[主題] 腎上腺素皮質機能亢進？

1. 品種 : 美短

2. 性別 : 女

3. 年齡 : 約4歲

4. 結紮 : Yes

5. 預防注射 : Yes No 預防針種類 / 品牌 :

6. 就醫前主訴 :
有一段時間不吃東西，貓咪從3.6瘦到2.6，並且脫毛、有皮屑；之後恢復食慾，常給她吃罐頭、起士等零食，甚至水煮小雞腿、蛋給她吃，可是卻怎麼吃也吃不胖，反而現在瘦到2.5。其他眼睛上有白膜、耳朵很髒。

7. 做過那些檢查 ( 包含抽血檢查的項目跟數據; 尿液分析值; 糞便鏡檢; 超音波; X光 ... )
血液檢查(2006.1.23)：
ALB:2.18g/dl
ALKP:33u/l
ALT:16u/l
AST:79u/l
BUN:14.6mg/dl
CREA:0.64mg/dl
GLU:98.0mg/dl
TP:7.53g/dl
GLOB:5.35g/dl
(檢查的醫生有說血蛋白非常低)
眼睛染色檢查
抹片檢查：不是黴菌引起脫毛
超音波(心臟部份)

8. 就醫後醫師的診斷病名 : ( 沒有診斷或不清楚醫師的診斷, 恕難回覆 )
目前這位醫生判為「腎上腺素皮質機能亢進」，他認為貓咪的脫毛是成對稱的，而且抹片並無發現黴菌，而檢查肚皮發現皮膚很薄，可以很容易看到微血管，他還問我貓咪是不是很愛喝水，的確是，於是他更確定是腎上腺素的問題。
另外他聽診時，發現心有雜音，做了超音波檢查，發現有點心肌肥大；醫生說有可能是因為腎上腺素分泌異常，使心臟跳動速度加快，造成心肌肥大。

9. 治療方式 :
目前吃腎上腺素的藥。點眼和點耳朵。

10.已治療天數 : 10天左右。

11.想問的問題 :
我想知道什麼是腎上腺素皮質機能亢進，雖然醫生稍微有解釋，可是聽不太懂，而他又忙著看下一位病人...我上網查了資料，發現這個病好像又叫庫新症，但在人的症狀卻是剛好相反，是會變胖、月亮臉、多毛...好奇怪？我很怕又是醫生誤診，我已經看了很多醫生，前後也拖了半年，從一開始有醫生把她的脫毛當黴菌治療，有的醫生說是憂鬱症，有的醫生說是甲狀腺的問題，到現在這個醫生，我想聽多方的意見，不要多浪費時間在錯誤的診療上(因為其實我發現醫生大多不會承認自己的錯誤，只會堅持用自己第一次的診斷去治療)，我想假如真的是腎上腺的問題的話，那早點治療正確也不至於到現在變成心肌肥大，我想這是台灣很多獸醫的問題！貓咪固然不會說什麼，可是我們飼主的醫學常識也不足以判斷醫生是否診療正確，只能當下相信醫生、信任醫生，但不料自己卻害了貓咪，唉！抱歉發起牢騷，我的問題以上。

12.怪叔叔的說明與建議 : ( 僅針對您的獸醫的診斷做解釋, 不做猜測性的答覆 )

腎上腺素皮質可以驗Cortisol (0.6-1.2)

右心應該確定一下是否有問題...肝跟脾有沒腫大??

下面引用由gsw在 2006/03/03 11:06pm 發表的內容：
ALKP:33u/l
ALT:16u/l
AST:79u/l

跟腎上腺素皮質機能亢進應該沒有關係.

對不起！兩位..
我實在不太懂你們所說的，可以解釋清楚些嗎？
1.Cortisol (0.6-1.2)是一種檢驗方法嗎？
2.右心指的是右心肌嗎？貓咪的心肌整體來看就是肥大的狀態(心肌厚度約等於心室的空間)
3.肝跟脾腫大是腎上腺素皮質亢進的病徵嗎？是怎麼造成的？
4.為什麼說和腎上腺素皮質亢進沒有關係呢？理由是什麼？
5.若不是這個腎上腺素皮質亢進的問題，那有可能是哪些問題呢?或我應該就哪些方向和醫生討論?

