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Biomedical subjects

H Lachkar

Publications and source records attributed to H Lachkar.

8 recordsLinked to original sources
PubMed2006

Thyroid disorders during interferon alpha therapy in 625 patients with chronic hepatitis C: a prospective cohort study.

AIM: to report the prevalence, risk factors, management and long-term outcome of thyroid disorders caused by INFalpha in patients with chronic hepatitis C. PATIENTS AND METHODS: From January 1991 to December 2004, 625 patients with chronic hepatitis C underwent INFalpha therapy. TSH assay was normal and antithyroperoxidase antibodies (anti-TPO) was performed before onset antiviral treatment; then TSH was performed every 2 months in all patients during therapy, and every 3 months after treatment. RESULTS: 58 patients developed thyroid disorder (8.9%). Mean age was 50.6+/-13 years; sex ratio: 1 M/2 F; the anti-TPO antibodies were positive before onset antiviral treatment in 9 patients (13.8%). 26 patients developed hypothyroidism (44.8%), 9 patients developed hyperthyroidism (15.5%) and among them 3 cases of Grave's disease. Biphasic thyroiditis occurred in 21 patients (36.2%), anti-TPO increase during treatment in 2 patients (3.5%) without hypothyroidism. The dysthyroidism was more frequent in risk in female gender (p<0.05) and in the group with positive antiTPO antibodies before treatment (p<0.02). CONCLUSION: Female gender and positive antiTPO antibodies are the predictive factors of development of the thyroid dysfunction during INFalpha therapy.

Antiviral Agents↗
PubMed1986

Trial of mild immunosuppression by methisoprinol in acute onset diabetes mellitus: effects on rate and duration of remission.

There is a lot of data that suggests the immune system plays a role in the pathogenesis of Type 1 DM. Methisoprinol, an immunomodulatory drug, has been reported as being efficient in preventing DM induced by a low dose of streptozotocin in mice. The efficiency of this drug in Type 1 DM was assessed by the rate and duration of remission obtained in recent acute onset DM by strict blood glucose control. We used 2 different therapeutic procedures successively: one was short in an anti-viral aim (50 mg/kg body wt. daily during 10 days) and the other longer given as immunomodulatory treatment (50 mg/kg body wt. daily during 2 weeks and 30 mg/kg body wt. daily during 4 weeks more) with reinduction (30 mg/kg body wt. daily during 4 weeks) every 5 months. No side effect was observed during the treatment. In both studies there was no improvement in the rate and duration of remission when compared to controls; residual beta-cell function was not increased after treatment by methisoprinol. Mild immunotherapy did not appear helpful in Type 1 DM.

Adolescent↗
PubMed1986

[Comparison of biosynthetic human insulin and purified pork insulin. Studies in insulin-resistant obese patients using the insulin suppression test].

An insulin suppression test performed in random order with either biosynthetic human insulin or purified pork insulin was used to compare biological activity of these two insulins in obese patients suffering from varying degrees of glucose intolerance. Blood glucose curve, steady-state blood glucose levels, insulin sensitivity indices and steady-state plasma insulin levels were identical during the two sets of tests. Furthermore endogenous insulin and glucagon secretion were similarly suppressed. The insulin suppression test is a simple and rapid procedure to compare the biological activity of fast-acting insulins. Our results confirm the insulin-resistance in obesity and clearly show that biosynthetic human and porcine insulins have similar biological potency.

Adult↗
PubMed1984

Plasma beta-thromboglobulin response to insulin-induced hypoglycemia in type I diabetic patients.

The effect of an insulin-induced hypoglycemia was examined in 14 type I diabetic patients. After an overnight blood glucose normalization, each patient received an additional intravenous bolus of 3 U regular insulin at 0900 h (time 0). Blood glucose was continuously recorded up to 180 min. Plasma samples were assayed for beta-thromboglobulin (beta TG, ng/ml), pancreatic glucagon (pg/ml), cortisol (microgram/dl), and growth hormone (ng/ml) 30 min before the insulin stress, at time 0, at blood glucose nadir, and at 180 min. The blood glucose fell from a baseline level of 85.0 +/- 3.2 mg/dl to a nadir value of 39.2 +/- 1.9 mg/dl (P less than 0.001) reached at an average time of 41.4 +/- 4.9 min. Plasma beta TG increased significantly (P less than 0.05) during the insulin stress: 93.4 +/- 23.7 ng/ml at nadir versus 42.5 +/- 5.9 at time 0. Plasma cortisol and growth hormone were significantly increased (P less than 0.02 and P less than 0.01) at nadir compared with time 0 values. Plasma pancreatic glucagon was higher at nadir than at time 0, but the difference was not significant. The present results indicate that in vivo platelet activation can be triggered by hypoglycemic episodes in insulin-treated diabetic patients.

Adolescent↗