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Introduction: Panton–Valentine leucocidin (PVL) is a bicomponent pore‑forming cytolytic toxin encoded by the lukF‑PV and lukS‑PV genes. Community‑acquired methicillin‑resistant Staphylococcus aureus (CA‑MRSA) may carry the pvl genes which may be related to increased disease severity. This study aimed to characterise the PVL‑producing MRSA recovered from different Taif Hospitals, Saudi Arabia. Methods: The study included 45 hospital‑acquired‑MRSA (HA‑MRSA) and 26 CA‑MRSA strains which were identified from 445 S. aureus strains isolated from different clinical samples. MRSA strains were identified by standard oxacillin salt agar screening procedure and by the detection of the mecA gene by the polymerase chain reaction (PCR). Detection of the S. aureus‑specific femA, mecA and pvl genes was performed by multiplex PCR. PCR‑restriction fragment length polymorphism (PCR‑RFLP) analysis was done for coagulase (coa) gene. Results: The staphylococcal cassette chromosome mec types of the 45 HA‑MRSA strains were Type I (n = 24), Type II (n = 7) and Type III (n = 14) whereas the 26 CA‑MRSA strains were Type IV (n = 14), Type V (n = 11) and one isolate was non‑typeable. All the HA‑MRSA and six CA‑MRSA strains were PVL‑negative PCR‑RFLP analysis of coa gene showed that PVL‑positive MRSA (n = 20) isolates showed six different patterns, and five patterns were shared by PVL‑positive methicillin‑susceptible S. aureus (MSSA). The eighth pattern was the most frequent in both MRSA and MSSA. Conclusion: PVL is more frequent among CA‑MRSA than MSSA. All the HA‑MRSA and 25% of CA‑MRSA strains were negative for PVL. The pvl gene was related to the severity of infection but not related to coa gene RFLP pattern.
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Helicobacter pylori is one of the most common chronic bacterial infections in diabetic patients due to alteration of glucose metabolism, abnormal emptying of the stomach and autonomic neuropathy. So, this study was done to determine H. pylori infection in diabetes, to evaluate the different diagnostic methods of its infection and to estimate the efficacy of he current antimicrobial therapy to eradicate H. pylori. The study involved 40 patients with diabetes mellitus [12 with type 1 and 28 with type 2], and 20 non-diabetic patients as control group. Their sera were used for the assay of H. pylori specific lgG and IgA by enzyme immunoassay [EIA]. Biopsy specimens were tested by rapid urease test [RUT], stained by Gram's stain and cultured to isolate H. pylori. Antimicrobial susceptibility testing was performed using Epsilometer test [E-test]. Results showed that there was a significant increase in the incidence of H. pylori in diabetic patients, 77.5% by RUT, 75% by culture, 70% by lgG, 50% by IgA and 20% by direct smear. There was a significant association between age and smoking and the presence of IgG and IgA. The specificity of the direct smear and IgA was 100%, the sensitivity of RUT was 100%, positive predictive value [PPV] of direct smear and IgA was 100%, negative predictive value [NPV] of RUT was 100%. H. pylori was highly sensitive to tetracycline [93.3%] and amoxicillin [73.3%] and relatively resistant to metronidazol [70%]. We concluded that H. pylon infection is more common among diabetic patients. Culture is the method of choice in diagnosis of H. pylori as it allows testing for antimicrobial therapy. EIA for anti-H. pylori lgG could be of value in screening population and in excluding H. pylori negative infections. Anti-microbial sensitivity must be performed for better eradication of H. pylori in diabetic patients
