前回、ハリソン翻訳版を批判したが、そうしたら「でも、日本で書かれている教科書も結構ひどいよ」というレスポンスをいただいた。
同感である。
基本的に、ハリソンはとても良質な教科書で、ぼくは学生時代から長年愛用している。「最新のエビデンスが載っていない」と文句をいう人もいるが、本書は「そういう」本ではないのである。
日本の内科学の教科書は、ではどうか。確認のために、図書館でちょっと拾い読みしてみた。
けっこういろいろ出てるんですね、中山と朝倉しか知らんかった。
まあ、読んでみて治療やなんかもいろいろ突っ込みどころが多いです。でも、とくに「臨床像」を見れば、日本の教科書の「本質的な」問題点は分かる。比較して、考えてみてほしい、日本の内科学書に何が足りないのか、を。
中山書店「内科学書」（第７版 2009年）
レンサ球菌感染症より
「咽頭炎 pharyngitis 感染症法では五類感染症（小児科定点把握）に指定されている。潜伏期は２〜４日、急激に発症し、咽頭痛、発熱で始まる。咽頭発赤、扁桃腫大、灰白色分泌物を伴い、所属頸部リンパ節炎、中耳炎、副鼻腔炎、髄膜炎などを併発することがある」
ハリソン１８版（以下同様）
"Although seen in patients of all ages, GAS pharyngitis is one of the most common bacterial infections of childhood, accounting for 20-40% of all cases of exudative pharyngitis in children; it is rare among those under the age of 3. Younger children may manifest streptococcal infection with a syndrome of fever, malaise, and lymphadenopathy without exudative pharyngitis. Infection is acquired through contact with another indivisual carrying the organism. Respiratory droplets are the usual mechanism of spread, although other routes, including food-borne outbreaks, have been well described. The incubation period is 1-4 days. Symptoms include sore throat, fever and chills, malaise, and sometimes abdominal complaints and vomiting, particularly in children. Both symptoms and signs are quite variable, ranging from mild throat discomfort with minimal physical findings to high fever and severe sore throat associated with intense erythema and swelling of the pharyngeal mucosa and the presence of purulent exudate over the posterior pharyngeal wall and tonsiller pillars. Enlarged, tender anterior cervical lymph nodes commonly accompany exudatative pharyngitis" 以下鑑別診断や合併症へと続く。
医学書院「内科学」(2006年）
細菌性髄膜炎より
「発熱、頭痛、悪心・嘔吐、意識障害などがみられる。項部硬直、Babinski(バビンスキー）反射、Brudzinski(ブルジンスキー）反射が陽性となり、滑車、外転および顔面神経の麻痺を伴うこともまれではない」
ハリソン
"Meningitis can present as either an acute fulminant illness that progresses rapidly in a few hours or as a subacute infection that progressively worsens over several days. The classic clinical triad of meningitis is fever, headache, and nuchal rigidity, but the classic triad may not be present. A decreased level of consciousness occurs in >75% of patients and can vary from lethergy to coma. Fever and either headache, stiff neck, or an altered level of consciousness will be present in nearly every patient with bacterial meningitis. Nausea, vomiting, and photophobia are also common complaints.
Seizures occur as part of the initial presentation of bacterial meningitis or during the course of the illness in 20-40% of patients. Focal seizures are usually due to focal arterial ischemia or infarction, cortical venous thrombosis with hemorrhage, or focal edema" (以下続く）
文光堂 「内科学」第２版（2003年）
感染性心内膜炎より
「臨床症状および所見は感染症状、心症状、塞栓感染症状に分けると理解しやすい(表）。心症状は、弁破壊により逆流が生ずることによる心雑音や心不全所見である。塞栓感染症状は、疣贅が（一字コピー不鮮明）離し全身の塞栓症や感染症を呈するもので、脳、腎、脾、肺、（一字コピー不鮮明）管に多い。臨床症状・所見のうち、発熱・心雑音は80%以上にみられる。不明熱に遭遇した時は常に本症を念頭に置く必要がある。発熱＋心雑音、塞栓症が本症を疑わせる症状である」
ハリソンのcardiac manifestationsのとこだけ。(この前に一般論、その後で、noncardiac manifestations とmanifestations of specific predisposing conditionsと続く）。
"Although heart murmur are usually indicative of the predisposing cardiac pathology rather than endocarditis, valvular damage and ruptured chordae may result in newe regurgitant murmurs. In acute endocarditis involving a normal valve, murmurs may be absent initially but ultimately are detected in 85% of cases. Congestive heart failure (CHF) develops in 30-40% of patients; it is usually a consequence of valvular dysfunction but occasionally is due to endocarditis-associated myocarditis or an intracardiac fistula. Heart failure due to aortic valve dysfunction progresses more rapidly than does that due to mitral valve dysfunction. Extension of infection beyond valve leaflets into adjacent annular or myocardial tissue results in perivalvular abscesses, which in turn may cause intradcardiac fistulaee with new murmur. Abscesses may burrow from the aortic valve annulus through the epicardium, causing pericarditis, or into the upper ventricular septum, where they may interrupt conduction pathways near the atrioventricular node or in the proximal bundle of His. Emboli to a coronary artery occur in 2% of patients and may result in myocardial infarction"
朝倉書店「内科学」（第９版 2007) 6月に改定予定らしい。
結核より
「まず肺胞マクロファージに侵入した結核菌（１〜３個で病変をつくることができる）はそこで増殖し炎症により滲出性病変を生ずる（初感染巣）。一部は肺門リンパ節に到達し、そこでも病変を生じ、primary complex とよばれる。この初期感染から直接発病する場合を一次結核とよぶ。二次結核は既感染者に起こる結核で、肺尖部、上葉背部、下葉上区などに生ずる」（以下、検査所見、治療と移る（臨床像はどこ？？）。
ハリソン
"TB is classified as pulmonary, extrapulmonary, or both. Before the advent of HIV infection, ~80% of all new cases of TB were limited to the lungs. However, up to two-thirds of HIV-infected patients with TB may have both pulmonary and extrapulmonary TB or extrapulmonary TB alone.
