Chapter 2: Clinical Presentation of Portal Hypertension

Liver cirrhosis and portal hypertension (PHT) are common clinical findings, and according to the Centers for Disease Control and Prevention, chronic liver disease and cirrhosis is the 12th leading cause of death in the United States. The recent data suggest that it is the eighth leading cause of death overall and the third leading cause of death in persons 45 to 64 years of age, and deaths related to chronic liver disease and cirrhosis has increased 3.3% between 2009 and 2010. Current studies indicate that the mortality rate related to liver disease over the past 3 decades has remained unchanged.1,2 Liver disease continues to be a significant cause of morbidity and accounts for a substantial portion of health-care utilization in the United States and worldwide.³ Understanding the natural history of cirrhosis and PHT is important to identify patients at highest risk for complications of liver disease, including liver cirrhosis. Such knowledge would permit early intervention and potentially alter the clinical course of patients with chronic liver disease toward a favorable outcome. This chapter discusses the clinical presentation of cirrhosis and PHT.

Complications from Cirrhosis and Portal Hypertension

Regardless of the cause of cirrhosis, patients often remain asymptomatic until complications of end-stage liver disease develop ( Table 2.1). Diagnosing asymptomatic patients usually follows from noting abnormal laboratory markers during incidental screening tests or from radiologic findings. Diagnosis becomes easier when signs of decompensation, including jaundice, ascites, and asterixis, are present.^4,5 However, these patients are also at the highest risk for developing more serious and potentially life-threatening complications.⁵

Table 2.1 The Most Common Etiologies of Cirrhosis4,5

HBV: hepatitis B virus; HCV: hepatitis C virus; IBD: inflammatory bowel disease; NAFLD: nonalcoholic fatty liver disease; NASH: nonalcoholic steatohepatitis; PAN: polyarteritis nodosa; UC: ulcerative colitis.

Varices

Patients with cirrhosis often develop esophageal or gastric varices (GVs) caused by the portosystemic shunting that accompanies PHT.⁶ GVs usually form in the submucosal layer at the cardia or the fundus of the stomach because the posterior wall in this region of the stomach approaches the portosystemic collateral circulation. GVs receive most of their blood supply from the left, posterior, and short gastric veins and drain mainly through a gastrorenal shunt ( Fig. 2.1). About 85% of patients with GVs develop a significant shunt that is able to pass extraordinarily large volumes of blood at high velocities. These GVs and resultant shunts predispose patients to a higher risk of experiencing a massive variceal bleeding or hepatic encephalopathy (HE) ( Fig. 2.1; Fig. 2.2).⁷

Approximately 35% of patients with compensated cirrhosis and 80% of those with decompensated cirrhosis have varices at the time of diagnosis.⁸ Bleeding gastroesophageal varices is the most serious complication of cirrhosis ( Fig. 2.2; Fig. 2.3).⁹ One third of affected patients will experience a variceal bleed, which accounts for up to 90% of all bleeding episodes seen in these patients. Active bleeding at the time of endoscopy is one of the hallmarks for poor prognosis in patients with varices, particularly when accompanied by bacterial infection, portal vein thrombosis, and a hepatic venous pressure gradient (HVPG) greater than 12 mm Hg.⁶ Mortality rates from variceal bleeding have declined in recent years but still remain high. The 6-week mortality rate averages 15% to 20% per bleeding episode and correlates with disease severity.⁸ PHT may also lead to portal hypertensive gastropathy (PHG), a serious condition that can cause acute or even massive blood loss. Endoscopic investigation shows abnormalities in the gastric mucosa often described as a mosaic-like pattern that resembles snake skin. Pathologic changes responsible for these lesions originate from vascular ectasia rather than mucosal inflammation as originally thought.¹⁰ The low incidence of PHG, ranging from 2% to 12%, classifies this complication as a less common cause of upper gastrointestinal (GI) bleeding.¹⁰

Rectal varices, frequently confused with hemorrhoids, develop in about 4% of patients with PHT. Hemorrhoids develop in the submucosa of the anal canal and unlike varices do not communicate with the portal circulation, nor occur with a higher incidence in portal hypertensive patients. A correlation of the thickness of the rectal wall has been suggested by endoscopic studies, but this association remains a topic of debate.¹¹ Because rectal varices rarely bleed, they are of less clinical importance than either esophageal varices or GVs. Detailed discussions on the medical and endoscopic management of varices are given in other chapters.

