The McKittrick-Wheelock syndrome, a rare disorder, is caused by fluid and electrolyte hypersecretion from a rectal tumour and patients can develop a depletion syndrome characterised by severe dehydration, hyponatraemia, hypokalaemia and metabolic acidosis. We present a case of a 62-year-old man who presented with chronic diarrhoea that had resulted in numerous previous hospital admissions. On physical exam, the patient showed signs of volume depletion. A soft polypoid mass was appreciated on digital rectal examination. Laboratory tests showed renal failure and significant electrolyte abnormalities. Colonoscopy revealed a large, friable mass in the rectosigmoid region. Biopsies were consistent with tubolovillous adenoma. Subsequently, the patient underwent surgical resection, which on pathology exhibited evidence of high-grade dysplasia, and the patient was diagnosed with McKittrick-Wheelock syndrome. It is essential to identify this condition in a timely manner as it is associated with high morbidity and complications, some of which may be life threatening.

We described a case of Gitelman syndrome. A 56-year-old healthy man presented with facial paralysis. Initial laboratory tests revealed hypokalemia. Despite potassium supplements, kaliemia remains at low levels. Further investigations showed urinary potassium wasting, hypomagnesemia and hypocalciuria. Diagnosis of Gitelman syndrome has been confirmed by molecular diagnosis with identification of a composite heterozygote mutation on SLC12A3 gene. One of the mutations on exon 1 SCL12A3 gene wasn't yet known. In the patient family, the same genetic disorder has been found in the sister. Treatment and follow up schedule were proposed to patient.

Diuretics (thiazides, loop diuretics) are established as treatments of common diseases: arterial hypertension, heart failure, and renal disease. In aging societies, their prevalence sharply rises with age. Thus, diuretic efficacy and safety need to be considered in the elderly as main consumers. Diuretics expose several disadvantages with particular relevance for the elderly. The most acknowledged side effects concern electrolyte disturbances. Hypokalemia (up to 8%) may not only precipitate cardiac arrhythmias and related sudden death but also adynamia by muscular weakness. Hyponatremia (up to 17%) may contribute to confusion, delirium, and irreversible brain damage adding to age-related dementia. Thiazides are the antihypertensive drugs with the strongest diabetogenic activity. In heart failure treatment, overdosing of diuretics is common, as doses often reflect requirements for acute recompensation, which is two- to threefold the requirement of that in maintenance therapy. Trial data demonstrate a positive correlation between mortality and diuretic use/dose, which may also be related to volume contraction, related ACE-inhibitor intolerance, renal impairment, and venous thromboembolism. Combining loop and thiazide diuretics may be indicated for severe cardiac or renal failure, but it is also excessively used in less severe stages, causing an even more severe threat to patients; thiazides are often added unintentionally if overlooked in combination pills. Diuretics may be used to treat peripheral "edema" in obese patients, patients on calcium antagonists, or those with venous thrombotic disease. Here they are not indicated and may even induce edema. In statistics on adverse drug reactions leading to hospitalization, diuretics are among the 5 leading drug classes. Misleading interpretations of clinical trials and their low cost have pushed them into the front position of hypertension treatment. Here, side effects, including the urge of voiding, lead to the lowest adherence rate among first-line antihypertensives. It is proposed to term the syndrome of inappropriate diuretic application "morbus diureticus." It should be diagnosed by history taking, force assessment (timed-up-and-go, chair-rise tests), clinical hydration assessment, and laboratory tests (electrolytes, creatinine). In heart failure, dose reductions/step-down from loop to thiazide diuretics should be tested routinely at 3- to 6-month intervals. In hypertension treatment, diuretics should be third in line if control by RAS inhibitors and long-acting dihydropyridine calcium antagonists is insufficient. If symptoms improve after diuretic step-down (including improved tolerance to RAS inhibitors or renal function), this diagnosis may also be made "ex juvantibus."

OBJECTIVES:

: To determine urinary potassium loss (as measured by fractional excretion of potassium (FEK) and trans-tubular potassium concentration gradient (TTKG)) in children with acute liver failure (ALF) and acute viral hepatitis (AVH) at the time of presentation to the hospital and day 45 of follow up.

MATERIAL AND METHODS:

: Twenty five ALF and 84 AVH patients were worked up for clinical features, liver function tests and hepatitis viral infections and monitored for outcome. All ALF patients were hospitalized. FEK and TTKG were estimated on the day patients were first seen in the hospital or hospitalized and later on day 45 of follow up.

