A case report of posterior reversible encephalopathy syndrome in a patient receiving gemcitabine and cisplatin.

RATIONALE: Posterior reversible encephalopathy syndrome (PRES) is a subacute syndrome causing characteristic neurologic and radiologic findings. PRES is predominantly caused by malignant hypertension though it has been associated with immunosuppressive treatments such as chemotherapy. PATIENT CONCERNS: We describe a case of a 58 year old female who developed fluctuant level of consciousness, agitation. DIAGNOSIS: MRI findings were in keeping with posterior reversible encephalopathy syndrome following cycle 6 of palliative gemcitabine and cisplatin therapy for metastatic cholangiocarcinoma. INTERVENTIONS: The patient was managed with magnesium supplementation for hypomagnesemia and amlodipine. OUTCOMES: The patient's level of consciousness returned to normal though she had residual neurologic deficits impairing her ability to drive and impacting her balance. CONCLUSIONS: Cisplatin is a documented causative agent of PRES though gemcitabine is rarely associated with the syndrome. Combination cisplatin and gemcitabine therapy causing radiologically proven PRES has been documented in only 3 previous case reports. Gemcitabine's poor blood-brain barrier penetration makes it an unlikely culprit of central nervous system (CNS) toxicities. Our case and previous reports suggest higher doses may contribute to CNS toxicities such as PRES. Additionally, an emerging trend of hypomagnesemia associated with PRES has been documented inside and outside the context of malignancy and suggests a possible target for treatment and prevention warranting further investigation.

Tuberculosis of the genitourinary system-Urinary tract tuberculosis: Renal tuberculosis-Part I.

Tuberculosis (TB) remains a worldwide scourge and its incidence appears to be increasing due to various factors, such as the spread of human immunodeficiency virus (HIV) and acquired immunodeficiency syndrome (AIDS). The insidious onset and non-specific constitutional symptoms of genitourinary tuberculosis (GUTB) often lead to delayed diagnosis and rapid progression to a non-functioning kidney. Due to hematogenous dissemination of TB, there is a potential risk of involvement of the contralateral kidney too. Imaging plays an important role in the making of a timely diagnosis and in the planning of treatment, and thus helps to avoid complications such as renal failure. Imaging of GUTB still remains a challenge, mainly on account of the dearth of literature, especially related to the use of the newer modalities such as magnetic resonance imaging (MRI). This two-part article is a comprehensive review of the epidemiology, pathophysiology, and imaging findings in renal TB. Various imaging features of GUTB are outlined, from the pathognomonic lobar calcification on plain film, to finer early changes such as loss of calyceal sharpness and papillary necrosis on intravenous urography (IVU); to uneven caliectasis and urothelial thickening, in the absence of renal pelvic dilatation, as well as the hitherto unreported 'lobar caseation' on ultrasonography (USG). Well-known complications of GUTB such as sinus tracts, fistulae and amyloidosis are described, along with the relatively less well-known complications such as tuberculous interstitial nephritis (TIN), which may remain hidden because of its 'culture negative' nature and thus lead to renal failure. The second part of the article reviews the computed tomography (CT) and MRI features of GUTB and touches upon future imaging techniques along with imaging of TB in transplant recipients and in immunocompromised patients.

Tuberculosis of the genitourinary system-Urinary tract tuberculosis: Renal tuberculosis-Part II.

This article reviews the computed tomography and magnetic resonance imaging (MRI) features of renal tuberculosis (TB), including TB in transplant recipients and immunocompromised patients. Multi detector computed tomography (MDCT) forms the mainstay of cross-sectional imaging in renal TB. It can easily identify calcification, renal scars, mass lesions, and urothelial thickening. The combination of uneven caliectasis, with urothelial thickening and lack of pelvic dilatation, can also be demonstrated on MDCT. MRI is a sensitive modality for demonstration of features of renal TB, including tissue edema, asymmetric perinephric fat stranding, and thickening of Gerota's fascia, all of which may be clues to focal pyelonephritis of tuberculous origin. Diffusion-weighted MR imaging with apparent diffusion coefficient (ADC) values may help in differentiating hydronephrosis from pyonephrosis. ADC values also have the potential to serve as a sensitive non-invasive biomarker of renal fibrosis. Immunocompromised patients are at increased risk of renal TB. In transplant patients, renal TB, including tuberculous interstitial nephritis, is an important cause of graft dysfunction. Renal TB in patients with HIV more often shows greater parenchymal affection, with poorly formed granulomas and relatively less frequent findings of caseation and stenosis. Atypical mycobacterial infections are also more common in immunocompromised patients.