Ascites

Ascites develops secondary to PHT when excess fluids accumulate in the peritoneal cavity ( Fig. 2.4). It is the most common complication of cirrhosis seen in approximately 60% of compensated patients within 10 years of disease onset.¹² Arterial splanchnic vasodilation leads to arterial hypotension with activation of both sympathetic nervous and renin–angiotensin–aldosterone system (RAAS). Excessive sodium accumulation consequent to the body’s failure to adequately excrete sodium into urine ultimately results in ascites and edema. Performing a paracentesis and appropriate analysis of the ascitic fluid helps rule out other possible causes of fluid buildup.¹² Cirrhosis accounts for more than 75% of all causes of ascites. The remaining 25% of ascites cases are caused by malignancy (10%), cardiac failure (3%), pancreatitis (1%), tuberculosis (2%), or other factors.¹³ Patients who develop ascites tend to have a poor prognosis and diminished quality of life. Thus, they should be considered for liver transplantation upon diagnosis.¹²

Fig. 2.1 Anatomy of the portal circulation. Gastric varices caused by splenic vein thrombosis (SVT) tend to arise from the short gastric veins running from the hilum of the spleen to the greater curvature aspect of the stomach rather than through splenorenal or gastrorenal shunts common with portal hypertensive fundal varices. IVC: inferior vena cava; LGV: left gastric vein; LRV: left renal vein; PV: portal vein; SGV: short gastric vein; SMV: superior mesenteric vein.

Fig. 2.2 Photographs of gastric varices. (a) Large (>3 cm) gastric varices (IGV-1; isolated gastric varices-type 1) with no stigmata of bleeding. (b) A large IGV-1 with evidence of recent bleeding (blood in the stomach and a nipple or dimple sign). (c) The nipple sign area with active bleeding. (d) Mosaic (snake skin–like appearance) pattern of post-BRTO (balloon retrograde transvenous obliteration) findings of a GOV-2 (gastroesophageal varices-type 2).

Fig. 2.3 Classifications of esophageal varices. (a) Small, low-risk esophageal varices (or F1), almost flattened out with insufflation. (b) Medium-sized, low-risk esophageal varices (F2) that did not flatten with insufflation. (c) Large esophageal varices greater than one third of the esophageal lumen with some high-risk stigmata (red marks or wheals). (d) Esophageal varices with high-risk stigmata for recent bleeding and rebleed with red marks and a nipple sign or fibrin plug.

Pathogenic alterations responsible for ascites in patients with cirrhosis include 2 separate mechanisms.14 The first is caused by increased portal flow resistance at the sinusoids, creating sinusoidal PHT and an associated pressure backwash into the splanchnic capillaries. Excess fluid preferentially accumulates in the peritoneal cavity, and blood flow increases to the splanchnic area, leading to further increases in portal pressure. The second mechanism precedes ascites formation and relates to sustained renal sodium retention. The initiating process remains a subject of controversy but may involve hepatorenal baroreflex from PHT or nominal activation of the RAAS caused by subtle hypovolemia.¹⁴

The continuous escape of fluids into the interstitial space as a result of these hemodynamic changes is partly compensated by reabsorption into the systemic circulation via the lymphatic system and thoracic duct. When cirrhosis progresses to a point where the lymphatic system can no longer manage the overload, excess fluid progressively accumulates into the peritoneal cavity, which perpetuates sodium and water reabsorption caused by decreased intravascular systemic volume in addition to elevated norepinephrine and other systemic vasoconstrictors. Dietary changes and moderate doses of diuretics can usually manage ascites when presenting at an early stage. However, 10% of patients will become refractory when their condition becomes resistant to diuretics.¹⁴ An appropriate mode of treatment for ascites classified by its severity is shown in Table 2.2.

Increases in sodium retention (urine sodium <10 mEq/L) is accompanied by a decline in glomerular filtration rate. Patients with more advanced stages of decompensated cirrhosis develop low arterial pressure because of a further reduction of the peripheral vascular resistance. Eventually, sodium becomes primarily absorbed at the renal tubules and proximal to the site of diuretic action, explaining why treatment begins to fail in a subset of patients. At this stage, patient prognosis becomes dismal and implies a low 2-year probability of survival.¹⁴

Fig. 2.4 Illustration of ascites caused by cirrhosis and portal hypertension.

