Objective: To investigating the relationship between α-Klotho and FGF-23 with bone biochemical markers and bone density findings in extremely aged individuals. Methods: A total of 55 individuals with a mean age of 85.6 years were subjected to clinical, biochemical, and bone mineral density analyses and the enzyme-linked immunosorbent assay-based detection of α-Klotho and FGF-23. The mean, standard deviation, median, and interquartile ranges of the sample values were determined, and Spearman's test for association assessments was used for statistical analysis. Results: The study participants expressed median FGF-23 and α-Klotho levels of 69.81 RU/mL (51.43 RU/mL) and 733.43 pg/mL (360.83 pg/mL), respectively. The majority of the participants possessed osteopenia (54.5%) and a vitamin D deficiency (57%). The 25-hydroxyvitamin D concentrations ranged between 7.1 and 47.5ng/mL, with a median of 18.1ng/mL. Conclusion: No substantial associations were discovered between α-Klotho and FGF-23 levels and bone density in the study participants. Objective αKlotho α Klotho FGF23 FGF 23 FGF-2 Methods 5 856 85 6 85. clinical enzymelinked enzyme linked assaybased assay based FGF23. 23. deviation determined Spearmans Spearman s analysis Results 6981 69 81 69.8 RUmL RU mL 51.43 5143 51 43 (51.4 73343 733 733.4 pgmL pg 360.83 36083 360 83 (360.8 pg/mL, , pg/mL) respectively 54.5% 545 54 (54.5% 57%. 57 57% . (57%) 25hydroxyvitamin hydroxyvitamin 25 71 7 1 7. 475ngmL ngmL 47 5ng ng 47.5ng/mL 181ngmL 18 1ng 18.1ng/mL Conclusion FGF2 2 FGF- 8 698 69. 51.4 514 4 (51. 7334 73 733. 360.8 3608 36 (360. 54.5 (54.5 (57% 51. (51 360. 3 (360 54. (54. (57 (5 (36 (54 ( (3

ABSTRACT BACKGROUND: Osteoporosis compromises bone strength and increases the risk of fractures. Zoledronate prevents loss of bone mass and reduces the risk of fractures. OBJECTIVES: To determine the efficacy and safety of zoledronate in postmenopausal women with osteopenia and osteoporosis. DESIGN AND SETTINGS A systematic review and meta-analysis was conducted within the evidence-based health program at the Universidade Federal de São Paulo. METHODS: An electronic search of the CENTRAL, MEDLINE, Embase, and LILACS databases was performed until February 2022. Randomized controlled trials comparing zoledronate with placebo or other bisphosphonates were included. Standard methodological procedures were performed according to the Cochrane Handbook and the certainty of evidence for the Grading of Recommendations Assessment, Development, and Evaluation Working Group. Two authors assessed the risk of bias and extracted data on fractures, adverse events, bone turnover markers (BTM), and bone mineral density (BMD). RESULTS: Twelve trials from 6,652 records were included: nine compared zoledronate with placebo, two trials compared zoledronate with alendronate, and one trial compared zoledronate with ibandronate. Zoledronate reduced the incidence of fractures in osteoporotic [three years: morphometric vertebral fractures (relative risk, RR = 0.30 (95% confidence interval, CI: 0.24–0.38))] and osteopenic women [six years: morphometric vertebral fractures (RR = 0.39 (95%CI: 0.25–0.61))], increased incidence of post-dose symptoms [RR = 2.56 (95%CI: 1.80–3.65)], but not serious adverse events [RR = 0.97 (95%CI: 0.91–1.04)]. Zoledronate reduced BTM and increased BMD in osteoporotic and osteopenic women. CONCLUSION: This review supports the efficacy and safety of zoledronate in postmenopausal women with osteopenia for six years and osteoporosis for three years. PROSPERO REGISTRATION NUMBER: CRD42022309708, https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=309708. BACKGROUND OBJECTIVES metaanalysis meta analysis evidencebased based Paulo METHODS CENTRAL MEDLINE Embase 2022 included Assessment Development Group BTM, , (BTM) BMD. . (BMD) RESULTS 6652 6 652 6,65 alendronate ibandronate relative 030 0 30 0.3 95% 95 (95 interval CI 0.24–0.38 024038 24 38 0.24–0.38)) 039 39 95%CI 95CI (95%CI 0.25–0.61, 025061 0.25–0.61 25 61 0.25–0.61))] postdose post dose 256 2 56 2.5 1.80–3.65, 180365 1.80–3.65 1 80 3 65 1.80–3.65)] 097 97 0.9 0.91–1.04. 