急診小醫師ymmcc的醫學筆記: 2021

2021年12月15日星期三

口服抗糖尿病藥物

剛看到葉峻榳醫師整理的糖尿病口服藥. 覺得非常棒. 趕緊筆記一下網址

https://www.yehclinic.com/oral-antidiabetic-agents/

2021年9月25日星期六

糖尿病前期治療 Pre-DM stage treatment

糖尿病前期住院醫師陳筱筠1 主治醫師鍾嫈嫈2
基層醫學第二十一卷第七期 172頁

澎湖40歲以上民眾
空腹血糖 110 以下, 糖尿病年發生率 0.8%
空腹血糖 110-126, 糖尿病年發生率 3.2%

積極的生活型態介入治療
而健康生活型態介入治療則可能比藥物治療效果更好、無副作用、而且可以同時減少心血管疾病的危險因子，所以目前被認為是預防糖尿病及心血管疾病發生的最好方式。

健康生活型態計劃包括
一、減重(減少5~7%體重)；
二、減少脂肪攝取(少於25~30%總卡路里)；
三、飽和脂肪酸少於10%總卡路里；
四、增加纖維攝取(每1,000卡熱量大於15 公克)；
五、運動(中等程度運動，每星期150分鐘以上)

Diabetes Prevention Program顯示
積極的生活型態介入治療對於空腹血糖在 100~125mg/dL且有口服葡萄糖耐性異常的族群，可減少58%發生糖尿病的機會。
在高危險群中若7個人參加生活型態介入治療，3年內將可防止1個人發生糖尿病。
至於給藥組(metformin 850 mg bid)則可減少31%發生糖尿病的機會。
Finnish Diabetes Prevention study及中國研究(Da Qing IGT and Diabetes Study)顯示
飲食與運動的確可減少糖尿病的發生。

Acarbose 100 mg qd 減少糖尿病發生機率 24%
Troglitazone 400mg qd 減少糖尿病發生率 35%

而在STOP-NIDDM 及TRIPOD study中則分別顯示Acarbose 100mg tid及Troglitazone 400mg qd可減少 24%及35%糖尿病之發生機率。
由此可見健康的生活型態介入及藥物，都可能有助於延緩糖尿病之發生。
然而，藥物治療不僅花費昂貴、需監測血糖以防低血糖發生、有其他副作用
而且對於是否能預防或延緩糖尿病之併發症目前仍屬未知，也需要更多的研究來比較其效果與成本效益。

根據陳國東等人1995-1999年於澎湖對40歲以上600位民眾所做研究，發現在整個族群，空腹血糖正常(<110mg/ dL)及空腹血糖異常者(110~125mg/dL)其糖尿病的年發生率分別為 0.8%及3.2%。另外根據陳國東等人1995-1999年於澎湖對40歲以上600位民眾所做研究，發現在整個族群，空腹血糖正常(<110mg/ dL)及空腹血糖異常者(110~125mg/dL)其糖尿病的年發生率分別為 0.8%及3.2%。

空腹血糖異常者相較於空腹血糖正常者, 發生糖尿病的危險比為4.4倍。

糖尿病前期增加微小血管病變發生之危險性

Momin MG等人追蹤5,023位美國原住民的報告中指出，當空腹血糖大於 108mg/dL或兩小時飯後血糖大於162mg/ dL時，發生視網膜及腎臟病變的危險性就已經開始上升。

糖尿病前期增加心血管疾病發生之危險性
心血管疾病是造成第二型糖尿病患最常見的死亡原因，其所佔比率高達66% 以上。良好的血糖控制，可以延緩糖尿病患微小血管的破壞(如蛋白尿的產生 )，但是對冠狀動脈疾病的預防效果卻不佳。可能的解釋為：高血糖對心血管的傷害，早在糖尿病前期就已開始。挪威，Bjornholt JV.等人對40-59歲且空腹血糖小於110mg/dL的1973位男性做過22年的追蹤，發現空腹血糖大於85mg/dL的男性，其因心血管疾病之死亡率為空腹血糖小於 8 5 m g / d L 者的 1 . 4 倍 (1.04~1.8)。DECODE Study 分析歐洲10個回溯研究共15388位男性，7126位女性的研究，則顯示在預測心血管疾病死亡率方面，葡萄糖耐性異常的影響較空腹血糖異常為大。另外發現糖尿病前期者的心血管疾病危險因子如：血壓、血脂肪、身體質量指數、CRP等，都比正常組高。而這些因子也正是我們診斷新陳代謝症候群的條件因子，與胰島素阻抗性有關。

第三次美國健康和營養調查(NHANES III)也顯示在25~75歲且空腹血糖在 1 0 0 ~ 1 0 9 m g / d L 的成人，百分之八十九併有身體質量指數增加、高血壓或高血脂等需採取運動、飲食控制之問題。因此在面對糖尿病前期的病人時，要同時注意是否合併其它心血管疾病的危險因子。

預防糖尿病之發生積極的生活型態介入治療，對空腹血糖異常併有葡萄糖耐性異常的族群，的確可以預防或延緩發生糖尿病的機會。但是，對單純只有空腹血糖異常而無葡萄糖耐性異常者的成效，則仍有待研究證實（表2）。

Diabetes Prevention Program即顯示積極的生活型態介入治療對於空腹血糖在 100~125mg/dL且有口服葡萄糖耐性異常的族群，可減少58%發生糖尿病的機會。而在高危險群中若7個人參加生活型態介入治療，3年內將可防止1個人發生糖尿病。至於給藥組(metformin 850 mg bid)則可減少31%發生糖尿病的機會。Finnish Diabetes Prevention study及中國大陸大慶葡萄糖耐性異常及糖尿病研究(Da Qing IGT and Diabetes Study)也顯示飲食與運動的確可減少糖尿病的發生。而在STOP-NIDDM 及TRIPOD study中則分別顯示Acarbose 100mg tid及Troglitazone 400mg qd可減少 24%及35%糖尿病之發生機率。由此可見健康的生活型態介入及藥物，都可能有助於延緩糖尿病之發生。然而，藥物治療不僅花費昂貴、需監測血糖以防低血糖發生、有其他副作用而且對於是否能預防或延緩糖尿病之併發症目前仍屬未知，也需要更多的研究來比較其效果與成本效益。而健康生活型態介入治療則可能比藥物治療效果更好、無副作用、而且可以同時減少心血管疾病的危險因子，所以目前被認為是預防糖尿病及心血管疾病發生的最好方式。

健康生活型態計劃包括一、減重(減少5~7%體重)；二、減少脂肪攝取(少於25~30%總卡路里)；三、飽和脂肪酸少於10%總卡路里；四、增加纖維攝取(每1,000卡熱量大於15 公克)；五、運動(中等程度運動，每星期150分鐘以上) 。

野外與登山醫學---磺胺類抗生素過敏與丹木斯 2003 NEJM

https://www.nejm.org/doi/full/10.1056/nejmoa022963

2021-09-25 20:44
先是在 AAAAI 網站看到磺胺類抗生素與非抗生素磺胺交叉反應的文章, 裡面提到2003年NEJM這篇. 所以把這篇也看一看, 做做筆記.
先說簡單的結論, 發生過磺胺類抗生素過敏的人, 當然也可以對非抗生素磺胺過敏, 但醫師應該要知道, 這類患者其實對任何所有藥物都可能過敏, 甚至發生 penicillin 過敏機率還超過非抗生素磺胺類(例如丹木斯), 所以磺胺類抗生素過敏, 並不是丹木斯過敏的好指標
過去認為磺胺類抗生素過敏, 會發生非抗生素磺胺過敏, 是基於理論推導, 並非真實的數據

Abstract
BACKGROUND
The safety of sulfonamide nonantibiotics is unclear in patients with prior allergic reactions to sulfonamide antibiotics.