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Hyperthyroidism is accompanied by osteopenia or osteoporosis with higher incidence of fracture rates. There is paucity of data about the relation between the degree or duration of hyperthyroidism or its etiology and the resulting bone changes. The aim of the present work was to study bone status in patients with hyperthyroidism including biochemical markers of bone turnover and bone mineral density, and to elucidate the impact of severity, duration, and etiology of hyperthyroidism on biochemical markers of bone turnover and bone mineral density. Subjects and Thirty-six male patients with hyperthyroidism, 21 with Graves' disease and 15 with toxic multinodular goiter, with an age ranging from 23 to 65 years and a mean of 43 +/- 10 years, were included, together with 10 healthy men with matched age as a control group. In addition to full clinical examination, patients were subjected to radioisotope scanning and uptake of the thyroid gland with Tc 99,and DEXA scanning of the lower half of the left radius. Laboratory work up included serum free T3, free T4, TSH. Special assays done for patients and controls included serum total and B-ALP, serum OC, serum calcium, serum phosphorus urinary calcium, urinary DXP cross-links, urinary creatinine and calculated urinary DXP/urinary creatinine ratio. Biochemical markers of bone turnover were significantly higher in patients with Graves' disease compared to controls. Serum B-ALP was 9,5 +/- 5.6 KAU/I versus 2.2 +/- 0.8 KAU/I [P=0.00], serum OC was12.7 +/- 5 ng/dl versus 6.6 +/- 1.6 ng/dl [P=0.00], urinary calcium was 22.6 +/- 7.5 mg/dl versus15.5 +/- 5.1 mg/dl [P<0.05], and urinary DXP/urinary creatinine ratio was 12.6 +/- 5.5 versus 6.3 +/- 1.8 [P=0.00]. Biochemical markers of bone turnover were significantly higher in patients with toxic multinodular goiter compared to controls. Serum B-ALP was 4.3 +/- 2.6 KAU/I versus 2.2 +/- 0.8 KAU/I [P<0.05], serum OC was11.5 +/- 6.1 ng/dl versus 6.6 +/- 1.6 ng/dl [P<0.05], urinary calcium was 19.2 +/- 5 mg/dl versus15.5 +/- 5.1 mg/dl [P<0.05], and urinary DXP/urinary creatinine ratio was 13.5 +/- 7 versus 6.3 +/- 1.8 [P<0.05]. There was nonsignificant difference in the biochemical markers of turnover in patients with Graves' disease compared to those with toxic multinodualr goiter. Serum OC was 12.7 +/- 5 ng/d versus11.5 +/- 6.1 ng/dl, urinary calcium was 22.6 +/- 7.5 mg/dl versus 19.2 +/- 5 mg/dl, and urinary DXP/urinary creatinine ratio was 12.6 +/- 5.5 versus 13.5 +/- 7. However, serum B-ALP was higher in patients with Graves1 disease compared to those with multinodular goiter [9.5=/=5.6 KAU/I versus4.3 +/- 2.6 KAU/I [P< 0.05]. The Z -score at the lower half of the left radius in patients with Graves' disease [-1.7 +/- 0.5] was not significantly different from those with toxic multinodular goiter [-1.6 +/- 6]. Correlation between free T3 and biochemical markers of bone turnover revealed a significant positive correlation with all studied parameters: B-ALP [n= 0,37, P<0.05], serum OC [r= 0.62, P<0.05], urinary calcium [r=0.46, P<0.05], and urinary DXP/urinary creatinine ratio [r=0.52, P<0.05]. Correlation between free T4 and bone turnover markers revealed a significant positive correlation with B-ALP [r=0.43, P<0.05], serum OC [r=0.65, P<0.05], urinary calcium [r= 0.61, P<0.05], and urinary DXP/ urinary creatinine ratio [r=0.49, P< 0.05]. The duration of the thyrotoxic state did not correlate with the assessed bone turnover markers. However, the duration of the thyrotoxic state correlated significantly with the Z-score of the studied patients [r =0.68, P< 0.05]. The Z-score of the studied patients did not correlate with the free T3 and freeT4. Conclusions: It is concluded that men with hyperthyroidism have significant bone loss with higher biochemical markers of bone turnover. The severity of hyperthyroidism is directly related to the derangement of biochemical markers of bone turnover. Duration of the thyrotoxic state is related to the degree of bone loss. The etiology of the thyrotoxic state is not related to the degree of derangement in bone turnover markers or to the degree of bone loss