Симптомы дефицита тестостерона

Symptoms and Signs Suggestive of Testosterone Deficiency in Men

More Specific Signs and Symptoms – Reduced libido – Erectile dysfunction (ED) – Reduced intensity of orgasm and genital sensation – Osteoporosis or low bone mineral density – Decreased spontaneous erection – Oligospermia or azoospermia – Very small or shrinking testes – Hot flushes, sweats – Breast discomfort, gynecomastia – Loss of pubic and axillary hair, reduced shaving Less Specific Signs and Symptoms – Decreased energy or vitality, increased fatigue – Depressed mood – Reduced muscle mass and strength – Poor concentration and memory – Sleep disturbance; increased sleepiness – Mild anemia – Increased body fat, body mass index – Diminished physical or work performance

Risks and Comorbid Illnesses Associated With Testosterone Deficiency

– Metabolic syndrome – Obesity – Hyperlipidemia – Hypertension – Elevated fasting plasma glucose and serum insulin – Elevated C-reactive protein – Diabetes mellitus (type 1 or 2) – Cardiovascular disease (including aortic atherosclerosis) – Chronic obstructive lung disease – Inflammatory arthritis – Low trauma fracture – End-stage renal disease – HIV-related weight loss – Hemochromatosis – Sellar mass, radiation to the sellar region, or other diseases of the sellar region – Chronic pain syndrome and treatment with opioids – Treatment with glucocorticoids – Radical prostatectomy

Low Testosterone Medscape CME Expert Column Series. Issue 1: Testosterone Deficiency in Men: Common and Under-recognized

Назначение антидепрессантов при депрессивной симптоматике в рамках деменций не целесообразно

Antidepressants may provide little benefit but appear to increase adverse side effects in individuals with dementia and comorbid depression, suggesting that clinicians should reconsider use of these agents in this population, new research suggests.

Antidepressants of Little Use in Dementia Patients

Психоиммунологические разработки в терапии депрессии

Для повышения эффективности лечения антидепрессантами, в том числе и сертралином, нами предложен комплекс средств патогенетической терапии больных с депрессивными расстройствами, целью применения которого является восстановление иммунного и метаболического гомеостаза.

На первой неделе лечения мы считаем весьма полезным назначение 1,5% соли янтарной кислоты как средства детоксикации и улучшения энергетического метаболизма, который у больных депрессиями существенно снижен. Соль янтарной кислоты обладает выраженным детоксицирующим, антигипоксическим, антиоксидантным, гепато-, нефро- и кардиопротекторным действиями, что обусловлено способностью препарата усиливать аэробный гликолиз, увеличивать внутриклеточный фонд макроэргических соединений — АТФ и креатинфосфата, а также активировать систему АОЗ, снижать выраженность процессов ПОЛ и оказывать мембраностабилизирующий эффект, в том числе в отношении клеток головного мозга. При умеренно выраженных депрессиях мы вводим по 400 мл 1,5% раствора соли янтарной кислоты 2–3 раза с интервалом 1–2 дня между инфузиями. При тяжелых депрессиях реамберин желательно назначать ежедневно по 400 мл на инфузию, а количество инфузий увеличить до 5–6. Клинический опыт показывает, что введение 1,5% раствора соли янтарной кислоты способствует улучшению самочувствия у больных депрессиями, уменьшению астенического компонента и чувства тревоги.

В комплексе лечебных средств у больных депрессиями с целью снижения выраженности СМИ мы широко используем положительно зарекомендовавший себя метод энтеросорбции. Пациенты с первого дня лечения получают современные кремнеземные энтеросорбенты отечественного производства (атоксил, энтеросгель, силлард П и др.) в виде 1–2% водной суспензии 2–3 раза в день в перерывах между приемами пищи и других лекарственных препаратов по 200–250 мл курсами по 10–12 дней с перерывами между ними 7–10 дней. При легкой степени депрессии обычно проводится 2 курса энтеросорбции, при умеренно выраженной — 2–3 курса, у больных с тяжелой депрессией назначают до 5–6 курсов энтеросорбции.