METHODS
We conducted a retrospective cohort study using the General Practice Research Database in the United Kingdom, examining the risk of allergic reactions within 30 days after the receipt of a sulfonamide nonantibiotic. Patients with evidence of prior hypersensitivity after the receipt of a sulfonamide antibiotic were compared with those without such evidence. Similar analyses were also performed with the use of penicillins instead of sulfonamides, to determine whether any risk was specific to sulfonamide cross-reactivity.

RESULTS
Of 969 patients with an allergic reaction after a sulfonamide antibiotic, 96 (9.9 percent) had an allergic reaction after subsequently receiving a sulfonamide nonantibiotic. Of 19,257 who had no allergic reaction after a sulfonamide antibiotic, 315 (1.6 percent) had an allergic reaction after receiving a sulfonamide nonantibiotic (adjusted odds ratio, 2.8; 95 percent confidence interval, 2.1 to 3.7). However, the risk of allergic reactions was even greater after the receipt of a penicillin among patients with a prior hypersensitivity reaction to a sulfonamide antibiotic, as compared with patients with no such history (adjusted odds ratio, 3.9; 95 percent confidence interval, 3.5 to 4.3). Furthermore, among those with a prior hypersensitivity reaction after the receipt of a sulfonamide antibiotic, the risk of an allergic reaction after the subsequent receipt of a sulfonamide nonantibiotic was lower than the risk of an allergic reaction after the subsequent receipt of a penicillin (adjusted odds ratio, 0.7; 95 percent confidence interval, 0.5 to 0.9). Finally, the risk of an allergic reaction after the receipt of a sulfonamide nonantibiotic was lower among patients with a history of hypersensitivity to sulfonamide antibiotics than among patients with a history of hypersensitivity to penicillins (adjusted odds ratio, 0.6; 95 percent confidence interval, 0.5 to 0.8).

CONCLUSIONS
There is an association between hypersensitivity after the receipt of sulfonamide antibiotics and a subsequent allergic reaction after the receipt of a sulfonamide nonantibiotic, but this association appears to be due to a predisposition to allergic reactions rather than to cross-reactivity with sulfonamide-based drugs.

Results
Overall, 4.8 percent of patients (969 of 20,226) had an apparent allergic reaction within 30 days after receiving the initial sulfonamide antibiotic with use of the broad definition, and 0.4 percent (86 of 20,279) had an allergic reaction with use of the narrow definition. (These denominators differ slightly, because we excluded more patients with prior disease using the broad definition than using the narrow definition.) In both groups, 67.5 percent of patients were female and 43.5 percent of patients were 65 years of age or older at the time of exposure.

Overall, 2.0 percent of patients (411 of 20,301) had an apparent allergic reaction after subsequently receiving a sulfonamide nonantibiotic with use of the broad definition, and 0.1 percent (19 of 20,391) did so with use of the narrow definition. Patients with prior hypersensitivity after sulfonamide antibiotics and those without such a history were similar with respect to age (P=0.24), sex (P=0.94), and duration of follow-up in the General Practice Research Database (P=0.62).

A total of 9.7 percent of allergic reactions after the sulfonamide nonantibiotics (40 of 411) were serious enough to require hospitalization. The most common diagnoses included in our composite end point were asthma (288 of 411, or 70.1 percent), eczema (58 of 411, or 14.1 percent), and adverse drug reactions (47 of 411, or 11.4 percent). With the use of our narrow definition of outcome, the comparative results were not substantively different. Therefore, we used the broad definition for all subsequently presented results, unless specified otherwise.

The unadjusted odds ratio for the association between hypersensitivity or allergic reactions after receipt of a sulfonamide nonantibiotic and a history of hypersensitivity or allergic reactions to sulfonamide antibiotics, as compared with no such history, was 6.6 (95 percent confidence interval, 5.2 to 8.4) with use of the broad definition (Table 2) and 13.2 (95 percent confidence interval, 1.7 to 99.9) with use of the narrow definition. Results that included only the subgroup of patients whose symptoms were consistent with those of type I hypersensitivity or IgE-mediated reaction (i.e., anaphylaxis, bronchospasm, urticaria, laryngospasm, or angioedema) were substantively the same but imprecise, since only 18 patients had such reactions.

Since the majority of patients (98.4 percent) received trimethoprim–sulfamethoxazole as the initial drug, the results were identical between the group as a whole and the subgroup of patients who received trimethoprim–sulfamethoxazole as their initial sulfonamide antibiotic. The results also did not change substantively when the subgroups were classified according to the subsequent sulfonamide nonantibiotic that was prescribed: the unadjusted odds ratio was 5.7 (95 percent confidence interval, 4.0 to 8.3) for thiazides alone, 7.0 (95 percent confidence interval, 5.1 to 9.3) for loop diuretics alone, 6.9 (95 percent confidence interval, 3.0 to 15.9) for sulfonylureas alone, and 3.6 (95 percent confidence interval, 0.2 to 72.3) for other sulfonamide nonantibiotics.

Of the large number of potential confounders investigated, we found that the only variables that changed the odds ratio by at least 15 percent were preexisting asthma and prior use of asthma medications and corticosteroids. The adjusted odds ratio (after controlling for sex, age at outcome, and the presence or absence of preexisting asthma, prior use of asthma medications, and prior use of corticosteroids) was 2.8 (95 percent confidence interval, 2.1 to 3.7). The odds ratio was 2.9 (95 percent confidence interval, 1.9 to 4.2) for those younger than 65 years old and 2.6 (95 percent confidence interval, 1.7 to 4.0) for those 65 years of age or older. With the use of cessation of the sulfonamide nonantibiotic therapy (instead of allergic reactions) as the outcome, prior hypersensitivity to sulfonamide antibiotics was not a predictor for stopping therapy with a sulfonamide nonantibiotic (unadjusted odds ratio, 1.1; 95 percent confidence interval, 0.9 to 1.2).

