Intriguing findings of liver fibrosis following COVID-19.

BACKGROUND: Studies on a new coronavirus disease (COVID-19) show the elevation of liver enzymes and liver fibrosis index (FIB-4) independently on pre-existing liver diseases. It points to increased liver fibrogenesis during acute COVID-19 with possible long-term consequences. This study aimed to assess liver fibrosis in COVID-19 patients by serum hyaluronic acid (HA) and FIB-4. METHODS: The study included the acute COVID-19 group (66 patients, 50% females, mean age 58.3 ± 14.6), the post-COVID group (58 patients in 3-6 months after the recovery, 47% females, mean age 41.2 ± 13.4), and a control group (17 people, 47% females, mean age 42.8 ± 11.0). Ultrasound elastography was performed in the post-COVID and control groups. RESULTS: Sixty-five percent of the acute COVID-19 group had increased FIB-4 (> 1.45), and 38% of patients had FIB-4 ≥ 3.25. After matching by demographics, 52% of acute COVID-19 and 5% of the post-COVID group had FIB-4 > 1.45, and 29% and 2% of patients had FIB-4 ≥ 3.25, respectively. Increased serum HA (≥ 75 ng/ml) was observed in 54% of the acute COVID-19 and 15% of the post-COVID group. In the acute COVID-19 group, HA positively correlated with FIB-4, AST, ALT, LDH, IL-6, and ferritin and negatively with blood oxygen saturation. In the post-COVID group, HA did not correlate with FIB-4, but it was positively associated with higher liver stiffness and ALT. CONCLUSION: More than half of acute COVID-19 patients had increased serum HA and FIB-4 related to liver function tests, inflammatory markers, and blood oxygen saturation. It provides evidence for the induction of liver fibrosis by multiple factors during acute COVID-19. Findings also indicate possible liver fibrosis in about 5% of the post-COVID group.

Targeting Microbiota: What Do We Know about It at Present?

The human microbiota is a variety of different microorganisms. The composition of microbiota varies from host to host, and it changes during the lifetime. It is known that microbiome may be changed because of a diet, bacteriophages and different processes for example, such as inflammation. Like all other areas of medicine, there is a continuous growth in the area of microbiology. Different microbes can reside in all sites of a human body, even in locations that were previously considered as sterile; for example, liver, pancreas, brain and adipose tissue. Presently one of the etiological factors for liver disease is considered to be pro-inflammatory changes in a host's organism. There are lot of supporting data about intestinal dysbiosis and increased intestinal permeability and its effect on development of liver disease pointing to the gut-liver axis. The gut-liver axis affects pathogenesis of many liver diseases, such as chronic hepatitis B, chronic hepatitis C, alcoholic liver disease, non-alcoholic liver disease, non-alcoholic steatohepatitis, liver cirrhosis and hepatocellular carcinoma. Gut microbiota has been implicated in the regulation of brain health, emphasizing the gut-brain axis. Also, experiments with mice showed that microorganisms have significant effects on the blood-brain barrier integrity. Microbiota can modulate a variety of mechanisms through the gut-liver axis and gut-brain axis. Normal intestinal flora impacts the health of a host in many positive ways, but there is now significant evidence that intestinal microbiota, especially altered, have the ability to impact the pathologies of many diseases through different inflammatory mechanisms. At this point, many of the pathophysiological reactions in case of microbial disbyosis are still unclear.

THINK PORPHYRIA: CASE REPORT AND REVIEW OF LITERATURE.

Porphyrias are a group of rare disorders caused by enzyme defects in haem biosynthesis pathway. Acute intermittent porphyria is the most common hepatic porphyria. The disorder presents with severe neuropathic abdominal pain that can be accompanied by a wide range of gastrointestinal, psychiatric and neurological symptoms, making the diagnosis clarification very challenging. We report a case of a 27-year-old female patient who presented with acute abdominal pain, vomiting and marked hyponatremia, developed seizures and disorientation, and eventually required intensive care unit treatment to maintain breathing. Her symptoms were initially misinterpreted as a functional gastrointestinal disorder, thus delaying the needed specific treatment. She was diagnosed a week after the initial hospital admission, and her condition improved after receiving treatment with intravenous glucose and haemin. For patients with acute neurovisceral attacks, early clinical recognition is essential. Severe hyponatremia, urine that develops orange colour on exposure to light and gastrointestinal symptom combination with neurologic symptoms are three valuable clues that may lead to the right diagnosis faster. Pathophysiology of hyponatremia in case of acute intermittent porphyria in only partly understood and can be associated with syndrome of inappropriate antidiuretic hormone secretion, gastrointestinal or renal sodium loss.

Current opinion on the management of iron deficiency anaemia in gastrointestinal diseases.

