Because no information is available on the use of systemic dexamethasone during breastfeeding, an alternate corticosteroid may be preferred, especially while nursing a newborn or preterm infant. Local injections, such as for tendinitis, would not be expected to cause any adverse effects in breastfed infants, but might occasionally cause temporary loss of milk supply.

This study aimed to investigate the role of ganoderma lucidum polysaccharides (GLP) in mitigating dexamethasone (DEX)-induced immune injury in goslings. Dexamethasone (DEX) is commonly used to establish an animal model of immune suppression, which mimics the immune injury caused by stress or certain pathological conditions in poultry. A total of 180 one-day-old goslings were randomly assigned to three groups: control (Con), DEX, and DEX + GLP, with six replicates of 10 goslings each. The Con and DEX groups were fed a basal diet, whereas the DEX + GLP group received feed supplemented with 0.2% GLP. From days 14 to 21, the DEX and DEX + GLP groups were injected with 3.5 mg/kg body weight (BW) of DEX, while the Con group received normal saline. Growth performance, immune organ indices, serum parameters, organ morphology, and intestinal microbiota were evaluated at 21 and 35 days. At day 21, the Con group exhibited significantly higher BW, average daily gain (ADG), spleen, thymus, and bursa indices, as well as serum total protein (TP), albumin (ALB), globulin (GLOB), IL-6, IgA, and IgG compared to the DEX and DEX + GLP groups (p < 0.01). By day 35, the DEX + GLP group demonstrated greater ADG than the DEX group (p < 0.01) and showed improved TP, ALB, and immune organ indices relative to DEX alone (p < 0.05). Histological analysis indicated that DEX induced bursa plica disorder, spleen parenchyma loosening, and thymus lobule atrophy, all of which were alleviated by GLP supplementation. Regarding the gut microbiota, the Con group displayed higher α-diversity at day 21 than the DEX group (p < 0.05), while at day 35, β-diversity in the DEX group differed markedly from that in the Con and DEX + GLP groups. Furthermore, DEX + GLP was associated with an enrichment of Bacteroidetes, Flavobacterium, and Lactococcus as microbial biomarkers. Overall, GLP effectively mitigated DEX-induced immune injury and partially restored growth performance by improving immune organ morphology, modulating serum factors, and reshaping gut microbiota.

Topical dexamethasone has not been studied during breastfeeding. Since only extensive application of the most potent corticosteroids cause systemic effects in the mother, it is unlikely that short-term application of topical corticosteroids would pose a risk to the breastfed infant by passage into breastmilk. However, it would be prudent to use the least potent drug on the smallest area of skin possible. It is particularly important to ensure that the infant's skin does not come into direct contact with the areas of skin that have been treated. Only the lower potency corticosteroids (e.g., hydrocortisone, triamcinolone) should be used on the nipple or areola where the infant could directly ingest the drugs from the skin. Only water-miscible cream or gel products should be applied to the breast because ointments may expose the infant to high levels of mineral paraffins via licking.[1] Any topical corticosteroid should be wiped off thoroughly prior to nursing if it is being applied to the breast or nipple area. Because absorption from the eye is limited, ophthalmic dexamethasone would not be expected to cause any adverse effects in breastfed infants. To substantially diminish the amount of drug that reaches the breastmilk after using eye drops, place pressure over the tear duct by the corner of the eye for 1 minute or more, then remove the excess solution with an absorbent tissue.

Indications for laparoscopic gynecologic surgery have been broadened. Although it is a rather noninvasive surgical procedure, it requires meticulous anesthetic management. Intraoperatively, hemodynamic and respiratory changes occur due to carbon dioxide insuf- flation, increased intraperitoneal pressure, and head- down position. Ventilator setting should be changed to cope with decreased chest-lung compliance and increased load of carbon dioxide during pneumoperitoneum in the head-down position. Mild hypercarbia may be per- mitted during this period to avoid ventilator-induced lung injury. Because the incidence of postoperative nausea and vomiting is high, it is recommended to use total intravenous anesthesia and prophylactic use of multiple antiemetics such as droperidol and dexameth- asone.

Purpose. To report a case of a patient with rheumatoid arthritis (RA) treated with tofacitinib citrate. Methods. Observational case report. Results. A 59-year-old patient, with a history of rheumatoid arthritis, on methotrexate 10 mg PO qwk and IV abatacept 750 mg/month, presented with photosensitivity, foreign body sensation, pain, redness, and blurry vision of her right eye (RE). Visual acuity of the RE was 20/200 and 20/20 of the left eye (LE). The slit lamp examination of the RE revealed dryness, 2+ injection of the conjunctiva, and pericentral ulceration of the cornea with 20-30% stromal thinning, pannus, and diffuse punctate epithelial erosions. The anterior chamber appeared normal. Laboratory values revealed elevated levels of rheumatoid factor, anticyclic citrullinated peptide antibodies, and C-reactive protein. The patient was switched to tofacitinib citrate 5 mg PO b.i.d, underwent corneal gluing, and was given prednisone acetate 1% gt TID, polytrim gt TID, neomycin-polymyxin-dexameth gt QD, FreshKote lubricant 1.8% gt QID, moxifloxacin 0.5% gt QID, and preservative free artificial tears Q1H. Within one week, laboratory values normalized, symptoms diminished, and the cornea reepithelialized. Conclusion. RA can present with ulcerative keratitis. Tofacitinib citrate, steroids, and corneal gluing were found to halt the progression of keratolysis and promote reepithelialization.