Amphetamine Misuse and Social Phobia

Abstract

Lithium carbonate is an effective, commonly used treatment for manic-depressive illness. The drug is known to produce a number of renal side effects, including impaired urinary acidification, polyuria, and impaired renal concentrating ability, which have been summarized elsewhere (1, 2). Lithium is a rare cause of nephrotic syndrome, a complication that reduces renal lithium excretion and precipitates lithium toxicity (1). We describe here a case in which the clinical features of lithium toxicity appeared after nephrotic syndrome, due to focal segmental glomerulosclerosis, developed in a patient treated with lithium. We report the case of a 59year-old woman with bipolar affective disorder.For 3 weeks Ms. A had been experiencing progressive lethargy and diarrhea. She was finally admitted to the hospital because of anemia and leukopenia of unknown origin. She had bipolar disorder, which had been well controlled for 3 years with a regimen of 2.5 mg/day of haloperidol, 50 mg/day of doxepin, 2 mg/day of biperiden, and 800 mg/day of lithium carbonate. There had been no recent change in her medication regimen. Three days after admission Ms. A developed cerebellar ataxia, dysarthria, and bilateral pleural effusions.The following laboratory values were noted: 6.9 g/dl of hemoglobin, 2.4 × 10 9 /liter of leukocytes, 52 mg/dl of urea, and 268 mg/dl of cholesterol. Both her electrolyte levels and creatinine values were normal. Ms. A's serum lithium level was markedly elevated at 1.9 mmol/liter (therapeutic range=0.6-1.2 mmol/liter). Her serum albumin level was 18 g/liter (normal range=36-47 g/liter). Her renal function had been normal during the previous 3 years of treatment. Her 24-hour urine protein excretion was 12.23 g (normal range: <0.15 g). Serum electrophoresis showed an increase in α 2 globulin, with no paraprotein detected. Antinuclear antibodies were absent. A renal biopsy analysis revealed focal segmental glomerulosclerosis. Ms. A's lithium therapy was discontinued, and her serum lithium level fell to 1.1 mmol/liter after only 2 days. Six weeks later her edema and effusions had completely disappeared, her serum albumin level had risen to 29 g/liter, and her 24-hour urine protein excretion had fallen to 3.19 g. After 3 months both her red and white blood cell counts had returned to normal, and her renal function had improved markedly, with only mild proteinuria (0.3 g/ 24 hours). The reason for her anemia and leukopenia remained unclear, despite a bone marrow biopsy.

The relationship between the characteristics of emotional regulation and social anxiety of persons dependent on psychoactive substances

“…По всей видимости, в это время на употребление ПАВ в наибольшей степени влияют склонность к поиску ощущений, склонность к гневу и психопатические черты в целом, протестность, низкий уровень конвенционального поведения, желание приобрести популярность, найти принятие в группе сверстников на фоне неблагополучной обстановки в родительской семье [5; 6]. Ситуация меняется во взрослом возрасте, когда обнаруживается значительная коморбидность социальной тревоги с употреблением ПАВ, что связывают с мотивами использования алкоголя и наркотиков для уменьшения собственных страхов [7][8][9][10]. Выход во взрослую жизнь связан со снижением материальной зависимости от родительской семьи, появлением многочисленных ситуаций экспертной оценки в профессиональной и личной сфере, где человек получает обратную связь по результатам собственных действий, значительно влияющую на его жизнь.…”

The response to sulpiride in social anxiety disorder: D2 receptor function

“…Conversely, drugs that reduce DA function, such as DA antagonists, have been reported to be associated with SAD symptoms in patients treated for Tourette’s syndrome (Mikkelsen et al, 1981; Scahill et al, 2003) and schizophrenia (Pallanti et al, 1999). There has also been a report of chronic amphetamine abuse (resulting in DA depletion) leading to the onset of social phobia (Williams et al, 2000).…”

O papel do sistema dopaminérgico na fobia social

“…11 Outras evidências de envolvimento do sistema dopaminérgico na fisiopatologia da FS provêm de estudos sobre abuso de substâncias. Williams et al (2000) relataram um caso de desenvolvimento de fobia social após abuso de anfetamina, que pode produzir depleção de dopamina no striatum, tanto em modelos animais quanto em humanos. 12 Após o uso crônico de 1,5 g de anfetamina quase diariamente por seis anos, a paciente descrita por Williams et al apresentou sintomas de ansiedade intensos desencadeados por situações sociais.…”

“…Williams et al (2000) relataram um caso de desenvolvimento de fobia social após abuso de anfetamina, que pode produzir depleção de dopamina no striatum, tanto em modelos animais quanto em humanos. 12 Após o uso crônico de 1,5 g de anfetamina quase diariamente por seis anos, a paciente descrita por Williams et al apresentou sintomas de ansiedade intensos desencadeados por situações sociais. Antes desses episódios, era uma pessoa extrovertida sem história psiquiátrica prévia.…”

“…As crises não tinham relação com a ingesta da droga. 12 Ainda que as anfetaminas diretamente induzam ansiedade, a depleção de dopamina pelo uso crônico deve ser considerada para a compreensão da fisiopatologia da ansiedade associada às situações de interação social. Entretanto, a liberação de dopamina pela ação aguda da administração de anfetamina correlaciona-se à euforia em voluntários normais, 13 reforçando os achados de experimentos com animais que demonstravam a relação da atividade das projeções dopaminérgicas mesolímbicas para estriado ventral com comportamentos de motivação e recompensa.…”