Для снижения активности ПОЛ и повышения антиоксидантных потенций крови у больных депрессиями применяют витамины с антиоксидантной активностью — аскорбиновую кислоту до 500 мг в сутки внутрь, а при тяжелых депрессиях также внутривенно в виде 10% раствора по 10 мл 2 раза в день на 40% глюкозе или изотоническом растворе хлорида натрия, токоферола ацетат по 0,2 мл 50% раствора внутрь в капсулах 2–3 раза в день, а при тяжелых депрессиях внутримышечно по 1 мл 10% раствора 1 раз в день в течение 20–40 дней. У больных с фоновой соматической патологией — при хронических гепатитах и начальной фазе цирроза печени — дополнительно назначаем внутрь современные препараты эссенциальных фосфолипидов: ливолин, ливенциале форте или эссенциале Н по 2 капсулы 3 раза в день курсами по 25–30 дней. При необходимости у больных с тяжелыми соматоформными депрессиями этот курс лечения эссенциальными фосфолипидами может быть повторен через 1–1,5 месяца.

Депрессивные расстройства: иммунные и метаболические нарушения и их коррекция

Монотерапия антидепрессантами (STAR*D vs CO-MED)

Perhaps the HAM-D as administered across the CO-MED sites did not adequately capture the element of symptom severity most relevant to the emergence of clear drug effects. The CO-MED study group contained far fewer subjects with melancholia than did either of the groups of Blier et al., and depressed patients with melancholic features have been shown to have higher severity ratings on global and other symptom-based measures in comparison to those without melancholia, despite having nearly identical HAM-D scores (9). Group differences were only somewhat larger in the CO-MED subset with melancholic features than in the patients without them. The performance of melancholia as a response predictor, though, varies considerably by how its components are defined and applied (10), and the CO-MED report does not state how melancholic symptoms were assessed. The relative scarcity of melancholia in the CO-MED patients nevertheless indicates a correspondingly lower severity level on some dimension.

A particularly striking feature of the CO-MED study group is the coexistence of the absence of treatment resistance, as specified by the entry criteria, and a high rate of chronicity. Although none of the participants had had an adequate monotherapy trial of an FDA-approved antidepressant within the current episode, over one-half of the group had a depressive episode that had been fully syndromal for at least the preceding 2 years. Why had they not undergone even one adequate antidepressant trial before the CO-MED effort came to pass? Whatever the answer, it seems likely that the average interval between episode onset and the receipt of first treatment was quite long. A number of prospective studies of major depressive disorder have shown the no-treatment interval to be as robust a predictor of poor outcome with treatment as neuroticism (11). Why this is so is a matter of speculation, but the measure's association with poorer treatment response generally may well have narrowed differences between the regimens applied here.

The Search for Improved Antidepressant Strategies: Is Bigger Better?

Treatment-resistant schizophrenia: What can we do about it?

Антиконвульсанты при тревожных расстройствах

Can Anticonvulsants Help Patients With Anxiety Disorders?

Lurasidone at 40 mg/day and 80 mg/day did not show a statistically significant improvement over placebo in PANSS total score change at the six-week study endpoint, despite a significant within-group reduction of the total PANSS score after treatment. This clinical trial is viewed as a failed study, as it was unsuccessful in establishing assay sensitivity. Despite the failure, company leaders believe they obtained useful data, which will assist with the design of future studies to support the registration of lurasidone in Japan.

Перспективные стратегии лечения когнитивной симптоматики шизофрении

A randomized, double-blind, placebo-controlled study demonstrated that members of a sarcosine (2 g/day) group showed greater reductions in their Positive and Negative Syndrome Scale (PANSS) total scores than members of a placebo group or D-serine (2 g/day) group, suggesting that sarcosine is superior to D-serine in that benefits both patients with long-term stable disease and also acutely ill persons with schizophrenia .

Furthermore, a randomized, double-blind study reported that sarcosine (2 g/day) alone was effective in the treatment of acutely symptomatic drugfree patients with schizophrenia.

Nonetheless, all these findings suggest that GlyT-1 inhibition could be a novel pharmacotherapeutic target for enhancing cognitive dysfunction in schizophrenia and several clinical trials are underway with very promising results.

Gaining a better understanding of the role of GlyT-1 in the treatment of cognition in schizophrenia is expected to provide new perspectives for treating this disorder. The pharmacological modulation of glycine modulatory sites on NMDA receptors by GlyT-1 inhibitors could be beneficial in the treatment of the cognitive deficits and psychosis associated with schizophrenia and other psychiatric conditions.