Refractory ascites typically associates with other serious complications, including spontaneous bacterial peritonitis (SBP), muscle wasting, pleural effusion, and dilutional hyponatremia. The first line of treatment involves large-volume paracentesis and administering albumin if more than 5 L is removed.12,14 Patients may continue on diuretics if effective and perhaps undergo insertion of a transjugular intrahepatic portosystemic shunt (TIPS) to decompress the portal system (see Table 2.2).¹² Detailed management of ascites is discussed in a separate chapter.

Spontaneous Bacterial Peritonitis

Patients with cirrhosis have an increased susceptibility to bacterial infections, and development of an infection in cirrhotic patients is often associated with a poor outcome and high mortality rate. SBP is one the commonest infections in cirrhosis. It arises as an acute infection of the ascitic fluid and is defined by an ascitic polymorphonuclear leukocyte (PMN) count of 0.25 × 10⁹/L or greater.^15,16 Usually there is no obvious source of infection such as an abscess, hollow viscous perforation, acute pancreatitis, or cholecystitis. SBP infection is precipitated by bacterial translocation of gram-negative bacteria, including Escherichia coli and Klebsiella spp. from the intestine but may also originate from long-term antibiotic prophylaxis with fluoroquinolones.¹⁵ Most patients with SBP present with symptoms typical of peritoneal infection, especially abdominal pain, fever, and diarrhea, although a small percentage remain asymptomatic.¹⁷ Signs of liver or renal impairment suggestive of SBP include the development of HE and may offer important clues for diagnosis in asymptomatic patients.¹⁸

Whereas spontaneous bacterial peritonitis almost always develops in patients with cirrhosis who have large-volume ascites, low-volume ascites and ascites from other origins rarely cause concern for infection.¹⁷ Renal dysfunction develops in one third of patients with SBP likely because of a reduced effective circulating volume.¹⁸ Serum creatinine levels greater than 1 mg/dL at the time of diagnosis represents an important risk factor for death in these patients, and those at risk may benefit from renal volume expansion with albumin via intravenous infusion.^17,18 Although once considered a highly feared complication of cirrhosis, SBP has become a highly treatable condition, although it has a high recurrence rate.¹⁷

Table 2.2 Ascites Severity and Recommended Treatment12

TIPS: transjugular intrahepatic portosystemic shunt.

Table 2.3 Classification of Ascites Based on the Serum-Ascites Albumin Gradient

Paracentesis followed by an ascitic fluid analysis provides the most rapid and cost-effective approach for distinguishing portal from nonportal hypertension ascites because the ascitic fluid albumin (and protein) content can readily distinguish the two.12 Classification of ascites made using the serum-ascites albumin gradient (SAAG) allows reliable assessment of the ascites etiology. This method has largely replaced less reliable techniques that relied on sole measurement of ascitic fluid protein concentration.¹³ Calculating the SAAG involves subtracting the concentration of albumin in ascitic fluid from that in serum using samples withdrawn from the patient on the same day. Whereas a SAAG of less than 1.1 g/dL suggests an ascites etiology of nonportal hypertensive origin seen in about 15% of patients ( Table 2.3), a SAAG of 1.1 g/dL or greater predicts ascites caused by PHT with more than 97% accuracy.^13,16

Hepatic Hydrothorax

Hepatic hydrothorax (HH) is defined as serious pleural effusion (>500 mL) that occasionally develops in patients with cirrhosis who otherwise have no underlying pulmonary or cardiac disease.^19,20 This condition appears predominantly right sided in up to 87% of all HH cases but may also affect the left pleural cavity or present bilaterally. HH leads to significant patient morbidity because even modest volumes of pleural fluid can cause serious respiratory problems. Onset occurs when ascitic fluid leaks through small defects in the diaphragm, which is the most plausible explanation. The negative intrathoracic pressure generated by inspiration favors unidirectional passage of fluid from the abdomen to the pleural space that later gets trapped and absorbed. HH occurs when the rate of fluid accumulation exceeds the absorptive capacity of the pleura. Whether patients have clinically detectable ascites at the time HH presents depends on the pleural space leakage caused by the negative thoracic pressures during inspiration.²⁰

