Opercular myoclonic-anarthric status epilepticus due to glutamic acid decarboxylase antibody-associated encephalitis.

We report a patient who was diagnosed with opercular myoclonic-anarthric status epilepticus and found to have glutamic acid decarboxylase antibody (GADA)-associated encephalitis, a previously unrecognised aetiology of this condition. The patient was a 23-year-old female admitted for investigation of focal myoclonic status epilepticus in the right side of the face and glossopharyngeal area. Intravenous corticosteroid was administered and improvement was observed in seizure activity and overall general health. A video sequence of opercular myoclonia is included. Due to the presence of inflammatory elements based on brain MRI and CSF studies, a decision to investigate autoimmune encephalitis was undertaken. Anti-GAD65 radioimmunoassay was markedly positive. This case study highlights the need for awareness of the clinical presentation of GADA-associated encephalitis. [Published with video sequences].

Clinical and biochemical evaluation of HIV-related lipodystrophy in an ambulatory population from the Hospital Universitário Cassiano Antonio de Morais, Vitória, ES, Brazil.

We designed a retrospective cohort study to identify factors associated with HIV-1 related lipodystrophy at a tertiary HIV-care center in Vitória, ES, Brazil. Inclusion criteria were documented HIV diagnosis, anti-retroviral therapy and age above 17 years. Highly active antiretroviral therapy (HAART) was initially the exposure variable, but a second analysis was also performed, as a nested case-control, based on the presence or absence of lipodystrophy. Use of protease inhibitors (PI) was associated with an increase in serum triglycerides (243.7 +/- 189 mg/dL vs. 172.7 +/- 131 mg/dL, p = 0.015), but not of total cholesterol (TC) or HDL fraction levels. Non-nucleoside reverse transcriptase inhibitors (NNRTI) were associated with an increase in serum TC (180.6 +/- 46.8 mg/dL versus 162.4 +/- 41.4 mg/dL; p= 0.018) and an increase in HDL cholesterol (47.3 +/- 13.8 mg/dL versus 23.3 +/- 24.3 mg/dL; p < 0.001), with no significant effect on triglyceride levels. Lipodystrophy was diagnosed in 59.3% of the patients, but exposure to PI versus NNRTI did not affect the frequency of this disorder (43.4% versus 37.2%; p = 0.68). Serum TC, but not HDL cholesterol or triglyceride levels, was higher among the lipodystrophy cases (183.8 +/-47.5 mg/dL versus 162.1 +/-35.7; p=0.006). Among the controls (patients without lipodystrophy), HDL cholesterol (45.3 +/-14.4 mg/dL vs. 27.1 +/-26.3; p=0.001)and triglyceride levels (178.3 +/-146.3 mg/dL vs. 126.3 +/-126.9; p=0.013) also increased, but not TC. In conclusion, lipodystrophy was highly prevalent in our series. Lipid disorders were also frequent and apparently were related to lipodystrophy, except for triglyceride levels.

Clinical and biochemical evaluation of HIV-related lipodystrophy in an ambulatory population from the Hospital Universitário Cassiano Antonio de Morais, Vitória, ES, Brazil

We designed a retrospective cohort study to identify factors associated with HIV-1 related lipodystrophy at a tertiary HIV-care center in Vitória, ES, Brazil. Inclusion criteria were documented HIV diagnosis, anti-retroviral therapy and age above 17 years. Highly active antiretroviral therapy (HAART) was initially the exposure variable, but a second analysis was also performed, as a nested case-control, based on the presence or absence of lipodystrophy. Use of protease inhibitors (PI) was associated with an increase in serum triglycerides (243.7 ± 189 mg/dL vs. 172.7 ± 131 mg/dL, p = 0.015), but not of total cholesterol (TC) or HDL fraction levels. Non-nucleoside reverse transcriptase inhibitors (NNRTI) were associated with an increase in serum TC (180.6 ± 46.8 mg/dL versus 162.4 ± 41.4 mg/dL; p= 0.018) and an increase in HDL cholesterol (47.3 ± 13.8 mg/dL versus 23.3 ± 24.3 mg/dL; p < 0.001), with no significant effect on triglyceride levels. Lipodystrophy was diagnosed in 59.3 percent of the patients, but exposure to PI versus NNRTI did not affect the frequency of this disorder (43.4 percent versus 37.2 percent; p = 0.68). Serum TC, but not HDL cholesterol or triglyceride levels, was higher among the lipodystrophy cases (183.8 ±47.5 mg/dL versus 162.1 ±35.7; p=0.006). Among the controls (patients without lipodystrophy), HDL cholesterol (45.3 ±14.4 mg/dL vs. 27.1 ±26.3; p=0.001)and triglyceride levels (178.3 ±146.3 mg/dL vs. 126.3 ±126.9; p=0.013) also increased, but not TC. In conclusion, lipodystrophy was highly prevalent in our series. Lipid disorders were also frequent and apparently were related to lipodystrophy, except for triglyceride levels.