091104 0.91–1.04 91 04 0.91–1.04)] CONCLUSION NUMBER CRD42022309708 CRD https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=309708. httpswwwcrdyorkacukprosperodisplayrecordphpRecordID309708 httpswwwcrdyorkacukprosperodisplayrecordphpRecordID https //www.crd.york.ac.uk/prospero/display_record.php RecordID=309708. www crd york ac uk prospero display record php RecordID 309708 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=309708 202 (BTM (BMD 665 6,6 03 0. 9 (9 0.24–0.3 02403 0.24–0.38) 02506 0.25–0.6 0.25–0.61)) 5 2. 18036 1.80–3.6 8 1.80–3.65) 09 09110 0.91–1.0 0.91–1.04) CRD4202230970 phpRecordID https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=309708 httpswwwcrdyorkacukprosperodisplayrecordphpRecordID30970 wwwcrdyorkacukprosperodisplayrecordphp RecordID309708 RecordID=309708 30970 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=30970 20 66 6, ( 0.24–0. 0240 0250 0.25–0. 0.25–0.61) 1803 1.80–3. 0911 0.91–1. CRD420223097 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=30970 httpswwwcrdyorkacukprosperodisplayrecordphpRecordID3097 RecordID30970 RecordID=30970 3097 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=3097 0.24–0 024 025 0.25–0 180 1.80–3 091 0.91–1 CRD42022309 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=3097 httpswwwcrdyorkacukprosperodisplayrecordphpRecordID309 RecordID3097 RecordID=3097 309 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=309 0.24– 02 0.25– 18 1.80– 0.91– CRD4202230 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=309 httpswwwcrdyorkacukprosperodisplayrecordphpRecordID30 RecordID309 RecordID=309 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=30 0.24 0.25 1.80 0.91 CRD420223 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=30 httpswwwcrdyorkacukprosperodisplayrecordphpRecordID3 RecordID30 RecordID=30 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=3 0.2 1.8 CRD42022 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID=3 RecordID3 RecordID=3 https://www.crd.york.ac.uk/prospero/display_record.php?RecordID= 1. CRD4202 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID= RecordID= https://www.crd.york.ac.uk/prospero/display_record.php?RecordID CRD420 https//www.crd.york.ac.uk/prospero/display_record.phpRecordID CRD42 CRD4

ABSTRACT BACKGROUND: Fatigue is a frequent symptom in patients with primary Sjögren’s syndrome (pSS) and can be a cause of or be associated with sleep disorders. OBJECTIVE: To assess the sleep quality of pSS patients and its relationship with fatigue and disease activity. DESIGN AND SETTING: Analytical observational study conducted at an exercise psychobiology laboratory. METHODS: Sleep quality was evaluated using the Pittsburg sleep quality index (PSQI) and actigraphy. Fatigue was evaluated through the Profile of Fatigue and Discomfort - Sicca Symptoms Inventory (PROFAD-SSI-SF) and a visual analogue scale for fatigue (VAS-fatigue). Disease activity was evaluated using a visual analogue scale for pain (VAS-pain), EULAR Sjögren’s Syndrome Patient Reported Index (ESSPRI) and Disease Activity Index (ESSDAI). We summarized the data through descriptive statistics. RESULTS: A total of 50 female patients with pSS, of average age 56.4 years, were included in the study; 80% presented low disease activity. The total PSQI score showed that 74% had poor sleep. The actigraphy showed mean sleep latency of 26.2 minutes and mean nightly awakening of 48.2 minutes (duration of wakings after sleep onset, WASO). There were correlations between PSQI and VAS-pain, VAS-fatigue, PROFAD-SSI and ESSPRI. Actigraphy showed a correlation between the duration of WASO and ESSDAI. CONCLUSION: The present study provides important information regarding correlations between sleep disorders and disease activity. There is a need for proper control over disease activity and for development of strategies to help patients to sleep better in order to diminish their fatigue.