Hepatorenal Syndrome

Hepatorenal syndrome (HRS) is a type of acute kidney injury and is a serious complication of liver failure and cirrhosis. Its onset follows a severe compromise in renal perfusion, which might reverse with albumin infusion or with administering vasoconstrictors.²¹ Two types of HRS exist (types I and II), which may be differentiated based on laboratory findings and clinical features. Whereas renal failure in type II patients progresses slowly (average serum creatinine of 1.5 mg/dL), those with type I HRS experience an acute and rapid onset marked by quickly rising serum creatinine levels that reach above 2.5 mg/dL within 2 weeks.²¹ Regardless of the cause of HRS, it is associated with a poor prognosis. The expected survival time of these patients is diminished to weeks after the onset of HRS if left untreated.

Several precipitating events can lead to HRS development, including SBP, but also infections such as pneumonia, cellulitis or urinary tract infection, hepatitis, GI hemorrhage, and major surgical procedures. Type II HRS presents with refractory ascites and likely represents the end result of a complex series of circulatory and renal dysfunctions linked to cirrhosis. The peripheral arterial vasodilation theory best explains the mechanism behind type II onset.²¹ Enhanced local release of nitric oxide and other vasodilators during PHT stimulates arterial vasodilation in the splanchnic circulation. A slow deterioration in cardiac function may also precede the onset of HRS.²² Clinical features seen in individuals with type I HRS include impaired hepatic, renal, cardiovascular, and adrenal function thought to occur as part of a more complex syndrome called acute-on-chronic liver failure (ACLF).^21,23

Portopulmonary Hypertension and Hepatopulmonary Syndrome

Approximately one third of patients with cirrhosis will develop vascular pulmonary complications broadly categorized into portopulmonary hypertension (PoPH; 4%–8%) and hepatopulmonary syndrome (HPS; 15%–30%).²⁴ These 2 syndromes constitute opposing responses to the same clinical condition, and neither depends on the underlying cause or severity of PHT. PoPH is a state of pulmonary arterial hypertension defined by a mean pulmonary arterial pressure (mPAP) above 25 mm Hg at rest or above 30 mm Hg while exercising; a pulmonary vascular resistance above 240 dynes.s.cm^-5; and a capillary wedge pressure below 15 mm Hg.²⁴ Dyspnea upon exertion is a sign of PoPH, but patients frequently remain asymptomatic. In fact, PoPH often gets picked up during a routine echocardiogram that shows an elevated right ventricular systolic pressure (RVSP). An RVSP above 40 mm Hg requires following up with right heart catheterization to confirm changes from pulmonary arterial hypertension rather than other causes related to volume overload.²⁵ Reducing the pulmonary pressure with vasodilators provides an appropriate pharmacotherapy for managing PoPH. Liver transplantation, once contraindicated for patients with PoPH, may now be safely attempted as long as the patient has proper mPAP control and no right heart failure.²⁵

The second syndrome is HPS. HPS is due to intrapulmonary microvascular vasodilation and a widened alveolar–arterial oxygen gradient on room air (>15 mm Hg) with or without hypoxemia.^24,25 Although commonly seen in patients with cirrhosis who have PHT, HPS need not associate with either condition. This syndrome has also been described in individuals with acute or chronic hepatitis and no PHT as well as others with PHT and noncirrhotic liver disease such as nodular regenerative hyperplasia.²⁵ Patients with cirrhosis who have HPS experience increasing pulmonary vasodilation and diminished gas exchange as their condition worsens. HPS is associated with a high mortality rate, but orthotopic liver transplantation (OLT) can successfully reverse the condition.²⁴ Clinical studies so far have failed to confirm effective medical therapies for HPS; OLT currently provides the only definitive treatment.²⁵ Supplemental oxygen therapy gives relief when hypoxemia presents.