Finally, to place the above results in perspective (Table 2), the unadjusted odds ratio for an allergic reaction after the receipt of a prescription for a penicillin for those with a prior reaction after a sulfonamide antibiotic, as compared with those without such a reaction, was 7.8 (95 percent confidence interval, 7.1 to 8.5), with an adjusted odds ratio of 3.9 (95 percent confidence interval, 3.5 to 4.3). Among those with an allergic reaction after receiving a sulfonamide antibiotic, the unadjusted odds ratio for an allergic reaction to a subsequent sulfonamide nonantibiotic, as compared with a subsequent penicillin, was 0.7 (95 percent confidence interval, 0.5 to 0.9), and the adjusted odds ratio was 0.7 (95 percent confidence interval, 0.5 to 0.9). Indeed, comparing patients with prior evidence of hypersensitivity after sulfonamide antibiotics with patients with prior evidence of hypersensitivity after penicillins showed that an allergic reaction occurred in 9.1 percent (81 of 889) and 14.6 percent (693 of 4736), respectively, within 30 days after they had received a subsequent sulfonamide nonantibiotic drug (unadjusted odds ratio, 0.6 [95 percent confidence interval, 0.4 to 0.7]; adjusted odds ratio, 0.6 [95 percent confidence interval, 0.5 to 0.8]) (Table 2).

Discussion
Our results suggest that, although allergy to a sulfonamide antibiotic is indeed a risk factor for a subsequent allergic reaction to a sulfonamide nonantibiotic, a history of penicillin allergy is at least as strong a risk factor. The association initially seen in the primary analysis with the sulfonamide nonantibiotics might be explainable by a general predisposition to allergic reactions among certain patients rather than a specific cross-reactivity with drugs containing the sulfa moiety. Thus, our results suggest that, if sulfonamide-based nonantibiotics were to be avoided in those with a prior sulfa allergy, they would also have to be avoided in those with a prior penicillin allergy. Alternatively, and perhaps more rationally, prescribers should simply understand that patients with a history of any type of allergic reaction after the receipt of sulfonamides or penicillins may be at increased risk for reactions to other drugs, rather than consider sulfonamides a specific contraindication. Indeed, previous data have indicated that a history of an adverse drug reaction increases the risk of a subsequent adverse drug reaction.1,22 Some data suggest that persons with atopy are at higher risk for reactions to penicillin,23 radiocontrast dye,24,25 anesthetics,22 muscle relaxants,22 barbiturates,22 acetaminophen,26 nonsteroidal antiinflammatory drugs,27 and multiple antibiotics.28 Other data indicate that persons with atopy are not at increased risk for a drug hypersensitivity reaction,1,29,30 but that they may have more severe reactions.1,22,31

Although sulfonamide allergy is unpredictable and potentially life-threatening, there are few systematic investigations of these reactions and even fewer studies of the risk of hypersensitivity reactions after the subsequent receipt of a nonantibiotic sulfonamide. Understanding these risks is especially important, because sulfonamide allergy is common. In addition, sulfonamide nonantibiotics include members of many extremely important pharmacologic classes. Previous data indicating a link between an allergic reaction to a sulfonamide nonantibiotic and a history of a reaction to a sulfonamide antibiotic are limited primarily to case reports.6,32-34 One meta-analysis of data from clinical trials of celecoxib, an antiinflammatory agent containing an arylsulfonamide moiety, found no increased risk of an allergic reaction related to sulfonamide sensitivity.6 A small cohort study at two teaching hospitals did not find cross-reactivity between trimethoprim–sulfamethoxazole and dapsone.35 We used a much larger cohort to explore systematically the risk of allergic reactions to all sulfonamide nonantibiotics in patients with a history of sulfonamide allergy. However, we could not include data on the use of some newer drugs, including celecoxib. Because allergens, haptens, and other immune mechanisms for sulfonamide hypersensitivity have not been identified, this risk could not be studied with the use of immunologic methods.

Several limitations may have influenced our results. Information bias could have resulted if the two study groups were asymmetric with respect to the completeness of the information on outcomes. However, the assessment of outcome was not dependent on the patients' recall or on interviewers, since the information was obtained from computerized medical records. Furthermore, we did not rely on physicians' attribution of adverse drug reactions. Although there are codes in the General Practice Research Database for drug-induced disease, we have no way of ensuring that the general practitioners used such a code rather than a code for the outcome itself (e.g., urticaria). Therefore, we were hesitant to make such a distinction. In addition, the validity of the attributed link in such case reports is questionable in many instances, because a clinician cannot always determine whether urticaria is due to a patient's exposure to a sulfonamide antibiotic, is related to another precipitant, or is idiopathic. The uncertain validity of such subjective judgments is why comparative epidemiologic studies such as ours are needed.

So-called diagnostic suspicion bias could have occurred if patients who had the exposure of interest were more closely monitored for the outcome of interest than those without this exposure; that is, if physicians were more likely to monitor patients with a history of sulfa allergies for allergic reactions after administering a nonantibiotic sulfonamide. However, such bias would have increased the risk of a positive association in the comparison of sulfonamides with penicillins, in contrast to the inverse association that we found.

Outcome misclassification might have occurred if the outcomes did not come to medical attention. However, they would have been detected in our analyses in which cessation of sulfonamide nonantibiotics was the outcome variable. Outcome misclassification could also have occurred if physicians did not use a formal diagnosis to document milder outpatient drug reactions, such as maculopapular rashes. Since we relied on primary medical records, not on claims data, this possibility is less likely to have been a problem. In addition, there is no reason why this factor should have differed between the study groups. Outcome misclassification could also have occurred if a patient had chronic allergic symptoms (e.g., asthma) and coincidentally took a sulfonamide. However, we controlled for preexisting allergic reactions in the analysis.

A selection bias might be introduced from the loss of patients after enrollment (either due to death or to transfer out of the practice). Such a loss is unlikely in a medical-record data base of general practitioners in the United Kingdom and was unlikely to be unequal in the two study groups.

Selection bias could also have been introduced if a patient with a prior sulfonamide antibiotic reaction were less likely to be prescribed a nonantibiotic sulfonamide than a patient with no such history. However, when we compared those with an allergic reaction within 30 days after receipt of the initial sulfonamide antibiotic with those without such a reaction, examining the probability of being prescribed a subsequent sulfonamide nonantibiotic at least 60 days later, we found a relative risk of 1.13 (95 percent confidence interval, 1.06 to 1.21). In other words, those with an allergic reaction after a sulfonamide antibiotic were slightly more likely to receive a subsequent sulfonamide nonantibiotic than those without such a history (17.0 percent vs. 15.3 percent). It is possible, however, that those with certain types of initial reactions were preferentially steered away from subsequent exposures. However, our results did not differ substantively according to whether the initial reaction did or did not meet our strict definition or whether the initial reaction did or did not result in hospitalization. Thus, it seems very unlikely that such a selection process could have affected our results.