RESUMO Objetivo Validar o Pain Assessment Checklist for Seniors with Limited Ability to Communicate – Portuguese em idosos dementados e analisar as propriedades de suas medições. Métodos Foram avaliados 50 idosos dementados, residentes de uma casa de repouso e com capacidade de comunicação verbal limitada, quando expostos a situações potencialmente dolorosas. A ferramenta foi utilizada em dois momentos diferentes. Primeiro, foi aplicada por dois entrevistadores simultaneamente, e a intensidade da dor foi questionada com base na opinião do cuidador. Depois de 14 dias, sem intervenção de analgésico, a ferramenta foi aplicada novamente por um dos entrevistadores. Resultados A amostra teve predominância de mulheres, acima de 80 anos de idade, com demência de Alzheimer, apresentando dores musculoesqueléticas com intensidade moderada a grave. As propriedades psicométricas do instrumento demonstraram consistência interna adequada (coeficiente alfa de Cronbach de 0,827). A escala teve excelente reprodutibilidade, de acordo com o coeficiente de correlação intraclasse, e o instrumento demonstrou validade adequada. Conclusão O Pain Assessment Checklist for Seniors with Limited Ability to Communicate – Portuguese teve propriedades de medição adequadas para idosos com limitações de comunicação.

ABSTRACT Objective To validate the Pain Assessment Checklist for Seniors with Limited Ability to Communicate – Portuguese in demented elderly and to analyze its measurement properties. Methods We evaluated 50 elderly with dementia, residing in a nursing home and with limited communication ability, when exposed to potentially painful situations. The tool was applied at two different moments. First, two interviewers applied it simultaneously, and the intensity of pain was asked based on the caregiver’s opinion. After 14 days, with no analgesic intervention, one of the interviewers applied it again. Results The sample comprised more females, aged over 80 years, with dementia due to Alzheimer, presenting musculoskeletal pain of moderate to severe intensity. The psychometric properties of the tool demonstrated appropriate internal consistency (Cronbach’s alpha coefficient of 0.827). The scale had excellent reproducibility, according to the intraclass correlation coefficient, and the tool has been duly validated. Conclusion The Pain Assessment Checklist for Seniors with Limited Ability to Communicate – Portuguese had adequate measuring properties for use with elderly presenting limited communication.

RESUMO JUSTIFICATIVA E OBJETIVOS: As vitaminas do complexo B têm sido utilizadas em monoterapia ou combinada a outros fármacos, como os anti-inflamatórios, em diversas situações clinicas, como por exemplo, nas doenças degenerativas da coluna, doenças reumatológicas, polineuropatias e nos pós-operatórios diversos. O objetivo deste estudo foi identificar na literatura científica as evidências mais recentes do uso de vitaminas do complexo B como terapia analgésica e descrever as situações clínicas em que se pode verificar a sua ação analgésica. CONTEÚDO: Realizada a revisão bibliográfica na base de dados do Pubmed, Medline, LILACS, Biblioteca Cochrane e Scielo, contemplando os últimos 10 anos, títulos em português, espanhol e inglês. Os descritores utilizados foram: "Dor", "vitaminas do complexo B", "tratamento", "vitamina B1", "vitamina B6", "vitamina B12", "tiamina", "piridoxina" e "cianocobalamina". Dentre os 40 estudos encontrados selecionaram-se apenas os trials em dor musculoesquelética e neuropática com seres humanos, e em que as vitaminas do complexo B configuraram-se como agentes analgésicos. Foram selecionados então 13 estudos que satisfizeram esses critérios de inclusão. Em todos eles as vitaminas do complexo B desempenharam papéis na analgesia, inclusive quando em monoterapia. As vitaminas do complexo B também apresentaram ação anti-inflamatória, anti-pruriginosa, na funcionalidade e na qualidade de vida. CONCLUSÃO: Os estudos existentes, apesar de heterogêneos, demonstraram que as vitaminas do complexo B possuem efeito analgésico em síndromes dolorosas neuropática e nociceptiva, e que por serem esses fármacos seguros e de baixos custos poderiam representar boas opções na terapêutica analgésica no nosso meio.