下面引用由gsw在 2006/03/04 11:39pm 發表的內容：
4.為什麼說和腎上腺素皮質亢進沒有關係呢？理由是什麼？

就是肝功能指數會飆很高.
特別是ALKP.
很奇怪,這種常識應該是每個獸醫都知道的...@@
測可體松需要臨床症狀符合, 血檢方面也吻合才做.
未臨床診治驟下斷語...還是要小心...不要隨便亂嚇人...

下面引用由gsw在 2006/03/04 11:39pm 發表的內容：
對不起！兩位..
我實在不太懂你們所說的，可以解釋清楚些嗎？
1.Cortisol (0.6-1.2)是一種檢驗方法嗎？

Cortisol就是腎上腺皮質醇，這是腎上腺製造的一種主要類固醇。
腎上腺功能亢進，血液中的Cortisol應該會很高。
如果你還是很擔心的話，可以去驗這個項目。

你的貓咪食慾不振很久了嗎？
A/G ratio好低喔，只剩0.4了耶
請努力強迫灌食，替貓咪補充營養和體力吧

現在有吃比較多，可是還是很瘦，胖不起來....
唉！那我再問問醫生確認一下好了..看要不要驗Cortisol...

對稱性脫毛跟內分泌的疾病有關....
但是好像狗狗比較常聽到腎上腺皮值亢進~
貓咪甲狀腺抗進比較多耶~ ~

去大醫院驗cortisol和T4吧!!

[這篇文章最後由gsw在 2006/03/07 11:51pm 編輯]

之前那個醫生說是甲狀腺的問題，也吃了快半個月至一個月的藥，也沒有比較好...後來這個醫生否決掉了這個看法，說是甲狀腺的話會變的很胖才是，而貓咪的狀況則是很瘦很瘦，幾乎沒有皮下脂肪。
醫源性的我不清楚她之前吃的藥會不會造成那樣的情況，不過吃的藥很多倒是真的，有第一個醫生說的憂鬱症造成免疫力下降，吃增加免疫力的藥；第二個醫生說是甲狀腺的問題吃甲狀腺的藥，現在吃腎上腺素的藥吃了快半個月，明天還要帶去給醫生複檢，我想我會提出檢查可體松的請求。
另外貓咪的確有拉肚子的狀況，拉非常稀的稀便(很臭)，持續到現在都有，並且很愛喝水，大概是水一直跑離她的血管吧......為什麼會流失呢？可能有哪些原因呢？

下面引用由gsw在 2006/03/07 11:50pm 發表的內容：
之前那個醫生說是甲狀腺的問題，也吃了快半個月至一個月的藥，也沒有比較好...後來這個醫生否決掉了這個看法，說是甲狀腺的話會變的很胖才是，而貓咪的狀況則是很瘦很瘦，幾乎沒有皮下脂肪。

甲狀腺的功用是調節身體的新陳代謝。
當甲狀腺分泌過多的甲狀腺素，新陳代謝就會變快，造成神經緊張、心跳及呼吸加速
體重減輕、失眠、疲倦、凸眼、腹瀉等問題，這叫做甲狀腺機能亢進。
相反的，如果甲狀腺素分泌不足，新陳代謝就會變慢，就會造成怕冷、疲倦、嗜睡、
體重增加、水腫、精神遲鈍等症狀，這叫做甲狀腺機能低下。

並不是甲狀腺有問題就一定會變得很胖，你的醫生說錯了。

沒力氣翻譯. 先嘗試讀讀看, 有疑問再說.
從內科聖經摘錄下來的內容可知真的有人在胡說八道.
我氣是在氣這個!!

