Pulmonary function and health-related quality of life after COVID-19 pneumonia.

BACKGROUND: The COVID-19 pandemic has led to many cases of pneumonia with extensive lung abnormalities on CT-scans. The consequences of COVID-19 pneumonia on survivors' pulmonary function and quality of life are unknown. The purpose of this study is to examine the impact of COVID-19 pneumonia on pulmonary function, health-related quality of life (HRQoL) and perceived dyspnoea. METHODS: A prospective longitudinal cohort study regarding patients discharged from our hospital after PCR-proven, non-critical COVID-19 pneumonia was conducted. Cases were classified as moderate or severe pneumonia according to WHO definitions. Six weeks post-discharge subjects underwent interviews and pulmonary function tests, and completed questionnaires to assess their HRQoL, perceived dyspnoea (Borgscale and mMRC), and symptoms of depression and anxiety (HADS). RESULTS: 101 patients were included. Twenty-eight (27.7%) pneumonias were classified as moderate cases of COVID-19 pneumonia and 73 (72.3%) were classified as severe cases. Diffusion limitation (DLCOc < 80% of predicted value) was found in 66 (71.7%) of 92 cases, obstruction in 26 (25.7%) of 101, and restriction in 21 (21.2%) of 99. Diffusion capacity was significantly lower in cases after severe pneumonia. In the entire group, HADS scores ≥8 for depression were found in 16.6% and in 12.5% for anxiety. Across all SF-36 domains, except for bodily pain, significant impairment was found. FEV1 and DLCOc showed significant positive correlations with mMRC scores and multiple SF-36 domains, especially physical functioning. CONCLUSION: COVID-19 non-critical pneumonia survivors have significant impairment in diffusion capacity and HRQOL six weeks after being discharged from hospital.

[Fever and hypotension after treatment of syphilis; the Jarisch-Herxheimer reaction]. / Koorts en hypotensie na behandeling van syfilis.

A 73-year-old man presented with fever and hypotension, which had developed a few hours after receiving treatment with benzyl-penicillin for secondary syphilis. These symptoms were due to the so-called Jarisch-Herxheimer reaction. The patient was admitted to hospital and treated with prednisone and intravenous fluids. Within 24 hours the patient had fully recovered. The symptoms, pathogenesis and treatment of Jarisch-Herxheimer reaction are discussed.

[A blood culture containing coagulase-negative staphylococci: not always due to contamination]. / Coagulasenegatieve stafylokokken in een bloedkweek.

Staphylococcus lugdunensis (SL) is a species belonging to the group of coagulase-negative staphylococci (CNS). It can cause severe infections such as endocarditis. Three cases of endocarditis caused by SL are presented. The first case describes a 71-year-old man with a fever and endogenous endophthalmitis. The second case describes delirium in an 87-year-old woman, thought to be due to pneumonia. The third case describes a 76-year-old man with an infection of unknown origin. In all cases, the first blood cultures drawn were positive for CNS and considered to be contaminated. However, all three patients were finally diagnosed as having severe endocarditis caused by SL. Two patients underwent valve replacement, one patient died due to ongoing sepsis. The first CNS-positive blood cultures drawn were wrongly denoted as being contaminated. Physicians should be aware of the pathogenic potential of SL and rule out contamination.

Impaired NO-dependent vasodilation in patients with Type II (non-insulin-dependent) diabetes mellitus is restored by acute administration of folate.

AIMS/HYPOTHESIS: Patients with diabetes are characterised by endothelial dysfunction and cardiovascular mortality. In particular endothelium-derived nitric oxide has emerged as a first line mechanism against atherosclerosis. Hyperglycaemia causes oxygen radical stress but has also been associated with endothelial nitric oxide synthase uncoupling, both lead to decreased nitric oxide-availability. We recently showed that folate reverses eNOS uncoupling in vitro. Therefore we hypothesise that folate improves endothelial function in Type II (non-insulin-dependent) diabetes mellitus in vivo. METHODS: Using forearm plethysmography, we evaluated the effect of local, intra-arterial administration of 5-methyltetrahydrofolate (5-MTHF, the active form of folic acid, 1 microg/100 ml FAV/min) on forearm blood flow in 23 patients with Type II diabetes and 21 control subjects, matched for age, sex, blood pressure, body mass index, weight and smoking habits. Serotonin as a stimulator of nitric oxide-dependent vasodilation and sodium nitroprusside as a stimulator of endothelium-independent vasodilation were infused. RESULTS: Serotonin-induced vasodilation was blunted (53+/-30 vs 102+/-66 M/C%, p<0.005) and nitroprusside-induced vasodilation was mildly reduced (275+/-146 vs 391+/-203 M/C%, p<0.05) in patients with Type II diabetes compared to control subjects. 5-MTHF improved nitric oxide-mediated vasodilation (from 53+/-30 to 88+/-59 M/C%, p<0.05) in patients with Type II diabetes mellitus. As expected, 5-MTHF had no effect on forearm blood flow in control subjects. CONCLUSION/INTERPRETATION: These data imply that folate can be used to improve nitric oxide status and to restore endothelial dysfunction in patients with Type II diabetes. Our results provide a strong rationale for the initiation of studies that investigate whether supplementation with folic acid prevents future cardiovascular events in this patient group.

Insulin-like and fibroblast growth factors in spinal cords, nerve roots and skeletal muscle of human controls and patients with amyotrophic lateral sclerosis.

Insulin-like growth factors (IGF-I and IGF-II) and fibroblast growth factors [acidic FGF (aFGF) and basic FGF (bFGF)] are trophic for motor neurones in vitro and (in laboratory animals) in vivo. An immunohistochemical investigation was performed on the distribution of these factors in the neuromuscular system of control patients and patients with amyotrophic lateral sclerosis (ALS). Comparisons were made with rat tissue. IGF-I immunoreactivity (IGF-I-IR) was seen in motor neurone cell bodies and axons, astroglia and Schwann cells, and in muscle fibres. IGF-II-IR was weak in all these cells. aFGF-IR was present in motor neurone cell bodies and axons, oligodendroglia and muscle fibres, but was not demonstrable in Schwann cells. bFGF-IR was present in motor neurone cell bodies and axons, and in astroglia, but was not seen in Schwann cells or muscle fibres. The distribution of the IGFs and FGFs in material from motor neurone disease (MND) and controls was similar. A role for any of these factors in the etiology of MND is, therefore, unlikely. IGF-I-IR and aFGF-IR were stronger in type II than in type I muscle fibres and were increased in denervated fibres. Species differences were found for IGF-I and bFGF. The function of these factors is apparently not entirely similar in humans and rats.