ABSTRACT BACKGROUND AND OBJECTIVES: The B complex vitamins have been used as single therapy or combined to other drugs, such as anti-inflammatory drugs, in different clinical situations, such as degenerative spinal diseases, rheumatologic diseases, polyneuropathies and in different postoperative situations. This study aimed at identifying in the scientific literature most recent evidences of the use of B complex vitamins as analgesic therapy and at describing clinical situations where their analgesic action could be observed. CONTENTS: A search was carried out in Pubmed, Medline, LILACS, Cochrane Library and Scielo databases, contemplating the last 10 years and titles in Portuguese, Spanish and English. Keywords were: "pain", "B complex vitamins", "management", "vitamin B1", "vitamin B6", "vitamin B12", "thiamine", "pyridoxine" and "cyanocobalamin". Among 40 studies found, we have selected just musculoskeletal and neuropathic pain trials with humans, and where B complex vitamins were used as analgesic agents. From these, 13 studies were selected for meeting inclusion criteria. In all of them, B complex vitamins played roles in analgesia, even when in single therapy. B complex vitamins had also anti-inflammatory and anti-pruritus action, in addition to improving functionality. CONCLUSION: Existing studies, although scarce and heterogeneous, have shown that B complex vitamins have analgesic effect. They are considered safe and have low cost and have shown to be a good option as adjuvant analgesic therapy.

JUSTIFICATIVA E OBJETIVOS: A hiperleucocitose (> 100 x 10(9)/L) em leucemia mielóide crônica não é uma apresentação comum e pode determinar manifestações clínicas de hiper-viscosidade. As perdas auditiva e visual observadas em pacientes com leucemia são consideradas sintomas incomuns, mas fortemente associados à síndrome da hiper-viscosidade. O objetivo deste estudo foi relatar o caso de um paciente que apresentou perda da audição como manifestação inicial de leucemia mielóide crônica e síndrome de hiper-viscosidade e rever aspectos relacionados a seu tratamento em Medicina Intensiva. RELATO DO CASO: Paciente do sexo masculino, 41 anos, com queixa de tontura havia seis meses sem resposta ao tratamento sintomático, foi admitido no serviço de emergência com perda auditiva aguda. Ao exame físico encontrava-se normal, exceto por perda auditiva bilateralmente. Os exames laboratoriais demonstraram leucocitose importante (645.000), com 66,4% de blastos com características mielóides, 13,6% bastões, 15,3% segmentados, 1,4% linfócitos, 3,3% eosinófilos e plaquetas de 225.000. Devido à suspeição de leucemia com risco elevado para síndrome de hiper-viscosidade, o paciente foi admitido para tratamento na unidade de terapia intensiva. Realizado mielograma e biópsia de medula óssea que confirmaram o diagnóstico de leucemia mielóide crônica. Iniciadas hidratação, hidroxiuréia, alopurinol e dexametasona. A leucoaferese foi realizada uma semana após a admissão, quando a contagem leucocitária estava em torno de 488.000. Dez dias após o procedimento, o paciente não apresentou melhora da audição, apesar da leucometria de 10.000. Recebeu alta hospitalar em duas semanas para continuidade do tratamento ambulatorial. CONCLUSÕES: As freqüências das manifestações sensitivas em pacientes com leucemia incluem além das perdas auditiva e visual, vertigem, paralisia facial e infecções. A síndrome de hiper-viscosidade decorrente da hiper-leucocitose é uma causa possível para as perdas sensitivas, ocorrendo geralmente com contagem leucocitária superior a (> 100 x 10(9)/L). Este caso é representativo de raro caso de perda auditiva decorrente da hiper-viscosidade por leucemia.

