Beta-endorphin is a neuroendocrine peptide, with morphine-like effects, produced by anterior pituitary, cells of the immune system, and synovial cells. The clinical significance of Plasma Beta-endorphin was investigated in a well characterized cohort of 20 RA patients and 10 healthy controls. Beta-endorphin extraction and concentration were carried out according to Wardlaw. Plasma Beta-endorphin assay was measured as described by Naber. Plasma Beta-endorphin levels in severe RA patients were significantly lower (16.1 +/- 6.2 pg/ml) than in mild RA patients (45.4 +/- 2.8 pg/ml), P < 0.0001. The mean serum levels of Beta-endorphin were also significantly lower in both RA groups than those in normal controls (62.1 +/- 5.7 pg/ml), P < 0.001. The results indicate that there is an inverse correlation with the plasma Beta-endorphin levels, the rheumatoid disease activity score, and the duration of RA. The depressed plasma Beta-endorphin in patients with RA may be used as an indicator of the disease activity.

Musculoskeletal pains are sometimes misdiagnosed in some diseases, like rheumatoid and psoriatic arthritis, erosive OA, etc. Secondary hyperparathyroidism was not considered a differential diagnosis for RA, despite the fact that it can cause arthralgia or arthritis. Also, fibromyalgia is a psychosomatic condition marked by widespread pain and tenderness. This study included 400 patients attended certain outpatient clinics of Rheumatology in Egypt and Saudi Arabia, who were not fulfilling criteria for RA diagnosis. Criteria for classification of fibromyalgia syndrome were applied to all patients. We did lab tests and radiological imaging modalities for diagnosis or exclusion of suspected diseases were applied. All patients were fulfilling both old and new criteria of fibromyalgia syndrome, and not fulfilling any RA criteria, and had vitamin D3 deficiency or insufficiency. 75% of patients had abnormally high levels of PTH, without parathyroid gland pathology. Radiology showed subperiosteal and subchondral resorption of mainly thumbs, subchondral osteopenia of proximal and middle phalanges, mild subperiosteal resorption along the radial aspect of the middle phalanx and mild tuft erosions, besides changes in the carpus closely resembling those of rheumatoid arthritis, of ulnar styloid resorption, radiocarpal and scapho-trapezoid joint arthritis. Of special interest, the presence of tuft spur-like excrescences.

COVID-19 shares some features of giant-cell arteritis, in which the diagnosis needs a high suspicion for prompt investigation and therapy. When the diseases coexist this might lead to diagnosis delay with grave consequences. We reported a case of a post-COVID-19 giant cell arteritis and polymyalgia rheumatica with visual loss. We treated the patient with pulse methylprednisolone 1 gm daily for 3 consecutive days followed by 60 mg prednisolone for 4 weeks until normalization of ESR, and then, gradual withdrawal. Oral Paracetamol, vitamin-D3, and calcium carbonate were added to the treatment regimen. The headache continued, so, we started perineural injection therapy (PIT) once daily, for 6 sessions, at which the headache was completely resolved after the third injection. The vision was regained completely after the sixth injection.

