Volume 15 (2018): Issue 6 (December 2018)

Hepatocellular carcinoma (HCC), the third leading cause of cancer deaths worldwide, with incidence rising is expected to increase by another 81% by the year 2020, primarily due to the hepatitis C epidemic. The strongest risk factors for the development of HCC is a hepatitis B (HBV) and hepatitis C (HCV) virus infection, as well as cirrhosis of any cause. Other risk factors that have been reported include exposure to aflatoxin, alcohol, tobacco, obesity and diabetes. To detect potentially curable cases of hepatocellular carcinoma, outpatients with chronic liver disease who have been seen at the Dr. Ion Cantacuzino Hospital, since 10 years and examined periodically with real-time ultrasonography and measurement of serum alpha-fetoprotein.We analyzed the data on these patients for risk factors for hepatocellular carcinoma.

The risk of liver cancer in men was 1.33 times higher than in women; patients in their 60s had significantly higher rate ratios (6.46) than patients in their 40s; patients with liver cirrhosis diagnosed at enrollment had significantly higher rate ratios for liver cancer (1.93) than patients with chronic hepatitis. The high serum alpha-fetoprotein level at enrollment was also confirmed as a significant marker for a high risk, regardless of the stage of disease (chronic hepatitis or liver cirrhosis). The serum markers for hepatitis virus -- HBsAg, and anti-HCV - were significantly associated with the risk of liver cancer: the adjusted rate ratios for HBsAg, anti-HBc, and anti-HCV were estimated to be 6.92, 4.54, and 4.09, respectively. Hepatitis B surface antigen (rate ratio 6,92; 95% CI: 2.92 to 16.39) and hepatitis C antibody (rate ratio 4.09; 95% CI: 1.30 to 12.85) showed the most risk for carcinoma.

Further studies are required to clarify the roles of other risk factors, including drinking and smoking habits.

Introduction. Iatrogenic hypoglycemia increases cardiovascular morbidity sometimes even with fatalities, and also increases cognitive disorders in most people with type 1 diabetes (T1D) and type 2 diabetes (T2D). Hypoglycemia is characterized by unawareness if the sympathoadrenal response is attenuated during the night, in autonomic neuropathy or in elderly patients. Therefore, hypoglycemia is a limiting factor in the glycemic management of diabetes.

Methods. We aimed to analyze the hypoglycemic events and the time spent with low glucose level (glucose <3.9 mmol/l) in patients with diabetes (T1D, T2D) with insulin therapy (basal or basal-bolus), in ambulatory or hospital setting. The glucose variability was assessed via the interstitial glucose concentration, measured with a Continuous Glucose Monitoring (CGM) system over 72 hours.

Results. The incidence, severity and duration of hypoglycemia are not correlated with HbA1c, disease’s duration and patient’s age. In patients with T1D, severe hypoglycemia is more frequent in patients with a long duration of diabetes. In this analysis, the type of basal analog insulin did not influence the presence of hypoglycemia (p=0.7), but the duration of nocturnal hypoglycemia was longer with insulin glargine U100 than with insulin detemir. The basal regimen is more protective for hypoglycemia than basal-bolus insulin.

Conclusions. The study suggested that hypoglycemic events are common, silent and prolonged in 1/3 of patients with T1D and T2D. The CGM system is beneficial for all patients with T1D and for patients with T2D with hypoglycemic risk and complications, to adjust medication in order to prevent cardiovascular events.

Rapidly progressive glomerulonephritides are relatively rare but serious disorders of diverse etiology, which share some clinical features: rapid evolution, progressive to renal failure, often accompanied by oliguria or anuria. They are characterized histopathologically by an intense extracapillary proliferation, with the development of crescents (semilunar lesions) in over 50% of examined glomeruli. The following pathological entities are referred to as rapidly progressive glomerulonephritides: ANCA-positive pauci-immune vasculitides (microscopic polyangiitis, granulomatosis associated with microscopic polyangiitis, allergic granulomatosis associated with microscopic polyangiitis), extracapillary proliferative glomerulonephritides by immune complexes and glomerulonephritides by anti-glomerular basement membrane antibodies. Due to major histopathological and functional complications, their evolution to death or renal replacement therapy occurs within 6-2 months after the diagnosis, if they are not treated, but the evolution is favorably influenced by aggressive immunosuppression, whether or not associated with plasmapheresis.

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease that affects up to one third of the adult population of industrialized countries. The pathophysiological spectrum includes the following entities that are clinically and histologically distinct: hepatic steatosis and steatohepatitis; their subsequent evolution can lead to cirrhosis and hepatocellular carcinoma.The increase of the prevalence of NAFLD during the last decade is caused by the epidemiological and pathophysiological association with type II diabetes and obesity, NAFLD being present in about 70-80% of patients with type II diabetes mellitus. It has long been thought that the relationship between type II diabetes mellitus and NAFLD is unidirectional, fatty liver being secondary to insulin resistance and type II diabetes mellitus, but recent studies show that hepatic steatosis may precede insulin resistance and diabetes mellitus, thus demonstrating abidirectional causal relationship between these two disorders. Weight loss through diet andexercise is effective in preventing and treating NAFLD in diabetic patients; also, drugs that causeweight loss need to be evaluated. Both anti-diabetic medication and statins play an important vrole in the prevention and treatment of NAFLD.