HYPERADRENOCORTICISM IN CATS
Hyperadrenocorticism is an endocrine disorder not commonly recognized in cats. Over a 10-year period, one university clinic diagnosed Cushing's syndrome in more than 800 dogs and in only 34 cats.26
Similar to the incidence seen in dogs, 80% to 85% of cats have PDH, and 10% to 15% have an FAT. Adenomas and carcinomas occur with equal frequency. Adrenal tumors may secrete excessive amounts of steroids other than cortisol. Two recent case reports described cats with clinical signs of hyperadrenocorticism caused by a progesterone-secreting adrenal mass.87,88
Clinical Findings
Middle-aged to older cats are most commonly affected with hyperadrenocorticism. There does not seem to be a breed predilection; however, approximately 70% of feline cases are female. The most common clinical signs are polydipsia, polyuria, and polyphagia. Most authors have assumed that these symptoms are caused by diabetes mellitus, which develops in approximately 80% of cases, and that they therefore are late signs of hyperadrenocorticism. However, a recent case study described polydipsia and polyuria in two cats with hyperadrenocorticism that did not have concurrent diabetes mellitus and in one cat that had hyperadrenocorticism for 8 months before diabetes mellitus developed.89 Other frequent findings include pendulous abdomen, generalized muscle wasting, lethargy, and obesity. Many cats have dermatologic symptoms, including hair loss; unkempt haircoat; truncal or patchy alopecia; fragile, thin skin prone to traumatically induced tears (so-called feline fragile skin syndrome); and secondary infections (including demodicosis). Hepatomegaly and weight loss occur less frequently.
Hyperglycemia is the most frequent laboratory abnormality. Only 10% of dogs with hyperadrenocorticism develop overt diabetes mellitus, whereas as many as 80% of cats with Cushing's syndrome are diabetic. Cats seem to be more sensitive to the diabetogenic effects of steroids than dogs, and in many cases it is only after diabetes mellitus has been diagnosed that hyperadrenocorticism is suspected. Insulin resistance is a typical feature of diabetes mellitus caused by hyperadrenocorticism. However, it should be noted that not all cats with Cushing's syndrome and concurrent diabetes mellitus are insulin resistant.
page 1610

