Comparison of complications after Ahmed versus Baerveldt implant in glaucoma patients: one year follow-up

AIM: To compare surgical results of the Ahmed and Baerveldt implant procedures in glaucoma patients at 1y follow-up at Jakarta Eye Center (JEC) Eye Hospitals. METHODS: This cohort retrospective study was conducted on glaucoma patients aged ≥18y who had undergone Ahmed and Baerveldt implant surgery. Intraocular pressure (IOP), visual acuity, glaucoma medication, success rate, early and late postoperative complications, and the number of resurgeries were analyzed. RESULTS: A total of 351 eyes in the Ahmed group and 94 eyes in the Baerveldt group were included in this study. At 1y follow-up, the mean IOP was found to be significantly lower in the Baerveldt group (13±4.47 mm Hg) compared to the Ahmed group (15.02±5.73 mm Hg; P=0.025). Glaucoma medication was required in both the Ahmed and Baerveldt groups (58.92% vs 71.67%). Comparable success rate was found in both groups. The Ahmed group revealed a complete and qualified success of 86.82%, and failure of 13.17%. Similarly, the Baerveldt group showed complete and qualified success in 87.75% and failure in 12.25% cases. In the Ahmed group, 11.97% early complications, 26.06% late complications and 9.97% resurgeries were observed. In comparison, in the Baerveldt group, 23.40% early complications, 30.95% late complications and 11.70% resurgeries were observed. CONCLUSION: Both groups of glaucoma implants show significant IOP reduction, however, the Baerveldt implant group demonstrates greater IOP reduction with more failure rates and complications than the Ahmed implant group.     

Choroidal changes in eyes treated with high-dose systemic corticosteroids for optic neuritis

AIM: To analyze the effect of systemic high-dose corticosteroid on the choroid in patients with unilateral optic neuritis. METHODS: A retrospective comparative cohort study. Seventy-six eyes of 38 patients with unilateral optic neuritis that received systemic high-dose corticosteroid treatment were enrolled. Choroidal thickness (CT) and choroidal vascularity index (CVI) were measured in both affected and the fellow eyes at baseline, 1wk, 1 and 3mo. Changes in CT and CVI were analyzed in both eyes and compared between eyes. RESULTS: The mean CT and CVI were 349 μm and 0.70 in the affected eyes and 340 μm and 0.69 in the fellow eyes at baseline (P=0.503 and 0.440, respectively). Decrement of CT and CVI at month 3 were significant in affected eyes (P=0.017 and P<0.001). Decreased CVI began 2wk after treatment whereas CT decreased from 1mo. The CVI also decreased significantly in fellow eyes at 3mo compared to the baseline (P=0.001). CONCLUSION: A significant decrement in CT and CVI can appear after 3mo in optic neuritis patients treated with high-dose systemic corticosteroid treatment. The decrease in CVI appeared earlier than the decrease in CT, suggesting choroidal vasoconstriction caused by systemic steroid as a possible mechanism.     

Pneumothorax-associated pleural eosinophilia is tumour necrosis factor-alpha-dependent and attenuated by steroids

Background and objectives: The pathogenesis and the optimal treatment of eosinophilic pleural effusions are unknown. We aimed to examine whether pneumothorax‐associated pleural eosinophilia in mice is dependent on tumour necrosis factor (TNF)‐alpha, and whether it is affected by systemic administration of corticosteroids. Methods: Mice were injected intrapleurally with 0.4 mL air to create pneumothoraces. Animals were sacrificed 24 or 48 h later, and pleural lavage (PL) was performed. In the first experiment, comparisons were made between wild‐type and TNF‐α knockout mice with pneumothorax. In the second experiment, wild‐type mice were injected intraperitoneally with different doses of dexamethasone (0, 0.25, 0.5 and 1 mg/kg), 5 min before and 24 h after the induction of pneumothorax. Results: After induction of a pneumothorax, TNF‐α knockout mice had significantly fewer total number of cells (P = 0.004), mononuclear cells (P = 0.01), neutrophils (P = 0.017) and eosinophils (P = 0.002) in their PL compared with wild‐type animals. TNF‐α was detected in the PL of most of the control mice but not in TNF‐α knockouts. Dexamethasone induced a significant, dose‐dependent reduction of PL total cells (P < 0.001), eosinophils (P < 0.001), mononuclear cells (P = 0.007) and lymphocytes (P = 0.04) at 48 h, and significantly reduced the number of PL total cells (P = 0.045) and eosinophils (P = 0.005) at 24 h. Furthermore, dexamethasone prevented eosinophil infiltration of lung and pleural tissue. Conclusion: Pneumothorax‐associated pleural eosinophilia in mice is TNF‐α‐dependent and is significantly attenuated by corticosteroid treatment. In addition, both TNF‐α deficiency and dexamethasone treatment were associated with a significant reduction of other types of inflammatory cells in PL.     