Background:Cadmium is a naturally occurring minor element; it has been recognized as an occupational health hazard for many decades. Water and food are the main source of environmental cadmium exposure in non-smokers in most parts of the world. Cadmium accumulates gradually in the human body, where it gives rise to a number of adverse health effects and especially to kidney and bone. Several studies have addressed a possible association between long-term low-level environmental cadmium exposure and osteoporosis. Osteoporosis is a large and escalating public health problem.Objectives:This study was conducted to assess the bone mineral status in secondary school students in Egypt and to measure cadmium level in their blood and urine and possible relationship between cadmium retention and bone mineral abnormalities as well as its consumption from some food and drinks commonly utilized by those students.Methods:Two hundred secondary school students from different secondary schools in Egypt were included in this study(100 males, and 100 females). Bone mineral status was assessed in the 200 students by Quantitative Ultrasonography (QUS) of the calcaneus using the ultrasound bone densitometer unit PEGASUS PRESTIGE, OSTEOMED, FRANCE. Students with abnormal bone mineral status (T score < -1) were considered osteopenic, data obtained from this osteopenic group were compared to those from a group of apparently healthy students with normal T score (T score ≥ -1).Results:Osteopenic group were 52 students (26%); 16 males and 36 females, their mean age was 15.46 ± 0.40 years. Cadmium level in blood and urine was significantly higher in osteopenic group. Interpretation of dietary habits in the osteopenic and control groups revealed that carbonated beverages, potatoes chips, corn snacks intake were significantly increased in osteopenic group, whereas no significant difference was detected in milk, tea, and coffee intake. T score was negatively correlated with blood cadmium, urine cadmium, as well as carbonated beverages, potatoes chips, corn snacks. Cadmium concentrations in tap water as well as in commercial mineral water were negligible, but its concentration in carbonated beverages, potatoes chips, corn snacks was relatively high.Conclusion:Osteopenia and osteoporosis are not uncommon problem among secondary school students in Egypt. Cadmium exposure, evident by high blood and urinary levels, is a risk factor for development of low BMD. Fault dietary habits, including increased carbonated beverages, potatoes chips, and corn snacks intake, contributes to the occurrence of osteopenia.References[1] Abdel-Haleem AS, Sroor A, El-Bahi SM, et al.: Heavy metals and rare earth elements in phosphate fertilizer components using instrumental neutron activation analysis. Appl Radiat Isot 55:569-573; 2001.[2] Abdel-Sabour MF: Cadmium status in Egypt. J Environ Sci (China) 13:351–360; 2001[3] Abou-Arab AA and Abou Donia MA: Heavy metals in Egyptian spices and medicinal plants and the effect of processing on their levels. J Agric Food Chem 48:...

Background:Cigarette smoking supposed to be a risk factor for osteoporosis. There is an inverse relationship between smoking and both bone mass and fracture risk. Tobacco smoking is the most important single source of cadmium exposure in the general population. The absorption of cadmium from the lungs is much more effective than that from the gut.Objectives:This study was designed to evaluate the effect of cigarette smoking on bone mineral density, due to cadmium toxicity.Methods:this study was carried on 100 persons, selected from AL-Azhar university hospital and divided into three groups: group I: included 40 persons with active smokers; group II: included 40 persons with passive smokers and group III included 20 nonsmokers. All persons were subjected to full history taking, thorough clinical examination, routine lab tests, serum and urinary cadmium and lead, and bone mineral density was measured by DEXA.Results:Serum and urinary cadmium and lead were statistically significantly higher in group I in comparison to groups II or III and in group II in comparison to group III. Also, there was statistically significant decrease of BMD in group I in comparison to either group II or group III and in group II in comparison to group III. There was an inverse statistically significant correlation between serum and urinary cadmium and bone mineral density.Abstract AB0984 – Table 1Comparison between studied groups as regard serum and urinary cadmium levels*=statistically significant decrease in comparison to group I or group II#=statistically significant decrease in comparison to group IConclusions:Results of the present study revealed that: there are harmful effects of smoking on the bone mineral density and it may be occurred by direct (increased blood and urinary levels of both cadmium and lead) or indirect effects (effects of both renal and liver functions) of cadmium and lead.References[1] Aoshima K, Katoh T, Kasuya M. Renal effects of environmental exposure to cadmium in middle-aged population of Jinzu River basin in Toyama, Japan: 2000–2002 study. Nippon Eiseigaku Zasshi2006;61:69–80.[2] Bernard A. Cadmium& its adverse effects on human health. Indian J Med Res2008; 128:557–64.[3] Bhattacharyya MH. Cadmium Osteotoxicity in Experimental Animals: Mechanisms and Relationship to Human Exposures. Toxicol Appl Pharmacol2009; 238(3): 258–265.[4] Hapidin H, Othman F, Soelaiman IN, Shuid AN, Luke DA, Mohamed N: Negative effects of nicotine on bone-resorbing cytokines and bone histomorphometric parameters in male rats. J Bone Miner Metab2007, 25(2):93–8.[5] Noël L, Huynh-Delerme C, Guérin T, Huet H, Frémy JM, Kolf-Clauw M. Cadmium accumulation and interactions with zinc, copper, and manganese, analysed by ICP-MS in a long-term Caco-2 TC7 cell model. Biometals. 2006; 19(5):473–81.[6] Satarug S. Long-term exposure to cadmium in food and cigarette smoke, liver effectsand hepatocellular carcinoma. Curr Drug Metab. 2012Mar; 13(3):257–71.[7] Schutte R, Nawrot TS, Richart T, Thijs L, Vanderschueren D, Kuznetsova T, Van Hecke E, Roels ...