page 1611
Other findings include hypercholesterolemia and an increase in ALT activity, which may be caused by hyperadrenocorticism or diabetes mellitus. Some cats have elevated ALP activity. Because the activity of a steroid-induced isoenzyme is not increased, this elevation is thought to be associated with diabetes mellitus (and hepatic lipidosis) rather than with hyperadrenocorticism.90
Specific Endocrine Testing
A diagnosis of hyperadrenocorticism should be based on the results of one or more of the screening tests (urine C:C ratio, ACTH stimulation test, LDDS test). The endogenous ACTH concentration, an HDDS test, and adrenal ultrasonography can be used to differentiate PDH from an FAT in cats.
Urine Creatinine to Cortisol Ratio
Slightly more than 70% of cortisol (free cortisol and metabolites) is eliminated in the urine in dogs, whereas only 18% is eliminated in the urine of cats. Despite this difference, the urine C:C ratio of cats with hyperadrenocorticism is significantly higher than that of healthy cats, and this test can be used in the diagnosis of Cushing's syndrome.91 Urine should be collected by the owner at home. It is important to remember that false-positive results may be caused by other disease processes. Goosens et al.91 reported a reference range of 2 to 36 × 10-6 based on the results of 42 healthy cats. Our reference range, using 31 healthy cats, was 0 to 4 × 10-6. This discrepancy is possibly due to the different types of radioimmunoassay used. The amount of cortisol metabolites measured varies among assays, therefore it is critical that reference ranges be established for each assay.
ACTH Stimulation Test
In both dogs and cats, the ACTH stimulation test is mainly a test of adrenal reserve, and its major role is to rule in or rule out hypoadrenocorticism. The test's sensitivity is low, and because a variety of nonadrenal illnesses can cause abnormal test results, its specificity is also low. According to the test protocol most often used, blood samples for cortisol determination are taken before and 30 and 60 minutes after intramuscular administration of 125 μg/cat of a synthetic polypeptide containing the first 24 aminoacids of ACTH (e.g., Cortrosyn, Synacthen). The time to maximum peak cortisol response is longer and the maximum cortisol concentration is significantly higher after intravenous administration than after intramuscular administration. Therefore the protocol for intravenous administration is to collect blood samples before and 60 and 90 minutes after administration of ACTH. Because peak effect of cortisol is less consistent in the cat than in the dog, two post-ACTH samples are recommended. Reference ranges for the cat are slightly lower than those for the dog and should be established for the laboratory and protocol used. In our laboratory, the upper limit for the normal post-ACTH cortisol concentration using the intramuscular protocol is 13 μg/dL.92 We consider levels between 13 and 16 μg/dL to be borderline, and a concentration above 16 μg/dL to be consistent with hyperadrenocorticism.
Low-Dose Dexamethasone Suppression Test
The degree and duration of adrenocortical suppression after dexamethasone administration is more variable in cats than in dogs. It appears that a dosage of 0.1 mg/kg of dexamethasone suppresses cortisol levels in healthy cats and cats with nonadrenal illness more reliably than 0.01 mg/kg of dexamethasone, which is the dosage used in dogs. Currently, the protocol most often used involves collection of blood samples for production of plasma or serum before and 4 and 8 hours after intravenous administration of 0.1 mg/kg of dexamethasone. Cortisol levels of less than 1 μg/dL at 4 and 8 hours are considered normal, levels between 1 and 1.4 μg/dL are borderline, and levels greater than 1.4 μg/dL are consistent with hyperadrenocorticism. Post-dexamethasone suppression of cortisol concentrations at 4 and 8 hours does not occur in cats with an FAT. Approximately 70% of cats with PDH show no or inadequate suppression.90
Measurement of Endogenous ACTH
Healthy cats may have very low ACTH concentrations, therefore the measurement of endogenous ACTH test can be used only after a diagnosis of hyperadrenocorticism has been made. Normal to elevated levels of ACTH support a diagnosis of PDH, and low to undetectable levels indicate an FAT. Sample handling is critical (see discussion earlier in this chapter).
High-Dose Dexamethasone Suppression Test
Compared with dogs, a higher dose of dexamethasone (1 mg/kg) has been advocated to differentiate between PDH and an FAT in cats; however, very limited information is available. Blood samples should be taken before and 4 and 8 hours after administration of dexamethasone. Suppression (less than 50% of baseline or less than 1.4 μg/dL) is consistent with PDH. No or insufficient suppression may be due either to an FAT or to PDH and cannot be used to differentiate between the two conditions.
Adrenal Ultrasonography
High-resolution transducers have made ultrasonographic visualization of the adrenal glands possible in cats, and reference ranges have been reported.92 Symmetric adrenal glands of normal or enlarged size are suggestive of PDH, whereas unilateral enlargement or an adrenal gland with a masslike appearance suggests an FAT. Detailed information on the ultrasonographic appearance of the adrenal glands in cats with hyperadrenocorticism currently is limited.
===========================================================================
UPDATE Date Added: 17 March 2005
Edward C. Feldman, DVM, DACVIM
High urinary corticoid/creatinine ratios in cats with hyperthyroidism.
Measurement of the urine cortisol: creatinine ratio (UCCR) provides an assessment of cortisol secretion over a period of time. This test is generally agreed to be an extremely sensitive screening test for the diagnosis of hyperadrenocorticism (HAC) in dogs and cats. The major concern regarding use of UCCR as the sole screening test in dogs has been its lack of specificity. In other words, dogs with naturally occurring HAC almost always have an abnormal UCCR, but dogs that have disorders other than HAC also commonly have abnormal test results. Therefore, while an abnormal UCCR test result can be used to support a clinical suspicion that a dog has HAC, it is generally recommended that a more specific test -- low dose dexamethasone suppression -- be used to "confirm" a diagnosis.
It was hypothesized in this clinical study that chronic excesses in thyroid hormone could influence the metabolic clearance of cortisol, thereby causing the UCCR to be abnormal in cats with naturally occurring hyperthyroidism. To evaluate the effect of thyroid hormone excess, UCCR results were measured in 32 cats with naturally occurring hyperthyroidism and in 45 healthy control cats. In 7 cats, the UCCRs were measured before and after treatment for hyperthyroidism. With data from the healthy cats, the reference range for the UCCR was determined to be 8.0 to 42.0 X 10-6. The UCCR results from the cats with hyperthyroidism were significantly higher than those of the control population. UCCR results from 15 of the 32 hyperthyroid cats were above the established reference range. Treatment of hyperthyroidism caused a marked decrease in UCCR in those 7 cats evaluated.
The results of this study demonstrate that UCCR results may be abnormally increased in cats with hyperthyroidism, probably because of increased metabolic clearance of cortisol and activation of the pituitary-adrenocortical axis by disease. Although the clinical features of hyperthyroidism and HAC in cats are different, the authors suggest that hyperthyroidism be ruled out when any cat is suspected of having HAC on the basis of an abnormal UCCR.
Results of this study also have larger implications. This study can be added to the list of reports that demonstrate lack of specificity associated with abnormal UCCR results in both cats and dogs. This lack of specificity strongly suggest that HAC never be confirmed in any dog or cat based only on an abnormal UCCR result. Rather, the diagnosis of HAC in both dogs and cats should be suspected after careful review of the history, physical examination, CBC, serum biochemical profile, urinalysis, and imaging studies. The diagnosis of HAC should be confirmed by other tests, such as the low dose dexamethasone test, in both dogs and cats.
de Lange, M.S., et al: High urinary corticoid/creatinine ratios in cats with hyperthyroidism. J Vet Int Med 2004;18:152-155.

