1. A 54-year-old man with newly diagnosed acromegaly has residual disease after transsphenoidal surgery. His fasting glucose is 118 mg/dL and his HbA1c (hemoglobin A1c) is 6.2%, consistent with impaired glucose tolerance. Medical therapy is planned to control persistent GH (growth hormone) and IGF-1 (insulin-like growth factor-1) elevation. Considering his glucose status, which medical therapy is the most appropriate initial choice?
A) Pasireotide LAR (long-acting release), because its pan-somatostatin receptor (pan-SSTR) activity makes it the preferred first agent regardless of glucose status
B) Pegvisomant monotherapy, because it is the only option that will not worsen the tumor and shrinks the adenoma reliably
C) A first-generation somatostatin receptor analog (SSA) such as octreotide LAR or lanreotide Autogel, because these SSTR2-selective agents control GH and IGF-1 with a substantially lower risk of hyperglycemia than pasireotide in a patient who already has impaired glucose tolerance
D) Macimorelin, because it both confirms the diagnosis and provides ongoing GH suppression
E) Sermorelin, because stimulating endogenous GH release will normalize IGF-1 through restored feedback
ANSWER: C
Rationale:
In a patient with residual acromegaly who already has impaired glucose tolerance, the choice of medical therapy should weigh glycemic risk. First-generation somatostatin receptor analogs (SSAs) — octreotide LAR or lanreotide Autogel — are SSTR2-selective agents that effectively suppress GH and IGF-1 with a substantially lower risk of hyperglycemia (roughly 10 to 20%) than pasireotide (roughly 57 to 73%). They are therefore the appropriate initial choice for this glucose-intolerant patient.
Option A: Option A is incorrect because pasireotide carries the highest hyperglycemia risk of the SSAs owing to its high SSTR5 affinity; choosing it first in a patient with impaired glucose tolerance would predictably worsen glycemia and is not the preferred initial agent.
Option B: Option B is incorrect because pegvisomant does not shrink the adenoma (it has no tumor-volume effect), so the stated rationale is wrong; it is generally reserved for patients inadequately controlled on or intolerant of SSAs.
Option D: Option D is incorrect because macimorelin is an oral diagnostic ghrelin receptor agonist used to test for GH deficiency; it stimulates rather than suppresses the GH axis and has no role in treating acromegaly.
Option E: Option E is incorrect because sermorelin is a GHRH analog that stimulates GH release; using it in acromegaly would worsen GH excess rather than normalize IGF-1.
2. A 48-year-old woman with acromegaly remains biochemically uncontrolled (elevated GH (growth hormone) and IGF-1 (insulin-like growth factor-1)) despite maximum-dose octreotide LAR (long-acting release) for 9 months. She is normoglycemic with a normal HbA1c (hemoglobin A1c), and her pituitary tumor is small with no chiasmal involvement. Which change in medical therapy is most appropriate?
A) Switch to pasireotide LAR, a pan-somatostatin receptor (pan-SSTR) agonist whose high SSTR5 affinity provides additional GH and IGF-1 suppression beyond SSTR2-selective agents and can achieve biochemical control in a portion of patients refractory to first-generation agents; her normal glucose status makes the hyperglycemia risk acceptable with monitoring
B) Discontinue all medical therapy and observe, since octreotide failure indicates that no somatostatin-based agent can help
C) Add sermorelin to octreotide to stimulate the axis and overcome resistance
D) Switch to lanreotide Autogel, because it acts at entirely different receptors than octreotide and will succeed where octreotide failed
E) Begin macimorelin therapy to suppress GH through ghrelin receptor agonism
ANSWER: A
Rationale:
This patient has acromegaly refractory to a maximally dosed first-generation SSTR2-selective SSA, with a normal glucose profile and no mass-effect concern. Pasireotide LAR is the appropriate next step: as a pan-SSTR agonist with high SSTR5 affinity (roughly 40-fold greater than octreotide), it provides additional GH and IGF-1 suppression and can achieve biochemical control in a meaningful proportion of patients not controlled by first-generation agents (as shown in the PAOLA trial, a randomized comparison in inadequately controlled acromegaly). Because her glucose and HbA1c are normal, the principal drawback of pasireotide — hyperglycemia — is an acceptable, monitorable risk.