Galantamine, which acts as both a cholinesterase inhibitor and a nicotinic receptor modulator had the best result. The cognitive effects of galantamine may be accentuated by its nicotinic allosteric agonist action, which can improve attention and memory. Furthermore, galantamine appears to more powerfully elevate frontal cortical dopamine levels than cholinesterase inhibitors such as donepezil. This biological effect may be significant since frontal dopaminergic deficits have been proposed to underlie cognitive impairment in schizophrenia.

Importantly, significant improvement in attentional set shifting was seen. Modafinil may have potential as an important therapy for cognitive impairment in patients with schizophrenia, particularly because of its beneficial effects on attentional set shifting.

Patient with schizophrenia manifest signs of a dysregulation of the NPY system. Extensive preclinical studies suggest that the neuropeptide Y (NPY) counteracts the behavioral consequences of stress and anxiety to and maintain emotional homeostasis. Thus it is involved in stress regulation and coping.

Treatment of Cognition in Schizophrenia

Депо-формы классических антипсихотиков превосходят по эффективности пролонгированную форму рисперидона

In a large population-based cohort study, conventional depot antipsychotics turned out to be superior to risperidone long-acting injection, Danish researchers reported here at the New Clinical Drug Evaluation Unit (NCDEU) 51st Annual Meeting, sponsored by the American Society of Clinical Psychopharmacology.

Older Antipsychotics Trump Newer Agents for Schizophrenia

Blepharospasm as an Obsessive-Compulsive Phenomenon

Маниакальная симптоматика ассоциированная с приступами мигрени

This is a case report of a previously diagnosed "treatment-refractory bipolar" patient whose successful treatment of atypical migraine resulted in the questioning of any psychiatric diagnosis.

A 47-year-old man was referred to the Mood Disorders Clinic for severe migraine associated with mood, "psychic," and neurologic symptoms. He had first presented to Psychiatry 8 years earlier, for acute "mania" with agitation, extreme lability, intense anger, and religiosity necessitating hospitalization. Subsequently, he had recurrences of similar manic "crises" followed by a "depressive" states consisting of cognitive dysfunction, avolition, and anhedonia. He also experienced severe headache and nonspecific neurological symptoms. A diagnosis of migraine was suspected, and a thorough neurological work-up did not yield other diagnoses. Medical history revealed multiple recurrent migraine-equivalents since childhood (particularly, abdominal pain).

Each psychiatric "crisis" was preceded by weeks of increasingly frequent, severe, early morning migraine attacks, with subsequent sleep deprivation, and intensification of migraine symptoms, including aura, with disorganized speech and thinking and bizarre behavior. A prolonged period of complete rest would break the cycle of migraine, accompanied by complete resolution of psychiatric symptoms.

Previous treatments included lithium, buproprion, as well as nortriptyline, stemetil, valproic acid, and quetiapine, none of which were helpful. Family history was positive for migraine and negative for psychiatric disorders. On referral, his medications were propranolol 40 mg twice daily, valproic acid 500 mg twice daily, and lamotrigine 100 mg twice daily. Valproic acid level was therapeutic. A diagnosis of mood disorder, bipolar type secondary to severe migraine was made.

Discussion

This case illustrates the importance of inquiry of neurological symptoms, in particular headache, in patients with bipolar disorder. Patients with bipolar disorder have a greater-than-twofold risk of having migraine, as compared with the general population.1 Treatment for migraine, irrespective of mood disorder, includes amitriptyline, valproate, topiramate, and beta-blockers.2 In patients with bipolar disorder and migraine, judicious use of treatments for both disorders should be considered. Lamotrigine was used for this patient because valproate, although approved for both disorders,3 did not ameliorate the migraine symptoms. For bipolar disorder, lamotrigine is efficacious in the prevention of depressive episodes and, possibly, rapid-cycling type.4 Less evidence supports its use in acute depression or mania.4 For migraine, lamotrigine was not beneficial in a placebo-controlled trial, but had some effectiveness in two open pilot studies for the treatment and prevention of migraine aura.2

Lamotrigine is generally well tolerated, with an acceptable side-effects profile (mainly dizziness, nausea, and insomnia), and may be considered for a patient with aura nonresponsive to other medication. Slow and low dose increase is recommended for side-effects monitoring, especially for severe rashes and Steven's Johnson syndrome. In our patient, lamotrigine was increased to 200 mg twice daily. Use of lamotrigine with valproate may increase lamotrigine concentrations by up to 200% because of increased lamotrigine clearance inhibition,3,5 and valproate levels may also decrease.3 The patient's headache duration eventually decreased to 1 hour nightly, and he returned to work full-time with a 45-minute nap.