The role of protein synthesis in adrenocorticotrophin action: Effects of cycloheximide and puromycin on the steroidogenic response of isolated adrenocortical cells

The kinetics of the corticosteroidogenic response to adrenocorticotrophin (ACTH) have been investigated using collagenase dispersed adrenocortical cells. Following the addition of ACTH at a concentration that was maximal for steroidogenesis, there was a time-lag of about 3 min before increased steroidogenesis became apparent. This lag was extended (about two-fold) in the presence of a half-maximal concentration of ACTH. Preincubation of cells with submaximal concentrations of both cycloheximide and puromycin extended the time-lag observed following ACTH addition. Increasing doses of cycloheximide or puromycin concomitantly inhibited protein synthesis and steroidogenesis. Moreover cycloheximide, at a dose that halved protein synthesis, also inhibited steroidogenesis by 54–61% for a range of ACTH concentrations (1 × 10⁻⁴ to 1 × 10⁻² I.U./ml).It is concluded that the delay before ACTH-stimulated steroidogenesis is not attributable solely to the time taken for ribosomes to read of from the mRNA strand, the code for protein regulator(s). The results are discussed in terms of steroidogenic mechanisms whereby ACTH either induces de novo protein synthesis or activates a pre-existing, but labile, protein. In this latter scheme the steroidogenic rate observed under various conditions would be directly dependent upon the intracellular level of such an activated protein regulator. The half-life of labile protein, implicated as regulating steroidogenesis, was estimated at 2–4 min in this adrenal cell suspension system.     

Cyclical etidronate increases bone density in the spine and hip of postmenopausal women receiving long term corticosteroid treatment. A double blind, randomised placebo controlled study

OBJECTIVE: To study the effect of cyclic etidronate in secondary prevention of corticosteroid induced osteoporosis. METHODS: A double blind, randomised placebo controlled study comparing cyclic etidronate and placebo during two years in 37 postmenopausal women receiving long term corticosteroid treatment, mainly for polymyalgia rheumatica (40% of the patients) and rheumatoid arthritis (30%). Bone density was measured in the lumbar spine, femoral neck, and femoral trochanter. RESULTS: After two years of treatment there was a significant difference between the groups in mean per cent change from baseline in bone density in the spine in favour of etidronate (p = 0.003). The estimated treatment difference (mean (SD)) was 9.3 (2.1)%. Etidronate increased bone density in the spine (4.9 (2.1)%, p < 0.05) whereas the placebo group lost bone (-2.4 (1.6)%). At the femoral neck there was an estimated difference of 5.3 (2.6)% between the groups (etidronate: 3.6% (1.4)%, p < 0.05, placebo: -2.4 (2.1)%). The estimated difference at the trochanter was 8.2 (3.0) (etidronate: 9.0 (1.5)%, p < 0.0001, placebo: 0.5 (2.3)%). No significant bone loss occurred in the hip in placebo treated patients. CONCLUSIONS: Cyclic etidronate is an effective treatment for postmenopausal women receiving corticosteroid treatment and is well tolerated.     

Cryptococcal meningitis accompanying lymphocytic inflammation predominantly in cerebral deep white matter: A possible manifestation of immune reconstitution inflammatory syndrome

Cryptococcal meningitis is rarely complicated by immune‐mediated leukoencephalopathy, but the precise pathomechanism is uncertain. A 72‐year‐old Japanese man treated with prednisolone for Sweet disease developed a subacute progression of meningitis, which was considered as neuro‐Sweet disease. A treatment by methylprednisolone rapidly improved CSF findings with a remarkable decrease in lymphocyte numbers in the blood, but the patient's consciousness still worsened after the cessation of the treatment. The patient developed cryptococcal meningitis and MRI showed abnormal intensities predominantly in the cerebral deep white matter along with the recovery of lymphocyte numbers in the blood, which resulted in death. A postmortem examination of the brain revealed degenerative lesions, especially at the cerebral white matter and cortex adjacent to the leptomeninges abundantly infiltrated by Cryptococcus neoformans. In the affected cerebral deep white matter, perivascular infiltration of lymphocytes was prominent in coexistence with reactive astrocytes and vascular proliferation, but these findings were not observed in the subcortical and cortical lesions. Cryptococcus neoformans was not present within the brain parenchyma. This is the first report of a case suggesting that cryptococcal meningitis can accompany lymphocytic inflammation predominantly in cerebral deep white matter as a possible manifestation of immune reconstitution inflammatory syndrome.