Option B: Option B is incorrect because failure of a first-generation SSTR2-selective agent does not mean all somatostatin-based therapy will fail; pasireotide's broader receptor profile can still work.
Option C: Option C is incorrect because sermorelin stimulates GH release and would worsen acromegaly; it has no role in treating GH excess.
Option D: Option D is incorrect because lanreotide is also a first-generation SSTR2/SSTR5 agent with a receptor profile very similar to octreotide; switching between two SSTR2-selective agents is unlikely to overcome true resistance, and the claim that it acts at entirely different receptors is false.
Option E: Option E is incorrect because macimorelin is a diagnostic ghrelin receptor agonist that stimulates GH, not a therapy that suppresses GH in acromegaly.
3. A 60-year-old woman with acromegaly and type 2 diabetes is started on pasireotide LAR (long-acting release) after failing first-generation agents. Six weeks later her fasting glucose has risen to 210 mg/dL and her HbA1c (hemoglobin A1c) has climbed from 6.8% to 8.4%. Which antidiabetic strategy is most likely to be effective for her pasireotide-induced hyperglycemia?
A) Add a DPP-4 (dipeptidyl peptidase-4) inhibitor such as sitagliptin as the preferred first agent
B) Add metformin alone and expect full correction, since the hyperglycemia is due to insulin resistance
C) Reassure the patient that pasireotide hyperglycemia resolves spontaneously and requires no treatment
D) Add an SGLT2 (sodium-glucose cotransporter-2) inhibitor as monotherapy, expecting it to fully restore euglycemia
E) Start a GLP-1 (glucagon-like peptide-1) receptor agonist or insulin, because pasireotide suppresses endogenous insulin and incretin secretion at the source, and agents that bypass that suppression (a GLP-1 receptor agonist acting directly on its receptor, or exogenous insulin) restore effective insulin action
ANSWER: E
Rationale:
Pasireotide causes hyperglycemia chiefly by suppressing endogenous insulin secretion and incretin (GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic polypeptide)) release at the source through high-affinity SSTR5 activity. The effective strategy bypasses that suppressed pathway: a GLP-1 receptor agonist acts directly on the GLP-1 receptor, and exogenous insulin directly replaces the suppressed secretory drive. These are the preferred agents for pasireotide-induced hyperglycemia.
Option A: Option A is incorrect because DPP-4 inhibitors work by preventing degradation of endogenous incretins; since pasireotide suppresses incretin secretion upstream, there is little substrate to preserve, and these agents are largely ineffective — not the preferred first choice.
Option B: Option B is incorrect because pasireotide hyperglycemia is predominantly a secretory defect rather than insulin resistance, so metformin alone does not address the core mechanism and is unlikely to fully correct it.
Option C: Option C is incorrect because the hyperglycemia does not reliably resolve spontaneously while the drug is continued; it requires active management, often for the duration of therapy.
Option D: Option D is incorrect because SGLT2 inhibitors reduce renal glucose reabsorption but do not restore the suppressed insulin secretory drive, so monotherapy is generally insufficient for pasireotide-induced hyperglycemia.
4. A 45-year-old man with acromegaly has been on pegvisomant for 4 months. He reports marked symptomatic improvement. Laboratory results show a serum GH (growth hormone) of 32 ng/mL (elevated) but a serum IGF-1 (insulin-like growth factor-1) squarely within the age- and sex-adjusted normal range. Liver enzymes are normal. What is the most appropriate next step?
A) Discontinue pegvisomant immediately because the elevated GH indicates treatment failure
B) Continue pegvisomant at the current dose without change, because during pegvisomant therapy serum GH rises (from loss of IGF-1 negative feedback) and is not a valid monitoring marker; the normal IGF-1 with symptomatic improvement indicates adequate biochemical control
C) Add a high-dose somatostatin receptor analog urgently to bring the GH below 1 ng/mL, the standard target
D) Recheck both values, since a high GH with a normal IGF-1 must represent a laboratory error
E) Obtain an urgent pituitary MRI (magnetic resonance imaging) and hold the next pegvisomant dose because the elevated GH signals rapid tumor growth
ANSWER: B
Rationale:
During pegvisomant therapy, serum IGF-1 (insulin-like growth factor-1) is the sole reliable monitoring marker. Pegvisomant blocks the peripheral GH receptor, lowering IGF-1, but does not suppress pituitary GH secretion; because the fall in IGF-1 removes negative feedback, serum GH actually rises during therapy. A high GH with a normal IGF-1 and symptomatic improvement therefore indicates adequate biochemical control, and the correct action is to continue therapy unchanged.
