|
Presentation of a
Case
A 28-year-old man was
admitted because of prolonged fever and progressive headache
for two weeks. He had been well until two week earlier before
this admission when he experienced flu-like symptoms which
consisted of fever, chills, nausea, sore throat, and cervical
lymphadenopathy. The symptoms did not resolve after taking
medications prescribed at a local clinic. Faint erythematous
rashes were noted at the trunk. Headache developed which was
mainly located at the bilateral tempero-parietal regions and
was constant and dull in character. There was no focal motor
or sensory deficits or sphincter dysfunction. Headache
worsened in association with fevers. One week prior to entry
to this hospital, he was seen at another hospital where a
first-generation cephem and a macrolide were given without benefit.
Blood tests show leukopenia and examination of a urine
specimen was negative. Chest radiography was negative. One
day before admission, he developed worsening headache.
Therefore, he was referred to this hospital.
He had been a bank clerk for several years and remained single.
He did not smoke, use illicit substance or consume alcohol.
He lived alone and had no history of contact with children
who were recently known to have flu symptoms, nor did he
have a history of contact with animal or travel out of
metropolitan areas.
On admission, he appeared in no acute distress while
breathing ambient air and not dehydrated. Body temperature was
38.5℃, respiration 20/min, pulse 100/min and blood pressure
120/70 mmHg. Fading rashes were noted at the forechest.
Consciousness was clear and oriented. Neck was stiff. Multiple
cervical and inguinal lymph nodes were palpable. Chest and
heart examinations were normal. There was no organomegaly.
Neurologic examinations were normal except that he could not
perform tandem gait because of headache. Finger-to-finger and
finger-to-nose tests were normal.
Results of blood examinations showed WBC, 3400/μL with 38%
lymphocytes and 12% atypical lymphocytes, hematocrit, 43%,
platelet 111 x 103/μL, GOT, 105 IU/L, GPT, 162 IU/L,
ALP 266 IU/L, and g -GT
197 IU/L. Studies for viral hepatitis were negative
for hepatitis A, B, and C. MRI of the brain performed after
administration of contrast medium showed leptomeningeal enhancement
at the both cerebral hemisphere and cerebellum and diffuse
brain edema without other focal lesions. The findings were
suggestive of meningitis. Lumbar puncture showed an initial
pressure of 240 mmH2O, lymphocytic pleocytosis with lymphocytes
to neutrophils of 44/12. CSF protein level was 86 mg/dl and
glucose 62 mg/dl. India ink and acid fast stains were
negative. Cerebrospinal fluid (CSF) specimen was submitted for
bacterial, mycobacterial, viral, and fungal cultures which
were subsequently shown to be no growth. A CSF specimen was
tested for herpes simplex virus by polymerase chain reaction
and was reported to be negative. Ceftriaxone and acyclovir
were given by vein after performance of lumbar puncture and
glycerol was infused for increased intracranial pressure. On
the second hospital day, fever continued and headache did not
abate. Blood tests did not show significant changes. Serology
showed a titer of 16 for CMV-IgG , 160 for EBV-VCA IgG, and
negative for toxoplasma IgG, IgM and syphilis.
One of his male friends who came to
visit him informed physicians of the patient’s homosexual
practice and a recent sexual encounter about 4 months prior to
the onset of symptoms. On the fourth hospital day, a test for
anti-HIV antibody was reported as positive which was
subsequently confirmed by Western blot. His CD4+ lymphocyte
count was 146 cells/μL (9.2%) and CD8+ count, 1,123 cells/μL
(70.7%).
Plasma viral load by RT (reverse transcriptase)-PCR was
>750,000 copies/ml.
Ceftriaxone and acyclovir were discontinued when cultures
and HSV-PCR were negative. Headache gradually improved with
infusion of glycerol. He become afebrile on the 10th hospital
day. Antiretroviral therapy was initiated with zidovudine,
lamivudine and efavirenz with a good and sustained virological
suppression and increase of CD4+ lymphocyte count.