BACKGROUND AND OBJECTIVES: Hyperleukocytosis (> 100 x 10(9)/L) is an uncommon presentation of chronic leukemias and it can present clinical symptoms of hyperviscosity syndrome. Hearing loss and blindness rarely occurs in patients with leukemia; however, it can be strong association with hyper-viscosity syndrome. The purpose of this paper is to report a case of acute hearing loss as the initial manifestation of acute leukemia and hyper-viscosity syndrome and also mainly aspects of the intensive care treatment. CASE REPORT: A 41 year-old, male patient, who has been complaining about dizziness for six months with no response to symptomatic medications, was admitted to the emergency department with acute hearing loss. The physical examination was normal except for a bilateral hearing loss without an apparent cause. Laboratory exams showed total leukocyte: 645.000 with 66.4% blasts, hemoglobin: 7.0, hematocrit: 20.5, urea: 94, creatinine: 1.59, K: 5.6, Na: 138, INR: 1.38, TTPa: 0.89, troponin lower than 0.2, CK: 218, CKMB: 50, uric acid: 11.1. After a first hypothesis of leukemia with a high risk of hyper-viscosity complications, the patient was admitted to the Intensive Care Unit for monitoring and treatment. A bone marrow biopsy was performed and than started hidratation, hydroxyurea, allopurinol, dexamethasone. According to hematologists the patient had a chronic myeloid leukemia. Leukopheresis was performed one week after admission when total blood leukocytes were around 488.000. Ten days after the procedure the patient had no improvement of the hearing loss but total leukocytes were 10.100. He was discharge to the ward and 2 weeks later went home to continue ambulatory treatment. CONCLUSIONS: The frequency of sensitive manifestations in patients with leukemia include not only visual and hearing loss but also many others manifestations such as conductive vertigo, facial palsy and infections. Hyperviscosity syndrome due to hyperleukocytosis is also a possible cause of sensorial loss, but the syndrome is often dependent on leukocyte counts greater than (>100 x 10(9)/L).This case is a representative of rare cases in which acute sensorineural hearing loss occurred as the initial manifestation of hyper-viscosity syndrome due to leukemia.

JUSTIFICATIVA E OBJETIVOS: O infarto hepático é definido como necrose isquêmica do parênquima hepático envolvendo pelo menos dois ácinos. Trata-se de evento considerado raro devido ao duplo suprimento sangüíneo, arterial e venoso. O objetivo deste estudo foi relatar um caso de paciente não sabidamente diabética que desenvolveu extensas áreas isquêmicas de infarto hepático, após quadro de descompensação aguda da diabete. RELATO DO CASO: Paciente do sexo feminino, 67 anos, hipertensa, procurou o Pronto Socorro com queixas de polidipsia, poliúria, turvação visual, náuseas e vômitos, dificuldade para deambular, havia aproximadamente 10 dias. Ao exame físico foi observado desidratação, palidez cutânea, cianose periférica, hipotermia, taquicardia, hipotensão, dor abdominal leve e difusa. Exames laboratoriais mostraram: leucócitos: 16800, creatinina (Cr): 3,7, uréia (Ur): 167, Na: 133, K: 6.9, glicose: 561; gasometria arterial (cateter de oxigênio: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, BE: -28,8, HCO3: 2,4, Sat 91,3%, lact: 79; urina I: pH: 6,0; leucócitos: 13; densidade: 1015; eritrócitos: 19; proteína: ++; glicose: +++; bilirrubina: negativa; corpos cetônicos: + denotando cetonemia. Eletrocardiograma com onda T apiculada, bloqueio de ramo direito. A paciente foi tratada com insulina, hidratação, bicarbonato de sódio e introduzido antibioticoterapia. Após o tratamento inicial, os exames laboratoriais mostraram: Cr: 2,2, Ur: 122, Na: 162, K: 4,3, Ca: 6,4, glicose: 504, pH: 7,01, HCO3: 7.1, BE: - 22. Um dia após, a paciente apresentou importante dor abdominal acompanhada de irritação peritoneal, além de sonolência e dificuldade para falar; exames laboratoriais mostraram: pH: 7,4, pCO2 : 31, pO2: 68, BE: -4,4, HCO3: 19, Sat.O2: 93,5%; Ur: 95; Cr: 1,4, albumina: 2,4, Ca: 0,95, Na: 