Finally, we controlled for a large number of potential confounders in the analyses, and substantial confounding was seen from preexisting asthma and its treatment, which can, of course, be related both to subsequent asthma and to the use of antibiotics and other medications. We also cannot be certain that there were no other variables for which we could not control.

Thus, although a history of allergy to sulfonamide antibiotics is a marker of increased risk on subsequent exposure to sulfonamide nonantibiotics, our results suggest that this risk is not unique to sulfonamide antibiotics. Indeed, patients with a history of hypersensitivity to sulfonamide antibiotics are at even greater risk for subsequent reactions to penicillins, a biochemically distinct group, than to nonantibiotic sulfonamides. Prescribers should understand that patients with a history of allergic reactions to drugs may be at increased risk for all drug-induced adverse events that appear to be allergic in nature.

2021年6月23日星期三

末梢神經障礙維生素B12 methycobal 500 ug

劑量 500ug tid.

Max 1500ug/day

若無明顯改善, 不建議服用超過一個月

2021年6月19日星期六

醫療人員採檢

疾管署QA

Q40.醫療照護工作人員COVID-19擴大採檢常見問與答

Q1. 醫療照護工作人員COVID-19擴大採檢相關規範有哪些？
「醫療照護工作人員COVID-19擴大採檢及個案處理流程」及「醫療照護工作人員COVID-19擴大採檢後注意事項」。

Q2. 醫療照護工作人員COVID-19擴大採檢之適用對象為何？
適用於醫院和住宿式衛福機構第一線照顧病人/服務對象的工作人員。。

Q3. 醫療照護工作人員COVID-19擴大採檢之條件為何？
具肺炎或嗅覺、味覺異常症狀者。或
具發燒/呼吸道症狀/不明原因腹瀉等症狀，醫師認為有進行 SARS-CoV-2 檢驗之必要者。

Q4. 經醫師評估符合醫療照護工作人員COVID-19擴大採檢之病人，該如何採檢送驗？
進行個案鼻咽擦拭液或咽喉擦拭液或痰液採檢，至傳染病個案通報系統「其他」項下「疑似新冠病毒感染送驗入口」通報送驗；個案如為醫事人員，需於通報單職業欄位選擇「醫師」、「護士」或「其他醫事人員」；如為醫院之非醫事人員，則選擇「醫院工作者（非醫事人員）」；如為照護機構工作人員，則選擇「醫療保健及社會福利服務業」。

Q5. 經醫師評估符合醫療照護工作人員COVID-19擴大採檢之病人，除了採檢送驗之外，醫療院所需配合哪些事項？
衛教個案落實「醫療照護工作人員COVID-19擴大採檢後注意事項」，且返家時應全程佩戴口罩，禁止搭乘大眾交通運輸工具。

Q6. 採檢時有哪些注意事項？
採檢應於單獨之病室或空間執行，並依感染管制措施指引，採取適當的防護措施。

Q7. 醫療照護工作人員COVID-19擴大採檢個案可否外出？
可外出，惟應遵循社區監測通報個案採檢後應注意事項。

Q8. 醫療照護工作人員COVID-19擴大採檢個案，何時可返回工作？
採檢個案於退燒超過24小時（未使用退燒藥）且相關症狀緩解後，不需等待檢驗結果陰性，可返回上班；惟返回工作後應遵循「醫療照護工作人員COVID-19擴大採檢後注意事項」所載事項。

Q9. 醫療照護工作人員COVID-19擴大採檢個案，返回工作有哪些注意事項？
遵循社區監測通報個案採檢後注意事項。
採檢後3日內(以採檢次日為第1日)或所有症狀尚未完全消失前，在醫療照護機構中應全程佩戴口罩，即使是在非照護區（如：休息區）；建議應依劃分的空間或使用時段間隔使用休息區，如因飲食等情況，需要脫除口罩時，須維持社交距離原則。
採檢後3日內(以採檢次日為第1日)或所有症狀尚未完全消失前，避免與嚴重免疫功能低下（如：移植、血液腫瘤等）的病人或服務對象接觸。
後續若症狀加劇，應立刻停止上班；若於工作中出現前述情形，則應立即離開照護區，進行自我隔離，並通知主管，且應全程佩戴口罩及採取適當防護措施，儘速就醫評估，且不得搭乘大眾運輸工具。

Q10. 醫療照護工作人員COVID-19擴大採檢個案，如何獲知檢驗結果？
若檢驗為陽性，衛生單位或採檢院所會主動通知；若採檢3日內未接獲通知，等同陰性。

Q11. 醫療照護工作人員若符合「嚴重特殊傳染性肺炎」通報定義，可否以醫療照護工作人員COVID-19擴大採檢送驗？
不可以。請依「嚴重特殊傳染性肺炎通報個案處理流程」進行處置。

Q12. 醫療照護工作人員若為「嚴重特殊傳染性肺炎」通報個案，是否適用「醫療照護工作人員COVID-19擴大採檢後注意事項」？
不適用。醫療照護工作人員若為通報個案（非確診），於2次（採檢間隔至少24小時）採檢陰性且退燒24小時（未使用退燒藥）且相關症狀緩解後，始可返回上班。

Q13. 醫療照護工作人員若於居家隔離或居家檢疫期間出現疑似症狀，可否直接到採檢院所進行擴大採檢？
不可以。應主動與與當地衛生局聯繫，或撥1922，依指示儘速就醫，並應全程佩戴口罩及採取適當防護措施，且禁止搭乘大眾運輸工具就醫。

Q14. 經醫師評估需進行COVID-19採檢之病人，該如何處置？
醫療院所若非COVID-19全國指定社區採檢院所，請依「COVID-19（武漢肺炎）社區採檢網絡轉診注意事項」進行轉診。
若病人符合「嚴重特殊傳染性肺炎」通報定義，不論是否為醫療照護工作人員，請依嚴重特殊傳染性肺炎「通報個案處理流程」進行處置。
若病人為未符合「嚴重特殊傳染性肺炎」通報定義之醫療照護工作人員，請依「醫療照護工作人員COVID-19擴大採檢及個案處理流程」處置。
若病人未符合「嚴重特殊傳染性肺炎」通報定義且非醫療照護工作人員，請依「社區監測通報採檢及個案處理流程」處置。

2021年6月1日星期二

原著文章疾管署網頁

COVID-19疫苗簡介投稿日期2021年03月31日, 刊登日2021 年 4月 13日

第 37 卷第 7 期蘇家彬(通訊作者)、陳孟妤、顏嘉嫺

表一、COVID-19 疫苗之不同平台比較

COVID-19 台灣死亡個案

COVID outbreak

COVID mortality cases

COVID-19 新冠肺炎全球確診病例數死亡病例數, 致死率

2021-06-01

2021年5月29日星期六

COVID確診個案處置解除隔離條件

2021-05-25 新北市衛生局建議: 留在家中等候公衛人員通知, 症狀嚴重打119或1922或當地衛生局

https://www.facebook.com/ntpchealth/photos/4081598395264325

2021-05-19 衛福部建議, 確診之後打電話給自己的密切接觸者, 建議他們自我隔離及健康監測, 輕症患者在家隔離等候公衛人員通知, 症狀嚴重打119或1922或當地衛生局

https://www.facebook.com/mohw.gov.tw/photos/a.484593545040402/1884870828345993

照顧確診的家人(自己沒症狀), 禁止訪客, 不得外出, 與患者最後一次接觸(患者住院隔離或死亡)之後需居家隔離 14 天(接觸日隔天開始算)

https://www.facebook.com/mohw.gov.tw/photos/a.484593545040402/1884273591739050

2020-04-21 附件1-嚴重特殊傳染性肺炎通報個案處理流程.pdf

去年2020年訂的通報流程, 原本陽性個案都要收住院隔離

2021-05-27 因疫情大爆發, 修改通報流程. 快篩陽性即可通報, 可居家隔離(無住院需求,且居家環境可一人一室)等候PCR結果

PCR陽性, 依照確診個案處置及解隔條件處理.