Pulmonary TB
Pulmonary TB can be conventionally categorized as primary or postprimary (adult-type, secondary). This distinction has been challanged by molecular ebidence from TB-endemic areas indicating that a large percentage of cases of adult pulmonary TB result from recent infection (either primary infection or reinfection) and not from reactivation
Primary disease
割愛
Postprimary (adult-type) disease
Also referred to as reactivation or secondary TB, postprimary TB is probably not accurately termed adult-type TB, since it may result from endogenous reactivation of distant latent infection or recent infection (primary infection or reinfection). It is usually localized to the apical and posterior segments of the upper lobes, where the substantially higher mean oxygen tension (compared with that in the lower zones) favors mycobacterial growth. The superior segment of the lower lobes are also more frequently involved. The extent of lung parenchymal involvement varies greatly, from small infiltrates to extensive cavitary disease. With cavity formation, liquefied necrotic contents are ultimately discharged into the airways and may undergo bronchogenic spread, resulting in satellite lesions within the lungs that may in turn undergo cavitation (fig). Masive involvement of pulmonary segments or lobes, with coalescence of lesions, produces caseating pneumonia. While up to one-third of untreated patients reportedly succumb to severe pulmonary TB within a few months after onset (the classic "galloping consumption" of the past), others may undergo a process of spontaneous remission or proceed along a chronic, progressively debilitating course ("consumption" or phthisis). Under thise circumstances, some pulmonary lesions beecome fibrotic and may later calicify, but cavities persist in other parts of the lungs. Individuals with such chronic disease continue to discharge tubercule bacilli into the environment. Most patients respond to treatment, with defervescence, decreasing cough, weight gain, and a general improvement in well-being within several weeks.
Early in the course of disease, symptoms and signs are often nonspecific and insidious, consisting mainly of diurnal fever and night sweats due to defervescence, weight loss, anorexia, general malaise, and weakness. However, in up to 90% of cases, cough eventually develops--often initially nonproductive and limited to the morning and subsequently accompanied by the production of purulent sputum, sometimes with blood streaking. Hemoptysis develops in 20-30% of cases, and massive hemoptysis may ensue as a consequence of the erosion of a blood vessels in the wall of a cavity. Hemoptysis, however, may also result from rupture of a dilated vessel in a cavity (Rasmussen's aneurysm) or from aspergilloma formation in an old cavity. Pleuritic chest pain sometimes develops in patients with subpleural parenchymal lesions or pleural disease. Extensive disease may produce dyspnea and, in rare instances, adult respiratory distress syndrome. Physical findings are of limited use in pulmonary TB. Many patients have no abnormalities detectable by chest examination, whereas others have detectable rales in the involved areas during inspiration, especially after coughing. Occasionally, rhonchi due to partial bronchial obstruction and dclassic amphoric breath sounds in areas with large cavities may be heard. Systemic features include fever (often low grade and intermittent) in up to 80% of cases and wasting. Absence of fever, however, does not exclude TB. In some cases, pallor and finger clubbing develop. The most common hematologic findings are mild anemia, leukocytosis, and thrombocytosis with a slightly elevated erythrocyte sedimentation rate and/or C-reactive protein level. None of these findings is consistent or sufficient accurate for diagnostic purposes. Hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone has also been reported" 以下長い長いextrapulmonary TB、HIV-associated TBへと続く。
日本の内科学の教科書は、一言で言うと、「臨床家のまなざし」が足りない。ハリソンと比較すると圧倒的な違いである。ぶっちゃけ、日本の内科の教科書を読んでもちゃんと病気が診断できたり治療できるようになるとは思えない。ハリソンとは天と地ほどのクオリティーの差を感じる。こういう本たちがアマゾンの評価がすごく高かったりするのを見るととても心配になる。まともな教科書読んだことないんじゃないの？
まあ、フェアに申し上げておくと、日本の教科書にも「執筆者によっては」なかなか良いことを書いていることもあるにはあった。また、感染症に割くページ数がそもそも少なすぎ、というのも大きな根幹的な問題である。もしかしたらレベルが低いのは感染症だけで、他の診療科はよいのかもしれない。しかし、そういうのを差し引いても、日本の内科の教科書は質においてハリソンの足元にも及ばない、と思う（神経とか循環器とか、横断領域も見ましたので）。６月に出る「朝倉」がぼくの評価をひっくり返すような良書であることを願っている。願っているけどね。
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