Hepatic Encephalopathy

Hepatic encephalopathy is the onset of brain dysfunction resulting from metabolic alterations accompanying liver cirrhosis or acute liver failure. The condition arises mainly from reduced clearance of gut-derived neurotoxins, although other substances normally cleared by the liver may also contribute. Initially, patients may appear confused, but if left untreated, this potentially reversible condition can quickly progress to irreversible cognitive dysfunction and coma.26 Treatment involves identifying and removing precipitating factors and reducing the load of ammonia reaching the liver by giving the patient lactulose.⁴ All patients with cirrhosis who present with an altered mental state should be evaluated for focal neurologic signs associated with HE, but these rarely appear and are regressive. After the first HE episode occurs, patient’s expected 1- and 3-year survival rates are 42% and 23%, respectively.²⁶

Hepatic encephalopathy is divided into 3 nomenclature types. The first, type A, refers to HE in acute liver failure; type B is HE associated with portosystemic bypass and no intrinsic liver disease; and type C describes HE in patients with cirrhosis with PHT.²⁶ Type C may present persistently, episodically, or minimally depending on the precipitating factors and clinical manifestations. Episodic HE usually occurs secondary to a precipitating event but can also initiate spontaneously. The common precipitating factors for HE are listed in Table 2.4.

The severity of mental disturbance, ranging from mild cognitive changes to coma, is most often graded by the West Haven Criteria ( Table 2.5).²⁷ Reliable classification in more severe cases relies on using the Glasgow Coma Scale (GCS), which provides a more objective and reproducible assessment of mental impairment than West Haven criteria. The portosystemic encephalopathy (PSE) score calculated based on the patient’s mental status, electroencephalographic abnormalities, and ammonia levels also objectively describes the clinical severity of HE.²⁷ The PSE serves primarily as a research tool and has not surpassed West Haven Criteria acceptance for classifying HE in clinical practice.²⁷

Table 2.4 Precipitants of Hepatic Encephalopathy27

GI: gastrointestinal; SBP: spontaneous bacterial peritonitis; SIRS: systemic inflammatory response syndrome.

Table 2.5 Stages of Hepatic Encephalopathy27

Despite significant research devoted to understanding the mechanism of HE, controversies still remain regarding its pathophysiology. Most experts believe that nitrogenous toxins originating from the gut adversely influence mental function. In healthy subjects with normal hepatocyte function, 80% to 90% of ammonia derived from the colonic bacteria gets excreted through first-pass metabolism.²⁷ Buildup of cellular ammonia as a consequence of liver failure may result in cerebral energy failure in addition to altered neurotransmissions by disrupting the GABAergic (gamma-aminobutyric acid) pathway.²⁸ Astrocyte swelling caused by ammonia detoxification in these cells and a consequent accumulation of glutamine are responsible for the brain edema observed in these patients. Astrocyte swelling may also accompany glutamate uptake or occur in response to extracellular acidosis.²⁹

Symptoms and Physical Examination

The majority of patients with cirrhosis are asymptomatic. The onset of symptoms in these patients usually occurs insidiously but can also be abrupt. Cirrhosis may be suspected when the patient presents with mild symptoms, including weakness, fatigue, muscle cramps, weight loss, or sleep disturbances or other symptoms of HE. More telling symptoms usually reflect decompensation, including hematemesis, hematochezia, melena, jaundice, and anorexia with nausea (which can be severe). Patients may complain of abdominal pain related to stretching of Glisson’s capsule or the development of ascites. About two thirds of patients will have signs of an enlarged, palpable liver predominantly affecting the left lobe. Women sometimes experience menstrual irregularities, and men might experience erectile dysfunction or sterility.^30,31 Increased estradiol levels in men give rise to proliferation of glandular tissue in the breast, or gynecomastia.³⁰

Bulging flank and flank dullness to percussion caused by accumulation of fluid in the abdomen provides the most accurate prediction of ascites. In fact, the absence of flank dullness occurs in only about 10% of patients who have ascites.30 Examination of whether the dullness shifts with rotation of the patient or it persists when percussed anteriorly can help determine the extent of ascites development. Fever with hypotension, abdominal tenderness, and decreased bowel sound suggests the onset of SBP but can also manifest from alcoholic hepatitis or concurrent infection.

A physical examination may identify changes in the skin apart from jaundice that reveal liver disease. Vascular spider angioma commonly presents on the trunk, face, and upper extremities, and their number and size correlate with disease severity.³⁰ However, spider angioma can also indicate pregnancy or malnourishment. Palmar erythema characterized by an exaggerated and mottled redness on the thenar and hypothenar eminences develops as a result of changes in metabolism and sex hormones. The nails frequently show discoloration or clubbing and Dupuytren’s contractures manifested as thickening and shortening of the palmar fascia commonly occur. Evidence of vitamin deficiency, including glossitis and cheilosis, are frequently present.

