering, Heidelberg, Germany), the density of hyperreflective keratocytes and the number of hyperreflective spikes per image were manually analyzed, in the stroma. Results: In the first, second and third annular zone, light scattering was significantly higher in subjects with monoclonal gammopathy, than in controls (p ≤ 0.04). The number of hyperreflective keratocytes and hyperreflective spikes per image was significantly higher in stroma of subjects with monoclonal gammopathy (p ≤ 0.012). Conclusions: Our study confirms that increased corneal light scattering in the central 10 mm annular zone and increased keratocyte hyperreflectivity may give rise to suspicion of monoclonal gammopathy. As corneal light scattering is not increased at the limbal 10–12 mm annular zone in monoclonal gammopathy subjects, our spatial analysis provides evidence against the limbal origin of corneal paraprotein deposition. Using IVCM, stromal hyperreflective spikes may represent specific signs of monoclonal gammopathy