Option A: Option A is incorrect because the elevated GH is the expected, mechanistically predicted consequence of pegvisomant therapy and does not indicate treatment failure; IGF-1 is the marker of success.
Option C: Option C is incorrect because the SSA target of GH below 1 ng/mL applies to SSA therapy, not pegvisomant; applying it here misinterprets the drug's mechanism, and urgent SSA addition is not warranted in a well-controlled patient.
Option D: Option D is incorrect because the dissociation between a high GH and a normal IGF-1 is the predicted pharmacologic pattern during pegvisomant therapy, not a laboratory error.
Option E: Option E is incorrect because an isolated elevated GH during pegvisomant therapy does not signal tumor growth; periodic (not urgent) pituitary imaging is recommended because pegvisomant does not shrink tumor, but holding the dose for an expected GH rise is inappropriate.
5. A 51-year-old woman with acromegaly on pegvisomant monotherapy is seen for her scheduled 6-month visit. She feels well and is asymptomatic. Routine labs show ALT (alanine aminotransferase) at 6.4 times the upper limit of normal (ULN) and AST (aspartate aminotransferase) at 5.9 times ULN; total bilirubin is normal. What is the most appropriate action?
A) Continue pegvisomant unchanged and recheck enzymes in 6 months, since she is asymptomatic
B) Continue pegvisomant but reduce the dose by half and recheck in 3 months
C) Continue pegvisomant and attribute the enzyme elevation to resolving acromegaly-related hepatic steatosis
D) Discontinue pegvisomant and investigate the hepatotoxicity, because transaminase elevation exceeding five times the upper limit of normal meets the threshold for stopping the drug, regardless of the absence of symptoms
E) Continue pegvisomant and add a hepatoprotective agent, deferring any decision about the drug until enzymes exceed ten times ULN
ANSWER: D
Rationale:
Pegvisomant's principal safety concern is hepatotoxicity. The monitoring protocol calls for liver function tests at baseline and periodically (every 6 months); a transaminase elevation exceeding three times ULN warrants more frequent monitoring, and an elevation exceeding five times the upper limit of normal (ULN) meets the threshold for discontinuing the drug pending investigation. This patient's ALT (6.4× ULN) and AST (5.9× ULN) both exceed five times ULN, so pegvisomant should be stopped and the hepatotoxicity evaluated, even though she is asymptomatic and bilirubin is normal.
Option A: Option A is incorrect because continuing unchanged ignores a transaminase elevation that has crossed the discontinuation threshold; the absence of symptoms does not justify continuation.
Option B: Option B is incorrect because dose reduction is not the protocol response once enzymes exceed five times ULN; discontinuation is required.
Option C: Option C is incorrect because attributing a greater-than-five-times-ULN elevation to resolving steatosis would dismiss a genuine hepatotoxicity signal; new or marked elevations during therapy must be evaluated as a possible drug effect.
Option E: Option E is incorrect because the discontinuation threshold is five times ULN, not ten; deferring action until enzymes reach ten times ULN exposes the patient to avoidable risk.
6. A 39-year-old woman with panhypopituitarism on stable hydrocortisone and levothyroxine replacement begins somatropin (recombinant GH (growth hormone)) for confirmed adult GH deficiency. Three weeks later she develops progressive fatigue, nausea, anorexia, and a 3 kg weight loss. A morning cortisol is low. What is the most likely explanation and the appropriate intervention?
A) She has developed somatropin-induced primary hypothyroidism; increase her levothyroxine dose
B) She is experiencing expected somatropin fluid retention; reduce her somatropin dose and add a diuretic
C) Somatropin has induced CYP3A4 (cytochrome P450 3A4), accelerating hydrocortisone clearance and unmasking adrenal insufficiency in a patient with limited adrenal reserve; increase her hydrocortisone replacement dose
D) She has developed a pituitary tumor recurrence compressing the optic chiasm; obtain urgent neurosurgical consultation
E) Somatropin has caused acute hyperglycemia precipitating her symptoms; start insulin and continue somatropin unchanged
ANSWER: C
Rationale:
Somatropin induces CYP3A4 (cytochrome P450 3A4), which accelerates clearance of glucocorticoids including hydrocortisone and increases conversion of cortisol to inactive cortisone. In a patient with panhypopituitarism and limited adrenal reserve on a previously adequate hydrocortisone dose, this increased clearance can lower effective cortisol exposure and unmask adrenal insufficiency — presenting as fatigue, nausea, anorexia, and weight loss, with a low morning cortisol, exactly as seen here. The appropriate intervention is to increase the hydrocortisone replacement dose (commonly by 20 to 30%).