解隔離條件 2021-05-17 修訂

嚴重特殊傳染性肺炎>> 重要指引及教材>>通報定義及採檢

https://www.cdc.gov.tw/Category/MPage/np0wef4IjYh9hvbiW2BnoQ

無症狀或輕症發病(或採檢日)已經 10 天, 退燒至少一天, 症狀緩解, PCR陰性或CT值大於等於30, 可解除隔離

若CT值小於30, 但不需積極治療, 不需用氧氣, 可出院移至集中檢疫所繼續隔離七天

期滿不需採檢即可解除隔離. 

未滿七天若有採檢, 陰性或CT值大於等於30則解除隔離

非輕症住院, 退燒超過一天且症狀緩解, PCR一次陰性或CT值大於等於30, 發病(或採檢日)超過10天, 以上均達成可解除隔離

集中檢疫所隔離的個案(輕症或無症狀), 退燒至少一天, 症狀緩解, 發病超過10天, PCR採檢陰性或CT值大於等於30可解除隔離(還是需要採檢PCR) 

COVID-19 新冠肺炎

COVID-19 什麼人需要採檢

篩檢對象, 隨著時間和疫情進展而不同

要考量當地的醫療資源人力設備, 篩檢量能

2021-05-30 全國社區篩檢站設置補助上路，提高民眾採檢可近性

無症狀民眾

針對具有確診個案相關接觸史、活動史之無症狀民眾為主要篩檢對象

2021-05-25 新北市衛生局, 有症狀可打給衛生局 22586923或 1922 通報, 之後戴口罩去就近社區篩檢站採檢

2021-05-25 無症狀無接觸史不需採檢無症狀無接觸史不需篩檢

2021-05-22 如果您曾為 #萬華高風險區活動或 #接觸史者，建議您可就近 #社區篩檢站進行篩檢

2021-05-20 16:07 曾前往高風險區且有症狀

2021-05-19 無接觸史/活動史且無症狀不需篩檢

2021-05-16 22:12 目前以居住板橋區、有萬華高風險區活動或接觸史者為優先

2021年5月23日星期日

野外與登山醫學---戶外作業虎頭蜂攻擊預防手冊 104年勞動部出版

勞動部勞動及職業安全衛生研究所在 104年1月出版的戶外作業虎頭蜂攻擊預防手冊

毒性: 羅東博愛醫院急診科尤俊文醫師自1985年至1997年收集22份因為遭蜂螫住院的病人資料分析報告，是項資料顯示：
1. 8〜11月遭蜂螫的病例最多，蜂螫的數目超過10隻以上。
2.遭蜂螫後10〜30分鐘會發生過敏性休克。
3.被30〜50隻蜂螫後，累積足夠的毒素才會造成全身的嚴重症狀。
4.過敏反應與毒素的劑量無關，過敏體質的人受到1〜2隻蜂螫，就會引發嚴重症狀，局部腫脹超過10公分，且持續數天。
5.造成過敏性休克的機會有5-10 ﹪。在30分鐘內會發生全身蕁麻疹、舌咽腫脹、呼吸困難、哮喘、血壓降低、意識喪失等症狀。
6.被蜂螫刺的數目超過 10隻以上，必須住院觀察後續的併發症(急診教科書寫的是 100 隻)，包括休克、橫紋肌溶解症、溶血、腎衰竭，或產生延遲性全身反應，如全身性過敏反應或類似血清病等

七、戶外作業人員如何預防蜂螫 (我將原文修改成戶外活動版)
1. 觀察周圍是否由虎頭蜂個體活動, 或類似蜂巢結構物體
2. 無法確認是否為蜂巢, 當成是蜂巢. 行進中小心
3. 於虎頭蜂活動區行進, 可考慮攜帶含有DEET 成分的防蚊商品 (敵避、待乙妥、敵避胺、避蚊胺), 具有驅蟲效果, 噴灑於衣服或身體表面. 時間長了還要補噴.
4. 人少的山路或草叢是蜂類選擇築巢的好地方, 山岩或樹枝也可能有蜂巢, 仔細觀察是否有警戒任務的虎頭蜂. 盡量不要通過這些地區. 吃剩的果皮食物也可能引來蜂類.
5. 陰雨的天氣, 蜂類多留在巢內, 造成蜂巢內壅擠而容易被激怒, 之後螫人
6. 登山最好穿戴表免光華, 淺色衣帽. 避免深色. 毛織品. 或表面粗糙的衣帽, 帽子最好能紮到鞋子內. 避免噴香水. 使用化妝品. 或特殊氣味物品.
7. 發現蜂類經過身邊, 最好站立不動, 冷靜觀察, 不要拍打, 不要揮動衣物驅趕, 最好讓牠自行飛離, 以手拍打雖可暫時驅趕開, 但可能引來蜂群.
8. 如果發現兩三隻巡邏蜂在身旁打轉並盤旋不去, 表示蜂類已經懷疑你是敵人, 應鎮靜緩慢安靜離開現場, 稍後蜂類即可能自然離開. 人的肢體大動作即因緊張吼叫是非常危險的, 只要猛力揮趕閃避或動手驅蜂,拍蜂,必遭蜂螫.