RESULTS::

Sixty percent (15/25) of ALF patients were hypokalaemic (serum K+ <3.5 mEq/L) as compared to only 12% (10/84) in AVH group (p = 0.000) at the time of presentation in the hospital. Inappropriate kaliuresis was present in 80-100% of hypokalaemic children compared to 0 to 30% of normokalaemic individuals at the time of first contact in either ALF or AVH group. Inappropriate urinary potassium loss and serum K+ levels in the hypokalaemic individuals improved as the hepatic functions recovered by day 45 of follow up. (p between 0.014 and 0.000) No significant change in kaliuresis was observed among normokalaemic subjects between first contact and later on day 45 of follow up. (p between 0.991 and 0.228) Despite different physiologic mechanisms, appropriateness of kaliuresis measured by FEK and TTGK showed results in the same direction.

CONCLUSION:

: Hypokalemia and inappropriate kaliuresis observed during acute phase of ALF and AVH reversed with clinical and biochemical recovery. In the absence of major gastro-intestinal losses, and renal abnormalities, there is need to investigate the contributory role of factors like hyper-aldosteronism and food intake which may have therapeutic implications.

OBJECTIVE

, To analyze the prevalence of prescription drugs, previously selected, that should be monitored by their analytical test, and the rate of alteration in these tests, with the aim of establishing priorities to facilitate monitoring.

METHOD

, Prospective observational study in the Internal Medicine department of a referral hospital of 350 beds. In a first phase, we selected some drugs which analytical monitoring is recommended for the medical literature, and after that, we reviewed the pharmacological treatment of all patients admitted with any of these drugs. The study was conducted in the last two month of 2011.

RESULTS

, We included 271 patients, 128 (47%) were women. The mean age was 74.5 ± 14.4 years and the average stay of 7 ± 5.8 days. These patients accounted for 83% of all patients admitted to Internal Medicine during the study period. There were 828 drugs that must be monitored; each patient had an average of 3.1 ± 2.3. We reviewed 1837 analytical test, of which 401 (22%) were altered and 154 patients (57%) were affected for it. The pairs drug-analytical test altered most frequently found were creatinine increased and nephrotoxic drugs, hypokalemia in patients taking high efficiency diuretics and thrombocytopenia in patients treated with low molecular weight heparins.

CONCLUSIONS

, Our study highlights the importance of monitoring laboratory test associated with some drugs from the pharmacy department, as it demonstrates a high incidence of warning results. Our proposal for selection of drugs makes monitoring easier, and reaches large numbers of patients.

To determine the utility (i.e., positive predictive value [PPV] and time requirement) of an adverse drug event (ADE) trigger tool in Veterans Affairs (VA) nursing facilities and to describe the most common types of potential ADEs detected with the trigger tool.Retrospective chart review.Veterans residing in three VA nursing facilities between September 29, 2010, and October 29, 2010.We used the Institute for Healthcare Improvement-endorsed nursing facility ADE trigger tool, modified to enhance its clinical relevance to detect potential ADEs. Electronic medical records were screened to identify residents with one or more abnormal laboratory values specified in the trigger tool.A potential ADE was defined as the concurrent administration of medication that could cause the abnormal laboratory value. An overall PPV, or proportion of residents with an abnormal laboratory value who had a potential ADE, and average time required to complete each trigger tool assessment, were calculated.Among 321 veterans, 50.5% (n = 162) had at least one abnormal laboratory value contained in the trigger tool. Ninety-nine potential ADEs involving 146 medications were detected in 65 veterans. The overall PPV of the ADE trigger tool was 40.1% (65/162), and the average time to complete resident assessments was 8.8 (standard deviation ± 5.7) minutes. The most common potential ADEs were acute kidney injury (n = 30 residents), hypokalemia (n = 18), hypoglycemia (n = 13), and hyperkalemia (n = 10).The modified nursing facility trigger tool was shown to be an effective and efficient method for detecting potential ADEs.

We report a case of a 59-year old Japanese woman with short bowel syndrome, whose hypokalemia and hypocalcemia were successfully treated with magnesium (Mg) supplementation. Two years previously, she underwent Mile's operation for advanced rectal cancer, which could have been the cause of subsequent extensive resection of the small intestine by strangulation. After serial resection, she gradually developed chronic diarrhea and anorexia. Three weeks before admission, she developed general fatigue and tetany, and was hospitalized at another hospital. On admission, her serum K and Ca were 2.5 mEq/L and 4.3 mg/dL, respectively, hence regular fluid therapy containing potassium (K) and calcium (Ca) was provided following admission. However, her hypokalemia and hypocalcemia persisted, and she also displayed renal dysfunction and thereafter was transferred to our department for further evaluation and treatment. Since the laboratory tests revealed severe hypomagnesemia (0.4 mg/dL), we started intravenous Mg supplementation together with fluid therapy containing K and Ca. After the combination therapy, her clinical symptoms and electrolyte disorders were remarkably improved within a week. As Mg is essential for PTH secretion in response to hypocalcemia and to inhibit the K channel activity that controls urinary K excretion, hypomagnesemia can cause hypocalcemia and hypokalemia, which is refractory to repletion therapy unless Mg is administered. Therefore, for patients who present with signs of Mg deficiency, early and accurate diagnosis of Mg deficiency should be made and corrected.