Primary biliary cirrhosis is an autoimmune liver disease, characterized by the progressive destruction of the small intrahepatic bile duct epithelial cells and the presence of antimithocondrial antibodies (AMA). Ankylosing spondilitis is a systemic, inflammatory, progressive disease, which usually affects the joints of the spine and the sacroiliac joints. The association of these two is very rare, in literature we found only one single study published in 1994, which describes the occurrence of primary biliary cirrhosis accompanying ankylosing spondylitis in amale patient. The aim of our study is to present the case of our patient, who had ankylosing spondylitis and has developed primary biliary cirrhosis. Our patient has ankylosing spondylitis with peripheral joint involvement, so according to the guidelines we initiated treatment with Sulfasalazine. We know from the literature about the hepatotoxicity of Sulfasalazine in some cases, so within each follow-up examination we monitored the liver function tests, and we also performed complete blood counts. The treatment of ankylosing spondylitis is challenging in this case due to the hepatotoxicity of the medications. Besides Sulfasalazine, our patient continued the treatment for primary biliary cirrhosis (ursodeoxycholic acid with hepatoprotective drugs in higher doses).

Giant cell arteritis (GCA), or temporal arteritis, is the most common systemic vasculitis, and the greatest risk factor for developing GCA is aging. The disease almost never occurs before age 50, and its incidence rises steadily thereafter, peaking between ages 70 to 79, the risk of development being two times higher in women.

Polymialgia rheumatica (PMR) is an inflammatory rheumatic condition characterized clinically by aching and morning stiffness at the shoulders, hip girdle, and neck. PMR is almost exclusively a disease of adults over the age of 50, with a prevalence that increases progressively with advancing age. The peak incidence of PMR occurs between ages 70 and 80, the same as in the case ofGCA. PMRis 2-3 times more common in women than in men.

PMR is two to three times more common than GCA and occurs in about 50% of patients with GCA. The percentage of patients with PMR who experience GCA at some point varies widely in reported series ranging from 5 to 30 percent. PMR can precede, accompany or follow GCA. The diagnostic in the case of PMR is made first of all on clinical features, in the patients in whom another disease to explain the findings is not present. For GCA we must follow the diagnostic algorithm presented below (figure 1) and keep in mind that a negative result for temporal artery biopsy does not exclude the diagnostic if clinical suspicion of GCA is high

We present the case of a 81 year-old male with signs and symptoms from both conditions, PMR and GCA.

Ulcerative colitis is a chronic idiopathic inflammatory disorder of the colon, characterized by a diffuse continuous superficial inflammation that always begins within the rectum and affects the proximal colon to a varying extent. One typical feature of the disease is that it does not involve the small intestine. A small percentage of patientsmay present a superficial inflammation of the terminal ileum. Clinically the disease is associated with rectal bleeding and urgency, tenesmus, abdominal pain and diarrhea. In the assessment of the disease severity, various factors are used, including the frequency of bowel movements, rectal bleeding, laboratory tests, endoscopic extension and appearance and patient’s quality of life.

The treatment of ulcerative colitis is adapted to the disease severity and to the individual patient, no treatment being universally effective. Treatment decisions should be based on disease activity (mild, moderate, severe) and distribution (proctitis, left-sided, extensive colitis) If mild to moderate inflammation is limited to the rectum and for left-sided colitis, the mainstay on the treatment are 5-aminosalicylates, which are highly effective as a topical treatment (suppositories, enemas, foams). Corticosteroids are indicated in patients with more severe disease, and in cases where mesalamine has failed in inducing remission.

For extensive mild to moderate ulcerative colitis, therapy recommendation consists of a combined therapy using oral and topical 5-ASA, which proved to be superior to single use of either. Use of systemic corticosteroids should be considered earlier for patients with extensive colitis and/or treatment failure. For patients with severe ulcerative colitis, hospitalization is generally required. In these cases, steroid therapy is still the gold standard. If there is no improvement in the first 72 hours after the initiation of treatment or symptoms are worsening, second-line conventional therapy must be attempted or proctocolectomymay be considered. In steroid-refractory patients, as well as in patients with severe ulcerative colitis, early introduction of immunosuppressive drugs may be effective during severe episodes, and for the prevention of complications, such as toxic megacolon. Without doubt, the introduction of anti-TNF antibodies have improved the therapeutic options available for patients with ulcerative colitis. But, there still is a substantial amount of patients not responding to anti-TNF antibodies or experiencing a secondary loss of response. Fortunately, for these cases, new classes of drugs have been developed and have been evaluated in early clinical trials.

To illustrate the heterogeneity of cases of ulcerative colitis, we present three particular situations.