Option A: Option A is incorrect because the picture is adrenal insufficiency, not primary hypothyroidism; somatropin can affect thyroxine-to-triiodothyronine conversion but does not cause primary hypothyroidism, and the low cortisol points to the glucocorticoid axis.
Option B: Option B is incorrect because fluid retention from somatropin produces edema and arthralgias, not anorexia, weight loss, and low cortisol; the clinical picture is glucocorticoid insufficiency.
Option D: Option D is incorrect because tumor recurrence with chiasmal compression would present with visual field changes and headache, not this constellation of adrenal-insufficiency symptoms with a low cortisol.
Option E: Option E is incorrect because somatropin can worsen glucose tolerance over time but does not typically cause an acute hyperglycemic crisis with weight loss and low cortisol; the findings indicate unmasked adrenal insufficiency requiring increased hydrocortisone, not insulin with unchanged somatropin.
7. A 50-year-old man with well-controlled HIV (human immunodeficiency virus) on long-term antiretroviral therapy has developed progressive central abdominal fat accumulation. Imaging confirms marked visceral adipose tissue (VAT) excess consistent with antiretroviral therapy-associated lipodystrophy. He has no active malignancy and his fasting glucose is normal. Which agent is specifically indicated to reduce his excess visceral adipose tissue?
A) Tesamorelin, a stabilized GHRH (growth hormone-releasing hormone) analog that stimulates endogenous GH (growth hormone) release and is FDA (U.S. Food and Drug Administration)-approved to reduce excess visceral adipose tissue in HIV-associated lipodystrophy
B) Octreotide LAR (long-acting release), because somatostatin receptor analogs reduce visceral fat by suppressing GH
C) Pegvisomant, because blocking the GH receptor mobilizes visceral adipose tissue
D) Macimorelin, because as a diagnostic agent it also reduces central fat during the stimulation test
E) Somatropin at high replacement doses, because direct GH replacement is the approved therapy for HIV lipodystrophy
ANSWER: A
Rationale:
Tesamorelin is a synthetic GHRH (growth hormone-releasing hormone) analog stabilized against dipeptidyl peptidase-4 cleavage; it stimulates endogenous GH release and is FDA (U.S. Food and Drug Administration)-approved specifically to reduce excess visceral adipose tissue (VAT) in HIV (human immunodeficiency virus)-infected patients with antiretroviral therapy-associated lipodystrophy. With no active malignancy (a contraindication) and normal glucose, this patient is an appropriate candidate.
Option B: Option B is incorrect because octreotide is a somatostatin receptor analog used to suppress GH in conditions such as acromegaly; it is not indicated for HIV lipodystrophy and reducing GH would not address the lipodystrophy mechanism, which involves blunted GH pulsatility.
Option C: Option C is incorrect because pegvisomant is a GH receptor antagonist used in acromegaly; blocking the GH receptor would not reduce VAT in lipodystrophy and is not indicated.
Option D: Option D is incorrect because macimorelin is a single-dose oral diagnostic agent for GH deficiency and has no therapeutic role in reducing visceral fat.
Option E: Option E is incorrect because the approved agent for HIV-associated lipodystrophy VAT reduction is tesamorelin (which stimulates endogenous GH), not high-dose somatropin replacement, which is not approved for this indication.
8. A 58-year-old man with a history of coronary artery disease and a prior seizure disorder is being evaluated for suspected adult GH (growth hormone) deficiency after pituitary surgery. A provocative GH stimulation test is required to confirm the diagnosis. Which test is the most appropriate choice given his comorbidities?