今天去看醫生本來要驗可體松，可是醫生那裡沒辦法化驗，他打了電話給一個化驗所那裡也沒辦法驗，有人知道台南哪裡可以驗嗎？

我說明貓咪一直腹瀉，還有吃喝正常卻又變瘦的問題，醫生檢查了一些便便說沒有蟲感染，於是醫生又驗了一次血，數據是：
ALB：2.3g/dl
AMYL：1285U/L
Ca：8.7mg/dl
GLU：109mg/dl
GPL：37.1
GOL：61.9
我不知道各個數值代表什麼意思，醫生跟我講大致上都正常，血蛋白雖然偏低但是還在正常範圍，血糖也正常，肝和胰都正常。

醫生說變瘦和拉肚子可能都是心臟病引起的，因為心臟肥大輸出的血液不足，因此無法傳送到末端，如腸子的絨毛，造成消化不良吸收不好，所以才會拉肚子和變瘦。

脫毛的地方還是禿禿的，醫生說再吃藥觀察看看。所以這次醫生除了腎上腺的藥又開了心臟病的藥，說看看能不能改善拉肚子的情況。

那個文章我看不懂，好像是很多檢驗的方法，那些檢驗方法醫院都有嗎？另外好像有些到一些症狀：像皮膚病、脫毛、倦怠是符合我的貓咪的且我的貓咪的確是母貓、年紀也不能說小；可是肥胖、下垂的腹部、伴隨糖尿病好像不一樣，所以這代表我的貓可能不是腎上腺的問題嗎？

最後兩項名稱寫錯了
不是GPL，應該是GPT (glutamate pyruvate transaminase) or ALT
不是GOL，應該是GOT (glutamate oxaloacetate transaminase) or AST

我不是醫生，不過我們家疑難雜症很多，手邊的檢驗報告也很多
我對照一下血檢的正常範圍，看起來的確是肝臟、胰臟都正常
上次血檢的數據，腎臟指數也正常

如果要檢驗甲狀腺素或腎上腺素，一般動物醫院又沒辦法做
我想嘉義大學獸醫系附設的動物醫院一定可以做的吧？

可是我有疑問的是"一直腹瀉，還有吃喝正常卻又變瘦的問題"
為什麼你的醫生們都是懷疑甲狀腺、腎上腺、心臟病這種比較遠的大方向
普通人第一個念頭不是應該先懷疑腸胃消化系統問題
難道不能先用消化酵素、止瀉劑之類的腸胃藥改善腹瀉的情況
讓貓咪消化吸收好一點，先不要一直消瘦下去嗎？

[這篇文章最後由gsw在 2006/03/28 11:32am 編輯]

那篇文章到底有什麼重要資訊呢？
可以講清楚一點好嗎？謝謝妳們，拜託拜託！

已經過了一個月，貓咪脫毛的地方還是沒有改善...
我不知道是不是要換醫生好...
到底貓咪生了是什麼病？有沒有對症下藥阿？
還是台南還有其他可以驗可體松的地方嗎？

既然怪叔叔已經說"跟腎上腺素皮質機能亢進應該沒有關係"
我覺得你就不用一直執著要驗可體松
最重要的是腹瀉和掉毛不是嗎?