Atypical Migraine Manifesting as Mania

Случаи психиатрической манифестации рассеянного склероза

Psychiatric disturbances, such as psychosis, have been often described during the course of multiple sclerosis (MS),1 but rarely at onset of the disease.2 In our work, we present two patients with psychotic disorders at onset of relapsing-remitting MS.

The first patient, a 26-year-old woman, was diagnosed with schizoaffective disorder after the acute appearance of auditory hallucinations and confusion; she was treated with antipsychotic drugs, without significant results. One year later, the patient developed weakness in the left leg and widespread paraesthesia. MR images showed demyelinating lesions in the white matter of the left temporal horn and in the dorsal spine. We made a diagnosis of MS,3 and she started glatiramer acetate treatment to prevent further relapses. To date, after 12 months from the beginning of treatment, the patient shows no relevant neurological and psychiatric alterations.

The second patient, a 30-year-old man, presented (2 years before our observation) with an episode characterized by psychomotor agitation with identity disturbances diagnosed as borderline personality disorder, and he started treatment with olanzapine without results. After a few months, he was referred to our department because of the development of lower-limb weakness and urge-incontinence. An MRI showed several lesions in the subcortical white matter and in the periventricular regions. All findings supported the diagnosis of MS, and the patient started beta-interferon treatment, with progressive clinical improvement, both in neurological and then in psychiatric alterations.

The exact percentage of psychiatric onset of MS is still unknown, but the number of MS patients with psychiatric onset may exceed 1%: in our experience, 2 among a cohort of 148 MS subjects had a psychiatric onset, about 1.3%. In our two cases, only the presence of abnormalities at the neurological examination induced clinicians to consider MS as cause of psychiatric disturbance.

Several reports highlight the association of psychotic symptoms with the presence of demyelinating lesions in the left temporal lobe. In our patients, one had temporal lesions, and the other had periventricular plaques, without significant relationship with the temporal lobe. In our opinion, it is not possible to establish a direct relationship between the sites of cerebral lesions and the psychiatric manifestations observed in MS.

After the psychiatric episode, both patients started long-term treatment with glatiramer acetate or beta-interferon. As reported in literature, glatiramer acetate also results in relief of affective disorders,4 whereas beta-interferon increases anxiety and depression.5 Nevertheless, in our patient, the administration of beta-interferon probably contributed to stabilizing the clinical picture.

Although studies on the prevalence of psychiatric onset of MS are few, we conclude that it may occur in more than 1% (in our experience, about 1.3%) and that, in previously healthy people with acute psychotic disorders, even the presence of the slightest neurological abnormality justifies a cranial MRI examination. Further studies are necessary to evaluate the factors that influence the development of psychiatric disorders in MS and the relationship between disease-modifying drugs and psychiatric disorders.

Psychiatric Onset Of Multiple Sclerosis: Description Of Two Cases

Интраназальный окситоцин в дополнение к эсциталопраму в терапии депрессии

Oxytocin (OT) is, first, a hormone synthesized in the hypothalamus and released by the neurohypophysis, but OT is also involved in the regulation of emotions, and OT receptors are distributed in various brain regions, including the limbic system and amygdala. There is much data suggesting a role for OT as an endogenous antidepressant/anxiolytic hormone and there is support for the idea that stimulation of OT receptors inhibits the hypothalamo-pituitary-adrenal (HPA) axis. The pathophysiology of stress-related diseases, such as depression or anxiety disorders, includes both endogenous/genetic predisposing factors and a dysregulated response to stress, and efficiency of antidepressants involves normalization of HPA-axis abnormalities.