A) Insulin tolerance testing (ITT), because the hypoglycemia it induces provides the most reliable GH stimulus and his comorbidities are irrelevant to test selection
B) An oral glucose tolerance test, because suppression of GH below 1 ng/mL confirms GH deficiency
C) A random single GH measurement, since a low value reliably establishes GH deficiency without provocation
D) A pegvisomant challenge test, since blocking the GH receptor reveals the underlying secretory capacity
E) The macimorelin stimulation test, an oral ghrelin receptor (GHSR-1a, growth hormone secretagogue receptor type 1a) agonist test that does not induce hypoglycemia, making it the safer choice in a patient with cardiovascular disease and a seizure disorder, in whom insulin tolerance testing is contraindicated
ANSWER: E
Rationale:
The macimorelin stimulation test uses an oral ghrelin receptor (GHSR-1a, growth hormone secretagogue receptor type 1a) agonist to stimulate GH release and does not induce hypoglycemia. This makes it the safer choice in this patient, because insulin tolerance testing (ITT) deliberately induces hypoglycemia and is contraindicated in patients with cardiovascular disease, seizure disorders, and older age — all relevant here. Macimorelin offers sensitivity and specificity comparable to ITT (a GH peak below 2.8 ng/mL establishes the diagnosis).
Option A: Option A is incorrect because the patient's comorbidities are highly relevant: ITT-induced hypoglycemia is hazardous and contraindicated in cardiovascular disease and seizure disorders, so ITT is not appropriate.
Option B: Option B is incorrect because the oral glucose tolerance test with GH suppression is used to diagnose acromegaly (GH excess), not to confirm GH deficiency.
Option C: Option C is incorrect because a single random GH measurement cannot establish GH deficiency owing to the pulsatile, often-low baseline secretion of GH; provocative testing is required.
Option D: Option D is incorrect because there is no pegvisomant challenge test for diagnosing GH deficiency; pegvisomant is a therapeutic GH receptor antagonist for acromegaly, not a diagnostic provocative agent.
9. A 46-year-old man with acromegaly has been treated with octreotide LAR (long-acting release) for 2 years. He now presents with intermittent right upper quadrant pain after fatty meals. Ultrasound reveals multiple gallstones in a previously normal gallbladder. What is the most likely explanation for his cholelithiasis?
A) Octreotide directly precipitates calcium bilirubinate stones through an osmotic effect confined to patients with pre-existing biliary disease
B) Octreotide, like other somatostatin receptor analogs, suppresses cholecystokinin (CCK) release and inhibits gallbladder contractility, producing bile stasis that promotes cholesterol gallstone formation; this occurs in roughly 20 to 30% of patients on long-term therapy
C) Octreotide increases hepatic cholesterol synthesis via CYP7A1 (cytochrome P450 7A1) induction, which is the dominant mechanism of stone formation
D) The gallstones are unrelated to octreotide and reflect only his dietary fat intake
E) Octreotide accelerates gallbladder emptying so forcefully that bile crystallizes in the cystic duct
ANSWER: B
Rationale:
Somatostatin receptor analogs (SSAs), including octreotide, suppress cholecystokinin (CCK) release and inhibit gallbladder contractility. CCK normally drives postprandial gallbladder emptying; with its suppression, bile stagnates, becomes supersaturated with cholesterol, and forms gallstones. Symptomatic gallstones develop in roughly 20 to 30% of patients on long-term SSA therapy, which fits this patient's 2-year octreotide course, postprandial right upper quadrant pain, and new stones in a previously normal gallbladder.
Option A: Option A is incorrect because SSA-associated cholelithiasis is not an osmotic calcium bilirubinate process confined to patients with pre-existing biliary disease; it arises in previously normal gallbladders through bile stasis and cholesterol supersaturation.
Option C: Option C is incorrect because octreotide does not cause stones by CYP7A1 induction or increased hepatic cholesterol synthesis; the mechanism is reduced gallbladder motility from CCK suppression.
Option D: Option D is incorrect because the stones are very plausibly related to long-term octreotide; attributing them solely to dietary fat ignores a well-established class effect occurring in 20 to 30% of treated patients.
Option E: Option E is incorrect because octreotide reduces, not accelerates, gallbladder contractility; the pathophysiology is stasis from impaired emptying, the opposite of forceful emptying.
10. A 55-year-old renal transplant recipient maintained on cyclosporine for immunosuppression is diagnosed with acromegaly and started on octreotide LAR (long-acting release) after incomplete surgical resection. Which monitoring action is most important to prevent a serious complication of this drug combination?