166, K:4, bilirrubina: 0,5, bilirrubina D/I: 0,2/0,3, amilase: 1157, Gama-GT: 56, AST 7.210, ALT: 2.470, VHS: 15, lipase: 84. Ultrasonografia abdominal não apresentou alterações significativas. Evoluiu com importante piora clínica, parada cardiorrespiratória e óbito. A necrópsia evidenciou múltiplas áreas de infarto hepático, trombose vascular, infarto esplênico, congestão visceral e aterosclerose de aorta e seus ramos e pâncreas normal. CONCLUSÕES: Os mecanismos de infarto hepático e esplênico neste caso não foram bem elucidados. Alguns fatores devem ter contribuído, tais como: desidratação e hipotensão devido a episódios de vômitos e febre que contribuem para diminuição do fluxo sanguíneo da veia porta e artéria hepática; o nível elevado de catecolaminas que ocorre em estado de hiperglicemia e cetoacidose metabólica pode induzir à vasoconstrição; aterosclerose difusa que é comumente vista em pacientes diabéticos e hipertensos. Este caso enfatiza a necessidade de investigar infarto hepático em pacientes diabéticos com cetonemia e com aumento de enzimas hepáticas. Anticoagulantes devem ser prontamente instituídos se houver trombose vascular.

BACKGROUND AND OBJECTIVES: Hepatic infarction is characterized by parenchyma ischemic necrosis involving at least two acinis. It is extremely uncommon due to the arterial and portal venous blood supply. We report a case of a patient not know to have diabetes who developed massive areas of ischemic infarcts of the liver after episode of acutely diabetes decompensated. CASE REPORT: A 67 year-old hypertensive female who has been presenting, for the last 10 days, polydipsia, high urinary volume, visual and gait impairment, nausea and vomiting was admitted to the emergency room (ER). During the physical examination it was observed dehydration, skin discoloration, peripheral cyanosis, hypothermia, tachycardia, hypotension and mild diffuse abdominal pain. Admissional laboratory exams demonstrated total leukocytes: 16.800, Cr: 3.7, Ur: 167, Na: 133, K: 6.9, glucose: 561; arterial gasometry (O2 catheter: 2 L/min): pH: 6.93, pCO2: 12.1, pO2: 107, B.E.: -28.8, HCO3: 2.4, Sat 91.3%, lactato: 79; urinalysis: pH: 6; leukocytes: 13; density: 1015; erythrocytes: 19; protein: ++; glucose: +++; bilirubin: negative; ketonic bodies: + denote ketonemia. EKG: sharp T wave, right branch block. Patient was treated with intravenous insulin, hydration, sodium bicarbonate and ceftriaxone. After initial treatment, the laboratory exams showed Cr: 2.2, Ur: 122, Na: 162, K: 4.3, Ca: 6.4, glucose: 504, pH: 7.01, HCO3: 7.1, B.E.: -22. One day after admission the patient presented with important abdominal pain and peritoneal irritation, followed by difficulty for talking and somnolence; routine laboratory exams showed arterial gasometry: pH: 7.4, pCO2: 31, pO2: 68, BE: -4.4, HCO3: 19, SatO2: 93.5%; Ur: 95,Cr: 1.4, albumin: 2.4, Ca: 0.95, Na: 166, K:4, bilirubin: 0.5, bilirubin D/I: 0.2/0.3, Amylase: 1157, Gamma-GT: 56, AST 7.210, ALT: 2.470, SR (sedimentation rate): 15, Lipase: 84. Abdominal ultrasound was unremarkable. Patient respiratory function and conscience level worsened, requiring intubation. Despite all resuscitation efforts, she died. Necropsy showed multiple ischemic infarcts of the liver with vascular thrombosis, splenic infarcts, generalized visceral congestion and atherosclerosis of aorta and its branches. Pancreas was normal. CONCLUSIONS: The mechanisms of hepatic and splenic infarctions in this case were unclear. The following factors may have contributed to necrosis: vomiting and fever should be considered to induce dehydration and hypotension, which further decreased portal and hepatic arterial inflows; elevated level of catecholamine in hyperglycemic states might induce vasoconstriction effects; widespread atherosclerosis is commonly seen in diabetic and hypertensive patients. This case underlies the importance of searching for hepatic necrosis or infarction in any diabetic patient with elevated liver enzymes. Anticoagulation therapy should be instituted promptly upon recognition of vascular thromboses.