【案例分析】
本案例是典型的急性反轉錄病毒感染症候群（acute retroviral
syndrome），以無菌性腦膜炎和類似傳染性單核球過多症（infectious
mononucleosis-like）為初發病症。患者在接觸人類免疫不全病毒（human immunodeficiency
virus;
HIV），發生感染後，可能在數週至數個月內出現所謂的急性反轉錄病毒感染症候群。這些症狀包括：不明原因的發燒、咽喉疼痛、全身淋巴腺腫（lymphadenopathy）、發疹、肝脾腫大、無菌性腦膜炎（aseptic
meningitis）等。這些症狀出現的機會，可能高達八成以上。但是，這些症狀並不特殊，和一般的感冒病症有些類似；和感染性單核球過多症（infectious
mononucleosis）的症狀，有許多重複之處。對於經驗較少的醫師而言，確實不易分辨。
急性病症在幾週內自然消失後，絕大多數的患者便進入了無症狀期。無症狀期可能長達五到十年。當CD4+淋巴球數減少到某一程度時（200-350/毫升左右），患者才開始出現一些皮膚、黏膜的病徵，例如：帶狀皰疹（herpes
zoster）、舌緣的毛髮狀白斑（oral hairy leucoplakia）、脂漏性皮膚炎（seborrheic
dermatitis）、卡波西氏肉瘤（Kaposi’s sarcoma）、口腔念珠菌感染（oral
candidiasis）、潰瘍性單純皰疹（ulcerative herpes simplex）等等。
當CD4+淋巴球數繼續減少時，嚴重、可能致命的伺機性感染和腫瘤，接連發生，例如：非何杰金氏淋巴瘤（non-Hodgkin’s
lymphoma; NHL）、結核病（tuberculosis; TB）、肺囊蟲肺炎（Pneumocystis
carinii pneumonia; PCP）、巨細胞病毒疾病（cytomegalovirus
disease）、全身性黴菌感染（例如：隱球菌「Cryptococcus
neoformans」、組織漿黴菌「Histoplasma capsulatum」、青黴菌「Penicillium
marneffei」等全身性感染）、全身性非結核分枝桿菌感染（non-tuberculous
mycobacteriosis）、卡波西氏肉瘤、弓蟲腦炎（cerebral
toxoplasmosis）、隱孢子蟲症（cryptosporidiosis）等等。
有一部份患者（5-10%）自感染十餘年後仍然沒有出現相關的併發症，CD4+淋巴球數仍然維持很高。這些患者被稱為long-term
non-progressor。有些病患感染後一到三年後，CD4+淋巴球數急速減少，患者很快出現相關的併發症（rapid
progressor）。
自西元1986年台灣發現第一例本國籍愛滋病毒感染病患後，感染患者也是逐年增加。根據衛生署疾病管制局的統計，截至2001年9月中，已累計有3,422例病患感染愛滋病毒。雖然，我們的感染愛滋病毒的盛行率和其它亞洲家較起來相距甚遠，但從我們新病例出現的情形看來，台灣地區愛滋病毒感染的流行似乎尚未成熟，流行曲線尚未趨緩。在未來五至十年內，我們仍會看到愛滋病毒感染的病例數急速增加。
HIV感染最主要的傳染途徑包括：性行為、靜脈藥癮者共用污染HIV的針器、輸入污染HIV的血液製品、週產期的垂直傳染（vertical
transmission）。少數的感染發生在醫療環境中遭銳器扎傷或黏膜接觸污染的體液。這些傳染途徑個別所佔的角色，隨時間和地區有所不同。雖然最初在歐美等已開發國家中發現的感染者，以男同性戀間的性行為和共用污染HIV的針器為主，但是，在非洲地區則是以異性戀間的性行為為主要的傳染途徑。近年來，在大多數地區，因異性戀間的性行為感染HIV所佔的比例逐年增加，連帶的垂直傳染的重要性也是與日俱增。台灣地區HIV感染的各種傳染途徑，根據衛生署發布的統計資料顯示，過去十年來，因異性戀間的性行為造成感染的比例，則逐年增加，在民國九十年的統計，異性戀間的性行為約佔48.4%，男同性戀間的性行為約佔45.8%。
HIV感染的診斷主要仰賴血清抗體檢驗。這可分兩種或兩步驟：一是ELISA（Enzyme-linked
immunosorbant assay），一是Western
blotting。我們用第一種方式篩檢，如果呈陽性反應，重複一次ELISA；陽性反應時，以Western
blot作為證實。若Western
blot出現了針對HIV特有抗原的抗體反應時，我們便可以確認HIV感染。其它的檢驗方式包括定量p24、病毒培養和分子生物學的方法，例如：reverse-transcriptase
polymerase chain reaction（RT-PCR）。
最後這種方法，目前已廣泛應用於HIV病毒的定量。
HIV 感染並不等於愛滋病（acquired immunodeficiency syndrome;
AIDS）！根據西元1993年美國疾病管制中心（Centers for Disease Control and
Prevention;
CDC）新的AIDS診斷標準，歸納共有二十餘種感染或腫瘤的併發症，如果HIV患者同時發生其中任何一種疾病時，便是符合AIDS診斷標準（不論CD4+淋巴球數）。另一AIDS診斷標準是HIV患者的CD4+淋巴球數少於200/毫升。因此，如果患者只有HIV血清檢查呈陽性反應，他並沒有CDC所定義的併發症或CD4+淋巴球數高於200/毫升，我們只能診斷該患者是HIV感染而不是AIDS。
| 
Case Discussion
繼續教育考題