Iron deficiency is the most common cause of anaemia in the world. Despite frequently weak and masked clinical presentation of iron deficiency anaemia (IDA), this disease is very serious with complications leading to early mortality. In the developed countries IDA is predominantly diagnosed as the complication of another disease or as the result of major bleeding events. Diagnosis of IDA should be based on laboratory findings i.e. haemoglobin, mean corpuscular hemoglobin concentration and ferritin. Latter is the most sensitive marker for iron deficiency. Anaemia of chronic disease should be taken into an account as a potential differential diagnosis or coexisting state. For women in fertility age with IDA, gynaecological disorders should be ruled out first. Males and postmenopausal women with IDA should undergo upper, lower and in certain cases capsule endoscopy and/or enteroscopy to find a plausible cause of IDA. The ultimate goal of therapy is to find out and treat the primary cause of IDA. Iron body stores should be restored using either oral or parenteral iron preparations. The use of parenteral iron preparations in patients with gastrointestinal pathologies is often clinically substantiated for the treatment of IDA. Red blood cell transfusion should be administered in emergency cases only.

Gut colonization with extended-spectrum ß-lactamase-producing Enterobacteriaceae may increase disease activity in biologic-naive outpatients with ulcerative colitis: an interim analysis.

BACKGROUND: Certain Enterobacteriaceae strains have been associated with the development of ulcerative colitis (UC). Extended-spectrum ß-lactamase (ESBL)-producing Enterobacteriaceae are the most commonly found multi-drug-resistant (MDR) bacteria colonizing the gut in UC patients and might trigger a more severe disease activity in UC patients. OBJECTIVE: The aim of this study was to evaluate whether disease activity is higher in UC patients with gut colonization with ESBL-producing Enterobacteriaceae. MATERIALS AND METHODS: A cross-sectional, pilot study was carried out in a tertiary medical center in Latvia. Demographic data were collected; UC disease activity and extent were evaluated according to the full Mayo score, Montreal classification, and adapted Truelove and Witt's index. Rectal swabs with fecal biomaterial were collected, ESBL-producing Enterobacteriaceae were isolated, and bacterial plasmid genes responsible for ESBL production, blaCTX-M, blaTEM, and blaSHV, were detected. UC disease activity was compared in patients with and without gut colonization with ESBL-producing Enterobacteriaceae. RESULTS: A total of 65 patients with UC were included in the initial analysis. Gut colonization with ESBL-producing Enterobacteriaceae was found in seven (11%) patients - mostly Escherichia coli [5 (71%)] containing the blaCTX-M bacterial plasmid gene. Patients with gut colonization with ESBL-producing Enterobacteriaceae had more severe disease compared with patients without gut colonization according to the full Mayo score (5.86 vs. 3.40; P=0.015), Montreal classification (moderate disease vs. clinical remission; P=0.031), and adapted Truelove and Witt's index (moderate disease vs. mild disease; P=0.008). CONCLUSION: Gut colonization with ESBL-producing Enterobacteriaceae may increase UC disease activity. Further research is needed to analyze the possible confounding factors that could contribute toward this outcome.

Replication study of ulcerative colitis risk loci in a Lithuanian-Latvian case-control sample.

BACKGROUND: Differences between populations might be reflected in their different genetic risk maps to complex diseases, for example, inflammatory bowel disease. We here investigated the role of known inflammatory bowel disease-associated single nucleotide polymorphisms (SNPs) in a subset of patients with ulcerative colitis (UC) from the Northeastern European countries Lithuania and Latvia and evaluated possible epistatic interactions between these genetic variants. METHODS: We investigated 77 SNPs derived from 5 previously published genome-wide association studies for Crohn's disease and UC. Our study panel comprised 444 Lithuanian and Latvian patients with UC and 1154 healthy controls. Single marker case-control association and SNP-SNP epistasis analyses were performed. RESULTS: We found 14 SNPs tagging 9 loci, including 21q21.1, NKX2-3, MST1, the HLA region, 1p36.13, IL10, JAK2, ORMDL3, and IL23R, to be associated with UC. Interestingly, the association of UC with previously identified variants in the HLA region was not the strongest association in our study (P = 4.34 × 10, odds ratio [OR] = 1.25), which is in contrast to all previously published studies. No association with any disease subphenotype was found. SNP-SNP interaction analysis showed significant epistasis between SNPs in the PTPN22 (rs2476601) and C13orf31 (rs3764147) genes and increased risk for UC (P = 1.64 × 10, OR = 2.44). The association has been confirmed in the Danish study group (P = 0.04, OR = 3.25). CONCLUSIONS: We confirmed the association of the 9 loci (21q21.1, 1p36.13, NKX2-3, MST1, the HLA region, IL10, JAK2, ORMDL3, and IL23R) with UC in the Lithuanian-Latvian population. SNP-SNP interaction analyses showed that the combination of SNPs in the PTPN22 (rs2476601) and C13orf31 (rs3764147) genes increase the risk for UC.