Laboratory Evaluation

A positive diagnosis for cirrhosis is made on the basis of laboratory and radiographic findings. Serum albumin and prothrombin time measurements provide clues regarding liver function, and serum bilirubin levels indicate the liver’s capacity to conjugate and excrete bilirubin.⁴ Elevated aminotransferases with aspartate aminotransferase (AST) greater than alanine aminotransferase (ALT) suggests cirrhosis, but the absence of this finding does not exclude the presence of cirrhosis. A low platelet count is suggestive of PHT and hypersplenism. When SBP is suspected, the patient should be investigated with a full blood count, urinalysis, and ascitic fluid cell count, as well as ascites, blood, and urine cultures.¹⁷ Laboratory tests also help identify the underlying cause of cirrhosis because specific findings can determine the different etiologies of cirrhosis ( Table 2.6).

Several laboratory tests, scores, and indices have emerged as noninvasive predictors of cirrhosis.^4,32 The APRI index measures the AST-to-platelet ratio and is able to predict cirrhosis with a high degree of accuracy.³² Scores generated by the patented FibroTest based on serum biomarkers (haptoglobin, α2-macroglobulin, apolipoprotein A1, γ-glutamyltransferase [γGT], and bilirubin) plus age and gender show a good correlation with PHT severity.³³ Other algorithms include the Hepascore combining hyaluronic acid, total bilirubin, γGT, α2-macroglobulin, age, and sex for predicting the degree of liver fibrosis but with limitations,³⁴ and the BARD score is composed of 3 variables—body mass index, AST-to-ALT ratio, and presence of diabetes—for identifying nonalcoholic fatty liver disease patients with advanced fibrosis. Despite advances in laboratory testing for evaluating chronic liver disease, liver biopsy remains the gold standard for the diagnosis of liver cirrhosis. However, liver biopsy is an invasive procedure and is costly and not appropriate for all patients (e.g., patients with prolonged prothrombin times or low platelet counts) with potential side effects and risks. Thus, liver biopsy is not necessary in the presence of decompensated cirrhosis or when imaging studies or laboratory tests have confirmed the presence of cirrhosis. The decision on whether to perform a histologic assessment should be reserved for selected patients.⁴

Radiologic Evaluation

Imaging techniques are an attractive method of evaluating cirrhosis because of their noninvasiveness and ability to detect structural changes and determine complications of liver cirrhosis, including ascites, varices, PHT, splenomegaly, and nodular liver or liver masses. Conventional imaging techniques, including ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI), provide initial evaluation of the hepatic architecture but are not particularly sensitive in detecting cirrhosis and have a low predictive value. Upper GI endoscopy currently sets the bar for reliable identification of esophageal varices, but abdominal CT scanning has shown promise as a reliable tool for identifying varices and is a safer and more cost-effective procedure.³⁵ Ultrasound color duplex Doppler helps visualize the upper abdominal vasculature changes caused by the development of portosystemic collateral circulation and enlarged portal and splanchnic veins from PHT.³⁵ Supporting information from CT and MRI also helps diagnose PHT by identifying venous structure alterations, particularly portosystemic collaterals.⁵ Endosonography, which combines ultrasonography and endoscopy, is the method of choice for identifying deep rectal varices.¹¹

Table 2.6 Diagnostic Laboratory Tests for the Most Common Causes of Liver Cirrhosis4,5

↑: increased; ↓: decreased; (+): positive test result; ALP: alkaline phosphatase; ALT: alanine aminotransferase; AMA: antimitochondrial antibody; ANA: antinuclear antibody; ASMA: anti–smooth muscle antibody; AST: aspartate aminotransferase; γGT: γ-glutamyltransferase; HbA1C: hemoglobin A1C; HBsAg: hepatitis B surface antigen; HBV: hepatitis B virus; HCV: hepatitis C virus; HDL: high-density lipoprotein; HFE: hemochromatosis; HLA: human leukocyte antigen; LKM: liver-kidney-microsomal; MCV: mean corpuscular volume; NAFLD: nonalcoholic fatty liver disease; NASH: nonalcoholic steatohepatitis; pANCA: perinuclear neutrophils cytoplasmic antigen; TSH: thyroid-stimulating hormone.

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