Rifampin is one of the most important drugs in first-line therapies for tuberculosis. The renal toxicity of rifampin has been reported sporadically and acute tubulointerstitial nephritis (ATIN) is a frequent histological finding. We describe for the first time a case of ATIN and Fanconi syndrome presenting as hypokalemic paralysis, associated with the use of rifampin.A 42-year-old man was admitted with sudden-onset lower extremity paralysis and mild renal insufficiency. He had been treated for pulmonary tuberculosis with isoniazid, rifampin, and ethambutol for 2 months. Laboratory tests revealed proteinuria, profound hypokalemia, hyperchloremic metabolic acidosis with a normal anion gap, positive urine anion gap, hypophosphatemia with hyperphosphaturia, hypouricemia with hyperuricosuria, glycosuria with normal serum glucose level, generalized aminoaciduria, and β2-microglobulinuria. A kidney biopsy revealed findings typical of ATIN and focal granular deposits of immunoglubulin A and complement 3 in the glomeruli and tubules. Electron microscopy showed epithelial foot process effacement and electron-dense deposits in the subendothelial and mesangial spaces. Cessation of rifampin resolved the patient's clinical presentation of Fanconi syndrome, and improved his renal function and proteinuria.This case demonstrates that rifampin therapy can be associated with Fanconi syndrome presenting as hypokalemic paralysis, which is a manifestation of ATIN. Kidney function and the markers of proximal tubular injury should be carefully monitored in patients receiving rifampin.

Hypokalemia is found in peritoneal dialysis (PD) patients. The problem may be severe and promote mortality. Several factors may trigger the hypokalemia in PD patients, such as preexisting malnutrition and the low protein and potassium food intake.To verify the prevalence of hypokalemia and its association with mortality, nutrition status, clinical, laboratory and electrocardiographic variables in PD patients.Serum K+ levels were evaluated retrospectively in PD patients. Hypokalemia was defined when the average of serum K+ was < 3.5 mEq/L in six consecutive measurements. Other available biochemical tests were also evaluated. Subjective Global Assessment (SGA) and body mass index (BMI) were used to assess the nutrition status. A questionnaire was applied to identify the most common symptoms and signals associated to hypokalemia. An electrocardiogram was performed. Demographic data, dialysis characteristics and survival rate were collected.Hypokalemia was present in 15 out of 110 patients (13.6%). The survival rate was lower in the hypokalemic group (p = 0.002). Hypokalemia was only associated with serum levels of albumin and urea, and with the SGA results.Low levels of serum potassium were associated to lower survival in PD patients and it seems to be related to malnutrition.

Hashimoto's encephalopathy (HE) is a completely treatable but relapsing neuroendocrine disorder associated with Hashimoto's thyroiditis (HT). Though numerous neurological manifestations are often associated with thyroid disorder, this entity is less documented. We are reporting a case of HE in a 65 year old female presenting with sudden onset deep coma following an attack of mild fever and vomiting for two days. Patient was a known diabetic. Hypoglycemic coma, diabetic ketacidosis and hyperosmolar coma were excluded by laboratory investigations. High blood sugar was corrected with insulin. She had hyponatremia and hypokalemia which were corrected with electrolyte replacement. Liver function tests were normal, but serum ammonia was mildly raised. CSF study was normal. Despite correction of her metabolic derangements patient failed to regain her consciousness. CT scan of brain was normal. MRI of brain revealed diffuse brain atrophy. Patient's thyroid function tests were normal but anti-thyroid peroxidase (anti-TPO) antibody was highly raised. EEG showed diffuse slow wave pattern. Intravenous dexamethasone (24 mg/d) was started. Patient regained consciousness slowly over a period of one month. To reduce the toxicity of steroid, oral azathiprine 50 mg/day was added later with tapering of steroid dose. HE must be kept in mind in comatose patients when other metabolic, infective and structural neurological causes have been excluded. Proper and timely treatment can salvage the patient.