Osteocalcin and bone-specific alkaline phosphatase in Sickle cell haemoglobinopathies

Osteocalcin or bone gamma-carboxyglutamic acid (gla) protein and Bone-specific alkaline phosphatase (b-AP) total protein levels were evaluated as indicators of bone turnover in twenty patients with sickle cell haemoglobinopathies and in twenty normal healthy individuals. The serum bonespecific alkaline phosphatase total protein level was measured by immunoradiometric (IRMA) method. The concentrations of serum bone-specific alkaline phosphatase total protein were higher in the study group than in the control group (p < 0.05). The serum osteocalcin (BGP) showed no significant difference with the control healthy subjects. There was no correlation between the serum osteocalcin and serum bone-specific alkaline phosphatase total protein in the patient group. In conclusion, serum bone-specific alkaline phosphatase total protein determined or measured by IRMA can be considered a sensitive marker of bone turnover and could be especially useful as valuable non-invasive biochemical marker for identifying sickle cell patients with bone complications.Key Words: Bone-specific alkaline phosphatase (b-AP); Osteocalcin; sickle cell haemoglobinopathie

Severe Acute Respiratory Syndrome-Coronavirus-2 Infection [Sars-Cov-2 (Covid-19)]: A Review

The outbreak of the new coronavirus disease-2019 (COVID-19) in December 2019 in China spread worldwide or globally developing into an emergency of primary international concern. SARS-CoV-2 infection leads to groups of severe respiratory disease similar to severe acute respiratory syndrome coronavirus. Human-to-human transmission through droplets, contaminated hands or surfaces has been described, with incubation times of 2 to 14 days. Early diagnosis, quarantine, and supportive treatments are essential to cure patients. This paper reviews the literature on all accessible information about the epidemiology, currently applied laboratory diagnosis, as well as therapeutical management and vaccines to prevent, treat and control further outbreaks of SARS-CoV-2 infection. Keywords: COVID-19, Diagnosis, SARS-CoV-2, Therapeutic management, Vaccine

Osteocalcin and specific markers of bone resorption in sickle cell disease

Sickle cell disease commonly causes avascular necrosis of bone. Plain radiographs are not useful if obtained early in the disease. Radionuclide scans do not appear to increase the sensitivity of the diagnosis. Magnetic resonance imaging can detect disease but this is expensive and hard to employ on a routine or regular basis. The determination of the following new biochemical markers of bone metabolism has not been previously performed in sickle cell disease: serum osteocalcin (S-BGP), urinary cross-linked aminoterminal telopeptide of type I collagen (INTP or NTx) and urinary deoxypyridinoline (U∼DPD). As a first step or preliminary study we evaluate the usefulness of these biochemical markers of bone metabolism, by measuring the plasma or serum and urine levels of these markers in 20 adult patients with sickle cell disease. There was no change in S-BGP (p<0.9) a biochemical marker of bone formation. The two markers of bone resorption, urinary NTx (p<0.002) and U-DPD (p<0.001) increased highly significantly. Although the mean values of urinary NTx and U-DPD were significantly elevated in five patients with clinical evidence of bone complications, only two of these subjects had values above mean +2 SD of normal (control) mean values. Hence the sensitivity and specificity of these measures need to be further investigated with a larger sample size. There was significant correlation (P < 0.001) between NTx and U-DPD. These preliminary findings indicate that urinary NTx and U-DPD should be further investigated as possible biochemical markers of skeletal changes in SCD

Colchicine therapy for hepatic murine schistosomal fibrosis: image analysis and serological study

Colchicine in a dose of 200 μg kg body weight/day (5 days/week) was administered to groups of Schistosoma mansoni infected mice 12 weeks post infection, either alone or following previous praziquantel therapy at the 8th week of infection. Certain groups received colchicine for 6 weeks and others received it for 10 weeks. Colchicine alone did not significantly change the light microscopic appearance of schistosomal liver fibrosis, or hepatic collagen content estimated histomorphometrically, and did not reduce the elevated IL-2 serum level. Colchicine induced hepatic injury consisted of intense inflammatory reaction in granuloma and portal tracts, hepatocytic degeneration, and elevation of serum AST and ALT levels. Colchicine seemed to postpone granulomatous reaction healing and collagen deposition rather than inhibiting collagen formation or degrading it. Colchicine inhibited proliferation of hepatocytes of infected mice by expanding G2-M phases of cell cycle, thus reduced Ag NOR count and raised cell ploidy and cyclic AMP serum level. Subsidence of schistosomal infection by praziquantel prior to colchicine therapy greatly reduced inflammatory cellular reaction, significantly diminished hepatic collagen deposition and serum IL-2 level, minimized the elevated nuclear ploidy and cyclic AMP serum level that followed colchicine therapy when administered alone