蜂螫後的現場緊急處置
就物種演化角度而言，蜂類螫針原本就是用來保護蜂巢、驅退敵人的武器。當被蜂螫的瞬間，隨即會感受巨大的疼痛感，接著患部出現抽痛與腫脹，腫脹的程度及持續時間會因個人體質、蜂毒種類及毒液量有關，一般需3〜5日始會逐漸消腫，消腫過程患部會呈現搔癢症狀。一般言之，從遭蜂螫到症狀消除，約需7日(一星期)左右。
當遭蜂類螫傷時，勿用手擠壓傷口，可以稍加消毒尖頭鑷子或利用刀片或信用卡輕輕將螫針挑出，然後清潔傷口、冰敷，減輕疼痛與腫脹症狀。有些人被蜂螫傷後10〜30分鐘會出現蕁麻疹，可考慮送醫施打抗組織胺，並讓患者處於通風涼爽之環境。但如出現暈眩、心悸、呼吸困難、意識不清等症狀，務必立即送醫急救。蜂螫後特別要注意是否出現過敏性休克症狀，少數對蜂毒過敏的人極可能會在短時間就出現休克反應，相當危險，此時現場的急救則極為重要，可由急救防護員施打腎上腺素，並立即就醫。

毒性反應
虎頭蜂螫叮之毒性反應，可分為下列三種情況：
1.少量螫刺，局部反應：
遭蜂螫刺數目少於20針次，且無過敏反應者，毒性反應大多只在螫刺部位引起因毒蛋白造成之局部紅、腫、熱、痛、癢等反應，較不會有生命危險。
遭蜂螫之傷患在離開現場後，應檢視被蟞傷的部位，如有螫針殘留(通常是一般蜜蜂螫刺會殘留螫針)，可利用指甲、刀片或信用卡輕輕將螫針挑掉，然後清潔傷口、冰敷、局部塗抹抗生素加類固醇軟膏，也可加上口服抗組織胺。
2.少量螫刺,過敏反應

(過敏性休克參考這篇anaphylaxis 嚴重全身性過敏反應治療藥物與頻次劑量)

anaphylaxis 翻譯成過敏性休克並不恰當. 會誤導醫護人員. 以為血壓降低才需要做緊急處置.

3.大量螫刺，全身性中毒反應：當遭蜂螫刺數目多過20〜30針時，有可能引起全身性中毒反應。
診療原則
♦此治療原則係以提供急診室作為遭蜂螫送急診之傷患就診治療參考。
1.穩定生命徵象，注意過敏休克的處置。
2.可利用指甲、刀片或信用卡輕輕的將蜂刺及毒液囊刮除(若有螫針遺留在皮膚上)。
3.用肥皂水或消毒水清洗傷口。
4.抬高患肢，可予以冷敷。
5.可給予止痛劑、抗組織胺
6.大片的局部反應可能需給予短期的類固醇治療。
7.如傷患遭多隻蜂螫，建議應觀察24小時，注意是否有腎衰竭或凝血異常的現象。
8.中度以上的過敏(如產生血管性水腫(angioedema)或支氣管痙攣(bronchospasm))，除給予靜脈注射抗組織胺(antihistamine)或吸入氣管擴張劑(bronchodilator)外，即適合使用腎上腺素(epinephrine)的時機，其劑量為肌肉注射(subcutaneous)1:1000之腎上腺素(epinephrine)0.3-0.5ml，如有必要可每20-30分鐘重覆使用。
9.如休克嚴重，除予以補充液體外，可給予1:10000之腎上腺素(epinephrine)3-5ml，如有必要可每3-5分鐘重覆使用。

(2010 ACLS 指引. 建議腎上腺素 5-15 分鐘使用一次)

anaphylaxis 全身性嚴重過敏反應腎上腺素劑量

查詢 2020 年 ACLS 的指引, 發現裡面的內容最後一次更新是在 2010 年. 2010 年 ACLS Part 12: Cardiac Arrest in Special Situations 建議, 腎上腺素每 5-15 分鐘可以給一次

2021年5月13日星期四

新冠武漢肺炎 COVID-19

具感染風險者=自主健康管理者, 根據110-03-01 公告.
https://www.cdc.gov.tw/File/Get/PrLPDhC3xFzQiGLzua8iAA

1. 需排除正在居家檢疫和居家隔離者

2. 採檢陰性

3. 居家隔離期滿之後再七天(隔離期滿的下一天為Day 1 ), 身分變為自主健康管理

4. 與確診病患最後一次接觸的隔天開始算 14 天

5. 居家檢疫期滿之後再七天. 七天內身分變成自主健康管理

6. 無症狀可外出, 但需配戴口罩, 不可與他人近距離接觸(例如聚餐, 聚會, 公眾集會

7. 近距離是指室內 1.5 公尺, 室外 1 公尺

8. 禁止到醫院探病

9. 醫療或檢查應延後, 除非有急迫性

10. 若採檢, 報告出來之前禁止外出.

11. 有症狀者禁止外出

12. 有症狀若需就醫, 需先打電話給衛生局或 1922, 禁止搭乘大眾交通工具去醫院

通報定義, 109年4月16日制定
https://www.cdc.gov.tw/File/Get/AyHd8990mKy62q9Ld0brqA

醫師懷疑即可通報
旅遊史或接觸史或群聚, 有症狀即可通報

嗅覺味覺異常或腹瀉 + 旅遊史/接觸史即可通報

採檢驗出病毒即可通報

疾管署針對新冠武漢肺炎的QA,

Q23-32. 我是醫療機構醫護人員，院內發生入院後才確診的COVID-19確定病例，我在何種情況下會被列為接觸者？

自個案發病日起至隔離前，如有以下情形，將被列為接觸者:

在無適當防護下曾有長時間（大於 15 分鐘）面對面接觸者，或提供照護、相處、接觸病患呼吸道分泌物或體液之同住者。
曾與確定病例在無適當防護下 2 公尺近距離接觸之醫護人員。

接觸者框列, 病患戴口罩, 醫護人員戴口罩, 不列入接觸者. 其他民眾有戴口罩, 不列入接觸者.
https://www.cdc.gov.tw/Category/QAPage/B5ttQxRgFUZlRFPS1dRliw

Q41.何謂密切接觸者?哪那些人會被列為接觸者?

依現行COVID-19之密切接觸者定義「自確診個案發病前2日起至隔離前，在無適當防護下曾有長時間（大於 15 分鐘）面對面之接觸者，或提供照護、相處、接觸病患呼吸道分泌物或體液之醫療人員及同住者。」，經衛生單位調查符合前述密切接觸定義而認定為與確定病例有密切接觸，將會匡列為接觸者，並納入居家隔離管制對象，應居家隔離至與確定病例最近一次接觸日後14天((如3月1日為最近一次接觸日，則應居家隔離至3月15日，3月16日零時起才可解除隔離))，惟衛生單位匡列之接觸者仍會視實際疫調情形作適當調整。

2021年5月12日星期三

Child-Pughs classification 肝硬化嚴重度

分數越高越嚴重, class C 一年存活率 45%

2021年5月11日星期二

氣喘患者若需使用乙型阻斷劑可先考慮給予 atenolon 100 mg

Asthma and beta-blockers
D S Lawrence, J N Sahay, S S Chatterjee, J M Cruickshank

PMID: 6127219
DOI: 10.1007/BF00609622

氣喘患者, 若需使用乙型阻斷劑, Atenolol 可與beta 2 agonist 同時開立
Abstract
In a randomized, blind crossover study in 14 hypertensive patients with asthma, involving placebo and chronically administered (3 weeks) equipotent beta1-blocking doses of atenolol 100 mg once daily and metoprolol 100 mg bid, atenolol and metoprolol produced a similar fall in blood pressure. Atenolol caused significantly (p less than 0.05) less bronchospasm in terms of fewer asthmatic attacks, more asthma-free days, less frequent sensations of moderate to very severe, wheeziness and less effect on the evening peak flow rate. It was concluded that, in patients with asthma who require beta blockade, atenolol is the preferred agent, co-prescribed with a beta2 stimulant.