A) Monitor for cyclosporine toxicity from elevated levels, because octreotide inhibits CYP3A4 (cytochrome P450 3A4) and raises cyclosporine concentrations
B) No specific monitoring is needed, because octreotide and cyclosporine do not interact
C) Monitor cyclosporine trough levels, because somatostatin receptor analogs reduce gastrointestinal absorption of cyclosporine, which can lower its plasma concentrations and precipitate acute allograft rejection
D) Monitor serum prolactin, because octreotide displaces cyclosporine from prolactin-binding sites
E) Reduce the cyclosporine dose preemptively, because octreotide predictably doubles cyclosporine plasma levels
ANSWER: C
Rationale:
Somatostatin receptor analogs (SSAs) such as octreotide reduce the gastrointestinal absorption of cyclosporine by inhibiting intestinal motility and secretion. Because cyclosporine already has variable and relatively low oral bioavailability, this reduced absorption can meaningfully lower plasma trough concentrations. In a transplant recipient, subtherapeutic cyclosporine levels risk acute allograft rejection — a serious, graft-threatening complication. The most important monitoring action is therefore to follow cyclosporine trough levels after starting the SSA, with upward dose adjustment as needed.
Option A: Option A is incorrect because octreotide does not inhibit CYP3A4 or raise cyclosporine levels; the interaction reduces cyclosporine absorption and lowers levels, the opposite direction.
Option B: Option B is incorrect because there is a clinically important interaction between SSAs and cyclosporine; ignoring it could lead to rejection.
Option D: Option D is incorrect because the interaction does not involve prolactin-binding sites, and serum prolactin is not the relevant monitoring parameter.
Option E: Option E is incorrect because octreotide lowers rather than raises cyclosporine levels, so a preemptive dose reduction would be exactly the wrong action and could precipitate rejection.
11. A 57-year-old man with adult GH (growth hormone) deficiency has been on stable somatropin (recombinant GH) replacement for several years. He is admitted to the intensive care unit with septic shock and acute respiratory failure requiring mechanical ventilation. The ICU team asks how to manage his somatropin during this admission. What is the most appropriate action?
A) Continue somatropin at his usual dose, because long-term tolerance means it poses no risk during acute illness
B) Increase the somatropin dose to provide anabolic support and accelerate recovery from critical illness
C) Continue somatropin but switch to a long-acting weekly formulation for convenience during the ICU stay
D) Discontinue somatropin for the duration of the acute critical illness, because acute critical illness is a contraindication to somatropin — pharmacological GH exposure increased mortality in critically ill patients in pivotal trials — and restart it after recovery
E) Continue somatropin and add a somatostatin receptor analog to offset any excess GH effect during the illness
ANSWER: D
Rationale:
Acute critical illness is a contraindication to somatropin, independent of prior tolerance, because pivotal controlled trials demonstrated increased mortality when critically ill adults received GH. The contraindication is tied to the patient's current physiologic state, so a patient established on replacement who becomes critically ill should have somatropin discontinued for the duration of the acute illness and restarted after recovery.
Option A: Option A is incorrect because prior long-term tolerance does not exempt the patient from a state-dependent contraindication; the risk arises from the acute critical illness itself.
Option B: Option B is incorrect because increasing the dose is the opposite of correct management; pharmacological GH exposure increased mortality in critically ill patients, so escalation is hazardous.
Option C: Option C is incorrect because switching formulations does not address the contraindication; somatropin should be held, not merely changed to a different schedule.
Option E: Option E is incorrect because adding a somatostatin receptor analog is not the appropriate strategy; the correct action is to discontinue somatropin during the critical illness rather than co-administer another agent.
This Web-based pharmacology and disease-based integrated teaching site is based on reference materials that are believed reliable and consistent with standards accepted at the time of development.
Possibility of error and on-going research and development in medical sciences do not allow assurance that the information contained herein is in every respect accurate or complete.
Users should confirm the information contained herein with other sources.
This site should only be considered as a teaching aid for undergraduate and graduate biomedical education and is intended only as a teaching site.
Information contained here should not be used for patient management and should not be used as a substitute for consultation with practicing medical professionals.
Users of this website should check the product information sheet included in the package of any drug they plan to administer to be certain that the information contained in this site is accurate and that changes have not been made in the recommended dose or in the contraindications for administration.
Medical or other information thus obtained should not be used as a substitute for consultation with practicing medical or scientific or other professionals.