Carpal tunnel syndrome treatment

Carpal tunnel syndrome, the most common peripheral neuropathy, results from compression of the median nerve at the wrist, and is a cause of pain, numbness and tingling in the upper extremities and an increasingly recognized cause of work disability. If carpal tunnel syndrome seems likely, conservative management with splinting should be initiated. Moreover, it has suggested that patients reduce activities at home and work that exacerbate symptoms. Pyridoxine and diuretics, since are largely utilised, are no more effective than placebo in relieving the symptoms. Non steroidal anti-inflammatory drugs and orally administered corticosteroids can be effective for short-term management (two to four weeks), but local corticosteroid injection may improve symptoms for a longer period. Injection is especially effective if there is no loss of sensibility or thenar-muscle atrophy and weakness, and if symptoms are intermittent rather than constant. If symptoms are refractory to conservative measures, the option of surgical therapy may be considered.     

Alpha2-Heremans-Schmid glycoprotein/fetuin-A is associated with insulin resistance and fat accumulation in the liver in humans

OBJECTIVE: The alpha(2)-Heremans-Schmid glycoprotein (AHSG; fetuin-A in animals) impairs insulin signaling in vitro and in rodents. Whether AHSG is associated with insulin resistance in humans is under investigation. In an animal model of diet-induced obesity that is commonly associated with hepatic steatosis, an increase in Ahsg mRNA expression was observed in the liver. Therefore, we hypothesized that the AHSG plasma protein, which is exclusively secreted by the liver in humans, may not only be associated with insulin resistance but also with fat accumulation in the liver. RESEARCH DESIGN AND METHODS: Data from 106 healthy Caucasians without type 2 diabetes were included in cross-sectional analyses. A subgroup of 47 individuals had data from a longitudinal study. Insulin sensitivity was measured by a euglycemic-hyperinsulinemic clamp, and liver fat was determined by (1)H magnetic resonance spectroscopy. RESULTS: AHSG plasma levels, adjusted for age, sex, and percentage of body fat, were higher in subjects with impaired glucose tolerance compared with subjects with normal glucose tolerance (P = 0.006). AHSG plasma levels were negatively associated with insulin sensitivity (r = -0.22, P = 0.03) in cross-sectional analyses. Moreover, they were positively associated with liver fat (r = 0.27, P = 0.01). In longitudinal analyses, under weight loss, a decrease in liver fat was accompanied by a decrease in AHSG plasma concentrations. Furthermore, high AHSG levels at baseline predicted less increase in insulin sensitivity (P = 0.02). CONCLUSIONS: We found that high AHSG plasma levels are associated with insulin resistance in humans. Moreover, AHSG plasma levels are elevated in subjects with fat accumulation in the liver. This is consistent with a potential role of AHSG as a link between fatty liver and insulin resistance.     

Paraneoplastic encephalomyelitis: a case report and review of the literature

BACKGROUND: The incidence of paraneoplastic syndromes varies with tumor histology. Uterine sarcomas rarely cause paraneoplastic syndromes. Furthermore, paraneoplastic encephalomyelitis has never been reported to accompany a uterine leiomyosarcoma. CASE: A 44-year-old female developed an ANNA-1 paraneoplastic encephalomyelitis after a diagnosis of a uterine leiomyosarcoma. CONCLUSION: Paraneoplastic encephalomyelitis usually causes progressive neurologic decline. Treatment rarely alters this course.     

The DGAT2 gene is a candidate for the dissociation between fatty liver and insulin resistance in humans

The enzyme DGAT (acyl-CoA:diacylglycerol acyltransferase) catalyses the final step of triacylglycerol (triglyceride) synthesis. Mice overexpressing hepatic DGAT2 fed a high-fat diet develop fatty liver, but not insulin resistance, suggesting that DGAT2 induces a dissociation between fatty liver and insulin resistance. In the present study, we investigated whether such a phenotype also exists in humans. For this purpose, we determined the relationships between genetic variability in the DGAT2 gene with changes in liver fat and insulin sensitivity in 187 extensively phenotyped subjects during a lifestyle intervention programme with diet modification and an increase in physical activity. Changes in body fat composition [MR (magnetic resonance) tomography], liver fat and intramyocellular fat ((1)H-MR spectroscopy) and insulin sensitivity [OGTT (oral glucose tolerance test) and euglycaemic-hyperinsulinaemic clamp] were determined after 9 months of intervention. A change in insulin sensitivity correlated inversely with changes in total body fat, visceral fat, intramyocellular fat and liver fat (OGTT, all P<0.05; clamp, all P< or =0.03). Changes in total body fat, visceral fat and intramyocellular fat were not different between the genotypes of the SNPs (single nucleotide polymorphisms) rs10899116 C>T and rs1944438 C>T (all P> or =0.39) of the DGAT2 gene. However, individuals carrying two or one copies of the minor T allele of SNP rs1944438 had a smaller decrease in liver fat (-17+/-10 and -24+/-5%; values are means+/-S.E.M.) compared with subjects homozygous for the C allele (-39+/-7%; P=0.008). In contrast, changes in insulin sensitivity were not different among the genotypes (OGTT, P=0.76; clamp, P=0.53). In conclusion, our findings suggest that DGAT2 mediates the dissociation between fatty liver and insulin resistance in humans. This finding may be important in the prevention and treatment of insulin resistance and Type 2 diabetes in subjects with fatty liver.