2021年5月4日星期二

IGRA 丙型干擾素

結核菌素皮膚試驗（tuberculin skin test，TST）

血液丙型干擾素釋放試驗(interferon-gamma release assay，IGRA)

IGRA 和 TST 一樣，對活動性結核病的發病風險預測不佳

接種卡介苗會造成偽陽性

IGRA 陰性無法排除結核菌感染

IGRA 可能會偽陽性

IGRA 陽性預測值偏低. 需挑選篩檢對象, 以提高陽性預測值

TST 在老年人或T細胞免疫功能低下, 會有偽陰性

TST: 用於五歲以下患者, 或無法抽血檢查 IGRA時

LTBI 診斷工具及其限制

目前的兩種診斷工具，為 TST 與 IGRA，陰性預測值都不錯，但陽性者發病的預測值偏低 (positive predictive value of active TB)，故應選擇結核病高危險族群來進行檢驗。臺灣過去廣泛採用的結核菌素，為丹麥製 PPD RT23 with Tween 80，劑量 2 tuberculin unit(TU)/0.1 mL，以 Mantoux test 之方法，於 48~72 小時判讀反應硬結。結核菌素測驗受結核菌素製劑（菌株）、測驗與判讀技術、使用劑量、宿主因素、卡介苗接種、環境中的非結核分枝桿菌等因素影響。在 1954 到 1986 年之間出生的世代，幾乎都有接種過一劑卡介苗，且超過六成接種過兩劑的卡介苗，且多半不是在新生兒時期接種，故結核菌素皮膚測驗的結果，常會有偽陽性的疑慮，以及是否需使用較大的臨界值判讀的問題。由於 TST 是依賴健全的 T 細胞免疫功能之體內(in vivo)測試，年長或者 T 細胞免疫功能低下時，往往又有偽陰性的問題。所以，若用在感染率較高的族群，例如近期接觸者，感染率可達 10~40%不等，陽性預測值可達八成以上。臺灣未滿 13 歲的兒童接觸者，若是未接受 LTBI 治療，接觸者檢查時 TST 的反應大小，是三年內發病風險最相關最可靠的預測因子。

從 2016 年起， TST 僅用在未滿 5 歲的接觸者或極少數無法完成IGRA 檢驗的民眾，其判讀標準維持在 10mm(接種過卡介苗者)。未接種過卡介苗者、愛滋感染者、接受anti-lymphokines 或其他免疫抑制治療者，改以 5mm 為陽性臨界值。IGRA 則是利用結核分枝桿菌特異抗原在體外刺激淋巴球產生丙型干擾素(M. tuberculosis specific Interferone-γ)，加以定量來判定是否有 LTBI。IGRA 較少有卡介苗及環境中非結核分枝桿菌所帶來的偽陽性，且只要抽血檢驗，不必像 TST 須回診判讀。IGRA 和 TST 一樣，對活動性結核病的發病風險預測不佳。此外，採檢時必須用力搖勻，採檢後必須在數小時內上機，且價格昂貴，是過去沒有被普遍使用的主要原因。從2016 年起，凡是五歲以上的接觸者，都優先使用 IGRA，以減少因大量接種卡介苗引起的偽陽性和不必要的LTBI 治療。

由於仍然有為數不少的細菌學確診結核病個案，IGRA 血液測驗結果是陰性，故許多指引都指出，當病人出現疑似結核病的症狀，就算 IGRA 血液測驗結果是陰性，也不能排除病人有結核病，應積極採檢進一步確定診斷，故臨床上在使用此類檢查時，需注意其限制性。

2021年4月22日星期四

2020台灣腦中風學會腦血管疾病血脂異常治療指引

觀察型研究發現，血中總膽固醇與或低密度脂蛋白膽固醇(low density lipoprotein cholesterol ［LDL-C］)的濃度升高，和腦中風的風險增加有相關性，特別是與大動脈粥狀硬化相關的缺血性腦中風。如果有血脂異常，無論是否使用藥物治療都應進行生活型態改善。

對於動脈粥狀硬化相關或非動脈粥狀硬化相關但合併有冠狀動脈疾病的的缺血性腦中風或短暫性腦缺血(transient ischemic attack［TIA］)的病人，應使用高強效或中強效statin治療以預防未來發生的主要心血管事件，必要時可合併ezetimibe，來降低LDL-C <70 mg/dL，且急性期過後持續使用statin是合理的。

急性缺血性腦中風或TIA病人，如LDL-C >100 mg/dL或中風前有使用statin，於急性期住院期間使用statin是合理的。

對於症狀性頸動脈狹窄或顱內動脈狹窄病人，控制LDL-C <70 mg/dL是合理的。

對於無症狀頸動脈狹窄或顱內動脈狹窄病人，控制LDL-C <100 mg/dL是合理的。

低血糖風險比較

參考資料 https://pubmed.ncbi.nlm.nih.gov/29108130/

以 metformin 做為基準值(1)來比較各種不同藥物的低血糖風險.

Glibenclamide(Glyburide) tab 低血糖風險 3.95

glimepiride 低血糖風險 3.28 發生率約 2-4%

Glipizide 低血糖風險 2.57

Nateglinide (Starlix) 低血糖風險 1.21

Repaglinide (novonorm) 低血糖風險 20.3

2021年3月25日星期四

DM CKD 糖尿病慢性腎病第四期以下, eGFR < 30 藥物選擇

糖尿病慢性腎病第四期以下, eGFR < 30 藥物選擇

BG二甲雙胍
台灣, eGFR < 30 不建議使用

加拿大規定血清肌酸酐濃度超過 1.5 毫克/毫升的病人，不適用 metformin

SU磺醯尿素
Glipizide 2.5~20 mg/day不須調整劑量
glimepiride 1-8mg/day 低劑量使用 1mg qd
Gliclazide 80-160 bid 或緩釋劑 30-120mg qd 不須調整劑量
gliqidone 45-60 mg/day 不須調整劑量

Meglitinides

Repaglinide 0.5-4mg 隨餐服用, 低劑量使用
Nateglinide 60-120mg 隨餐服用 , 低劑量使用

DPP4i

sitagliptin (Januvia) 2.5 mg QD (四分之一量)
Saxagliptin (Onglyza ) 2.5mg qd (半量)

Linagliptin (Trajenta) 不須調整劑量

Vildagliptin (Galvus) 50mg qd

TZD

pioglitazone 15-45 mg qd 不須調整劑量
rosiglitazone 4-8 mg qd 不須調整劑量

eGFR < 45 禁止使用SGLT2i.