JUSTIFICATIVA E OBJETIVOS: A cocaína é uma droga ilícita amplamente utilizada e o seu uso tem sido associado a efeitos decorrentes da toxicidade aguda e crônica em praticamente todos os órgãos, particularmente no sistema cardiovascular. Este artigo visou descrever um caso de cardiomiopatia em paciente jovem usuário crônico de cocaína. RELATO DO CASO: Paciente do sexo masculino, 19 anos, usuário de cocaína por inalação e crack desde os 15 anos de idade. Foi internado em fevereiro de 2006 devido a dispnéia progressiva aos mínimos esforços e expectoração sanguinolenta. Ao exame físico apresentava edema nos membros inferiores, estase jugular e dispnéia em repouso. Foram observados no ecocardiograma: dilatação das quatro câmaras cardíacas, com hipocinesia difusa de ventrículo esquerdo (VE), trombo mural em VE de 17 mm e fração de ejeção de 12%. Realizada broncoscopia pulmonar que identificou sangramento em língula ativo, tratado com embolização. Após 48h do procedimento, o paciente manteve-se assintomático e sem expectoração sanguinolenta. Iniciado tratamento antitrombótico com warfarina e enoxaparina. A cineangiocoronariografia não evidenciou lesões obstrutivas e o paciente recebeu alta após melhora clínica. Re-internado em julho de 2006 com dor precordial de forte intensidade e dispnéia de repouso. Nova cineangiocoronariografia evidenciou oclusão de terço médio da artéria descendente anterior. CONCLUSÕES: Os efeitos agudos da cocaína freqüentemente motivam atendimento de emergência. Já as suas manifestações crônicas, como as doenças cardiovasculares, podem produzir alterações de difícil correlação futura ao seu consumo prévio. O uso prolongado da cocaína está relacionado à alteração da função sistólica ventricular esquerda por hipertrofia ou dilatação miocárdica, aterosclerose, disritmias cardíacas, apoptose de cardiomiócitos e lesão simpática.

BACKGROUND AND OBJECTIVES: Cocaine is the most commonly used illicit drug and its acute and chronic effects are related to a variety of physiological changes, mainly in the cardiovascular system. This study is a case report of a patient with cardiomyopathy related to cocaine use. CASE REPORT: A 19 year old men, who has been using cocaine and crack since 15 years old, was admitted to the emergency department (ED) in February 2006 with progressive dyspnea during minimal efforts and bloody expectoration. During the physical exam it was observed legs edema, jugular stasis and dyspnea at rest. The echocardiogram demonstrated left ventricular hypocinesia, a 17 mm ventricular thrombus and a 12% ejection fraction. A bleeding from the left upper lobe was identified during a pulmonary bronchoscopy which was treated with arterial embolization. After 48h of the procedure, the patient was asymptomatic and an antithrombotic treatment with warfarin and enoxaparin was started. No obstruction was found at the cineangiography and the patient was discharged after clinical improvement. The patient was admitted again to the intensive care unit in July with intense chest pain and dyspnea at rest. A new cineangiography was performed and it was observed occlusion in the anterior descendent coronary artery. CONCLUSIONS: The cocaine acute effects are commonly seen at the ED but the chronic effects, as the cardiovascular manifestations, can take longer to be correlated as a side effect of cocaine use. Its prolonged use is related to left ventricular systolic dysfunction due to hypertrophy or myocardial dilation, atherosclerosis, arrhythmias, myocyte apoptosis and sympathetic damage.