A 56-year-old female with refractory adult-onset Still's disease presented with ocular herpes zoster infection during TCZ treatment. After three days of acyclovir treatment (5 mg/kg), she developed a severe headache and high fever. Viral DNA isolation and cerebral spinal fluid abnormalities led to a herpes zoster meningitis diagnosis. Her meningitis was cured by high doses of intravenous acyclovir (10 mg/kg for 14 days). To our knowledge, this is the first report of meningeal herpes zoster infection in rheumatic diseases under TCZ treatment.

Hypercapnia occurs in ventilated infants even if tidal volume (V T) and minute ventilation (V E) are maintained. We hypothesised that increased physiological dead space (V d,phys) caused decreased minute alveolar ventilation (V A ; alveolar ventilation (V A) × respiratory rate) in well-ventilated infants with hypercapnia. We investigated the relationship between dead space and partial pressure of carbon dioxide (PaCO 2) and assessed V A. Intubated infants (n = 33; mean birth weight, 2257 ± 641 g; mean gestational age, 35.0 ± 3.3 weeks) were enrolled. We performed volumetric capnography (V cap), and calculated V d,phys and V A when arterial blood sampling was necessary. PaCO 2 was positively correlated with alveolar dead space (V d,alv) (r = 0.54, p < 0.001) and V d,phys (r = 0.48, p < 0.001), but not Fowler dead space (r = 0.14, p = 0.12). Normocapnia (82 measurements; 35 mmHg ≤ PaCO 2 < 45 mmHg) and hypercapnia groups (57 measurements; 45 mmHg ≤ PaCO 2) were classified. The hypercapnia group had higher V d,phys (median 0.57 (IQR, 0.44-0.67)) than the normocapnia group (median V d,phys /V T = 0.46 (IQR, 0.37-0.58)], with no difference in V T. The hypercapnia group had lower V A (123 (IQR, 87-166) ml/kg/min) than the normocapnia group (151 (IQR, 115-180) ml/kg/min), with no difference in V E. Conclusion: Reduction of V A in well-ventilated neonates induces hypercapnia, caused by an increase in V d,phys .