Canaglu®可拿糖膜衣錠 canagliflozin

dapagliflozin/Forxiga 福適佳

empagliflozin/Jardiance 恩排糖膜衣錠

2021年3月11日星期四

甲狀腺疾病與糖尿病

參考資料 Thyroid Hormone Effects on Diabetes Jennal L. Johnson, MS, RNC, FNP, BC-ADM, CDE

Diabetes Spectrum 2006 Jul; 19(3): 148-153.

甲狀腺疾病造成的碳水化合物代謝影響, 可能會導致糖尿病失控, 雖然不是每次血糖都受影響, 但甲亢患者有可能因為血糖上升過快, 造成葡萄糖耐受試驗異常, 過多的甲狀腺素會增加消化道吸收. 增加胰島素阻抗及胰島素降解.
The effect on carbohydrate metabolism can potentially lead to disruptions in diabetes control. Although the glucose level does not always change, there can be an abnormal response to glucose tolerance testing in hyperthyroidism because glucose rises faster than normal.7 Additionally, excessive thyroid hormones increase the rate of digestive tract absorption and thyroid hormone levels and therefore increase insulin resistance and insulin degradation.

甲亢症肝醣合成與降解增加, 造成肝醣貯積下降, 葡萄糖吸收增加, 葡萄糖利用率與產生增加, 周邊組織攝入葡萄糖速率增加, 導致葡萄糖試驗時峰值上升. 胰島素需求量增加, 如果沒有適當解決, 會失去代償. 導致DKA, 此外, 尚未被診斷的DM患者, 甲亢症會增加胰島素阻抗而出現糖尿病, 在甲亢症治療過程, 可能需增加血糖藥物, 直到甲狀腺功能穩定且血糖穩定.
In hyperthyroidism, glycogen synthesis and degradation increase, leading to decreased glycogen levels.3 Glucose absorption is increased, as well as utilization and production. Peripheral tissues have increased rates of glucose uptake that can lead to the aforementioned exaggerated glucose peak during a timed glucose test. Insulin requirements are increased, and, if not addressed adequately, control can decompensate, leading to diabetic ketoacidosis. Additionally, in patients with undetected diabetes, hyperthyroidism can unmask diabetes because glucose levels can be abnormally elevated because of increased insulin resistance.3 Increased dosages of diabetes medications may be necessary in those already treated, until thyroid function is stabilized and resultant glucose stabilization occurs.

甲狀腺低下症, 肝臟分泌肝醣減少, 降解也減少, 導致肝醣貯積增加, 腸胃道吸收葡萄糖下降, 周邊組織葡萄糖利用率下降, 葡萄糖新生的受質減少. 胰島素半衰期增加, 胰島素濃度下降, 胰島素分泌下降. 導致胰島素需求量降低, 如果外源性胰島素沒有減少, 會導致低血糖.

甲狀腺低下症治療過程, 血糖可能呈現穩定狀態, 但經過治療之後, 當甲狀腺功能正常, 可能導致血糖濃度上升, 影響血糖控制

In hypothyroidism, liver secretion of glycogen decreases, but so does degradation, leading to increased levels of glycogen. Absorption of glucose from the gastrointestinal tract is slowed, and glucose utilization is slowed in the peripheral tissues. The availability of gluconeogenic substrate is decreased. Additionally, the insulin half-life is prolonged, insulin levels are lower, and insulin secretion is reduced, which may lead to reduced insulin requirements. If exogenous insulin is not decreased, hypoglycemia may occur. It is likely that glucose levels will stabilize during hypothyroidism treatment. But when thyroid function is normalized, this may lead to higher blood glucose levels and adverse effects on glycemic control.

2021年3月10日星期三

潛伏結核感染治療處方

參考資料: 疾管署第十章「潛伏結核感染 (LTBI)」有關LTBI治療處方說明
結核病診治指引-第10章潛伏結核感染10905修正版
https://www.cdc.gov.tw/Uploads/6b5c1be7-5666-4dea-aabe-0ecbd5826c7d.pdf

3HP 3HR 4R 9H

已服用3HP治療轉換處方建議表

2021年3月2日星期二

高三酸甘油脂治療 TG levels between 150-885 mg/dL

參考資料: uptodate

TG過高如果合併LDL超過目標值, 應使用 statin 治療.

中高劑量 statin 例如 atorvastatin 80 mg qd 或 rosuvastatin 20-40 mg qd. 可以降低 TGs 25-30%, 在TG超過 800mg/dL 的患者甚至可以降 40%

如果已經使用最大能忍受的statin劑量仍無法將LDL控制在目標值, 可加上 ezetimibe.

高心血管疾病風險患者, 包括已經確診心血管疾病患者, 糖尿病患, 十年內發生心血管疾病機率>10% 的族群

高心血管疾病風險患者, 如果經過上述治療, TG仍超過 150, 可考慮加上 Fenofibrate 或 icosapent ethyl (或 niacin, 但較少用). 沒有胰臟炎病史的人, 可先服用魚油萃取物 icosapent ethyl, 如果曾有胰臟炎, 可選用 fenofibrate. 如果是高心血管疾病風險患者, 已經服用 fenofibrate, TG仍過高, 可再加上 icosapent ethyl

icosapent ethyl=Vascepa= 魚油成份處方藥, 魚油中萃取高純度EPA(二十碳五烯酸)

The following is our initial approach to patients with TG levels between 150 and 885 mg/dL

●All patients should adopt lifestyle modifications similar to those recommended for individuals at high risk of ASCVD .
All patients not at their LDL-C goal should be treated with a statin.

Statins typically lower TG levels by 5 to 15 percent; however, high-intensity statin therapy can lower TGs by 25 to 30 percent in patients with fasting TGs <400 mg/dL. Larger reductions in TGs of 40 percent have been reported in patients with fasting TGs as high as 800 mg/dL with treatment with a moderate- to high-dose high-intensity statin (atorvastatin 80 mg daily, rosuvastatin 20 or 40 mg daily) [125,126]. Goals for the treatment of LDL-C are presented elsewhere.

●For patients who are not at LDL-C goal with maximally tolerated statin dose, we add ezetimibe.

●For patients with a TG level >150 mg/dL who have been managed with the above approach and who are at high risk of cardiovascular disease, we consider adding a drug that lowers non-HDL-C through effects of VLDL (eg, fenofibrate, icosapent ethyl, or rarely niacin) to further lower TG. High cardiovascular risk includes patients with known ASCVD or diabetes and those with a 10-year risk of a cardiovascular disease event >10 percent.

For these high-risk patients we usually start with icosapent ethyl. However, if the patient has a history of pancreatitis, we might start with fenofibrate. If after adding either icosapent ethyl or fenofibrate the TG level remains >150 mg/dL, we consider adding the other drug based on clinical circumstances. For example, if the cardiovascular risk is high and we had started with fenofibrate, we consider adding icosapent ethyl.