Case Report

RX is a 38-year-old man with a 15-year history of major depressive disorder without psychotic features. His depression severely worsened over a 5-year period despite various antidepressant treatments (tricyclics, serotonin reuptake inhibitors, and serotonin-noradrenaline reuptake inhibitors). He also received benzodiazepines and amisulpride without clinical success. His current treatment involves escitalopram 20 mg. After he gave full informed consent, intranasal synthetic OT (Syntocinon®, 1 puff per nostril each with 4 U.I., twice daily; Novartis Pharmaceuticals Corporation, Switzerland) was added. Initial severity of depression was scored at 17 on the Hamilton Rating Scale for Depression (Ham-D), and anxiety reached 57 on the Spielberger State-Anxiety Inventory (STAI–A). One week after OT initiation, his Ham-D score decreased to 11, and the STAI–A score to 49. At this time, the patient bought a car after several months of hesitancy. He contracted a loan and explained that he was offered good buying conditions. One week later, the patient was very much improved; his HAM-D score dropped to 2, and his STAI–A to 37. Unfortunately, Syntocinon® was stopped after 1 week because the patient missed the visit. After this period, the patient was much worse. Intranasal OT was then delivered at the dose of 36 UI per day in addition to escitalopram, 20 mg. His symptoms improved after 7 days (Ham-D: 5; STAI–A: 48). At the same time, he was very affected by the [bankruptcy] of his [step-]father, who raised him. One week later, he offered to install hardware [electronic equipment] in his parent's house. On The Quality of Life Enjoyment and Satisfaction Questionnaire (Q-LES-Q), he scored at higher levels, going from 1 to 4 by the end of the study.

Discussion

This is the first trial of OT as an adjunct to antidepressant in major depression. Our case report suggests that OT instillation significantly improves mood and anxiety. OT was already shown to reduce responses to social stress,1 to increase trust,2 and improve "mind-reading" in humans.3 It is possible that the efficacy of SSRIs in restoring interest in social interactions is due, in part, to their action on the reward circuit via the OT system.4 Further studies are needed to investigate the effects of OT or OT-receptor selective agonists in additional clinical models to promote the development of psychopharmacology targeting central OT receptors.

Intranasal Oxytocin as an Adjunct to Escitalopram in Major Depression

Акатизия при отмене габапентина

OBJECTIVE: To report a case of akathisia in a patient with type 2 diabetes after abrupt discontinuation of gabapentin.

CASE SUMMARY: A 76-year-old female with type 2 diabetes was admitted for change in mental status, agitation, and restless limb movements. She had been taking gabapentin 3600 mg daily for approximately 1 month for diabetic neuropathy. Her other home medications were glyburide 10 mg twice daily, oxycodone/acetaminophen 5 mg/325 mg every 6 hours as needed for leg pain, and zolpidem 5 mg at bedtime. She had taken none of these drugs for 4 days prior to admission because she was unable to have the prescriptions refilled. Subsequently, the patient exhibited repeated arm and leg motions in response to an inner restlessness. Upon admission to the emergency department, she was agitated and restless; all vital signs and results of laboratory studies were within normal limits. Gabapentin was restarted at the original dosage and the symptoms resolved within 8 hours. Because the patient developed lethargy, the gabapentin dosage was reduced and titrated to the original level over 2 days. After 3 days, the patient was well oriented and experienced no further symptoms. She was discharged on the original dosage of gabapentin.

DISCUSSION: To our knowledge, this is the first reported cases of akathisia induced by gabapentin withdrawal. Available case reports suggest that gabapentin withdrawal can occur at doses ranging from 400-8000 mg/day. Patients experienced symptoms similar to those that develop with benzodiazepine withdrawal and were taking gabapentin for as little as 3 weeks to as long as 5 years. This is the first case report to describe akathisia induced by gabapentin withdrawal. The Naranjo probability scale revealed a probable relationship between akathisia and gabapentin withdrawal.

CONCLUSIONS: If gabapentin discontinuation is desired, it is prudent to gradually taper the dose to avoid withdrawal symptoms, which may occur after as little as 1 month of treatment. Should the patient experience withdrawal symptoms, the optimal treatment is to restart gabapentin.

Akathisia Induced by Gabapentin Withdrawal

Пропранолол в профилактике рецидивов зависимостей

However, the research also suggests that treatment with the β-blocker propranolol can block stress-induced impairment in decision-making in these individuals, potentially reducing the risk for stress-related relapse.

Beta-Blocker May Prevent Stress-Related Relapse in Addicts