A 36-year-old man was diagnosed to be infected with HIV in November 2000 and was started on azidothymidine/lamivudine /nevirapine in January 2001. He tolerated this treatment well for 20 months, achieving suppression of the viral load to undetectable levels and increase of his CD4 count to 1,506 cells/ml. Then, he began to complain of nausea, fatigue, dyspnea, and pain in the epigastrium. He did not take any other prescription or over the counter medications.

On admission, he was slightly tachypneic (20 breaths/min); physical examination was notable only for mild epigastric tenderness. Laboratory work-up showed mildly elevated transaminases (AST: 44 U/L, normal: 7-40, and ALT: 64 U/L, normal: 7-40), elevated triglycerides (268 mg/dL, normal: 50-150), cholesterol (317 mg/dL, normal: <190) and a lactate level of 13.1 mmol/L (normal: 0.6-2.4), with mild metabolic acidosis (pH: 7.34, HCO3: 18.3 mmol/L). Hepatitis serologies for hepatitis B and C viruses were negative. Antero-posterior and lateral chest X-rays were normal.

What was the cause of his hyperlactaemia?

A 43-year-old male presented to the Emergency Department complaining for vomiting and dyspepsia. He refused persistently to give any more details. He asked for an intramuscular injection of metoclopramide, refusing further investigation, since "he already knew his problem ("recurrent gastritis")". However, he was convinced to undergo an electrocardiogram in our attempt to rule out vomiting of cardiac origin, which showed ST changes and minimal U wave, suggestive of hypokalemia (Figure 1). The physical examination on presentation was unremarkable except for epigastric tenderness. Routine laboratory testing on admission was unremarkable except for low serum potassium (K=2,1 mmol/liter). The arterial blood gas testing showed metabolic alkalosis (pH=7,66, bicarbonate = 55,2 mmol/liter, pC02 49mmHg, pO2 63mmHg, saturation O2 96%). Since his symptoms insisted, the patient accepted to be admitted.

During his hospitalization, he revealed that he had history of upper gastrointestinal bleeding four years earlier without undergoing further investigation. Since then he has been complaining for occasional vomiting that was empirically managed with metoclopramide. He didn't report chest pain, headache, fever, weight loss, or other symptoms. He was afraid of hospitals and doctors and he avoided visiting his family physician. The last two weeks prior to admission, his condition deteriorated. His other past medical history was unremarkable and he received no medications, except the occasional use of metoclopramide. He did not smoke and he did not drink alcohol.
Question
Based on the patient's history and physical examination, which one of the following is the most likely diagnosis?
A. Functional or non-ulcer dyspepsia
B. Peptic ulcer disease complicated by pyloric stenosis
C. Esophagitis or reflux without esophagitis
D. Gastric or esophageal cancer
E. Biliary track disease

A 55-year-old farmer was admitted to the hospital with low back pain without neurological compromise and nodulopustular skin lesions in the thighs and forearms. The patient reported recurrent episodes of right elbow bursitis as well as right heel pain during the last 8 months.

Past medical history revealed renal transplantation for end stage glomerulonephritis 15 years prior to the admission to the hospital and therapy with immunosuppressive agents since then. During the last 3 years, the patient received methylprednisolone, 4mg per day, and azathioprine, 75mg per day. Moreover, the patient had liver cirrhosis due to chronic hepatitis C viral infection diagnosed at the time of transplantation.

Physical examination and plain radiographs of the lumbar spine showed no abnormalities. The patient was discharged from the hospital with the advice to receive a 2-week treatment with non-steroid anti-inflammatory medications and bed rest for the low back pain and amoxicillin/clavulanic acid for the skin lesions.

Four weeks later, he presented with intense low lumbar pain, numbness of the lower extremities and gait disturbance. Furthermore, there was cervical spine pain, loss of dexterity, and numbness of the hands. The patient had malaise, vertigo, and tinnitus but no fever.

Physical examination revealed a palpable gibbus at the cervical region. Neck motion was decreased. The muscle strength of both lower and upper extremities muscles was mildly decreased (4/5). Deep tendon reflexes of the upper extremities were decreased. Deep tendon reflexes of the lower extremities were normal. There was no clonus.

Imaging evaluation with plain radiographs, computed tomography and magnetic resonance imaging of the spine showed spondylodiscitis at C4-C5, C5-C6, C7-T1, and T1-T2 intervertebral discs (Fig. 1) and spondylodiscitis at L4-L5 associated an epidural mass. Cervical kyphosis was present because of osteolysis with anterior wedged deformity of the C5 vertebra. Posterior C5-C6 spondylolisthesis resulted in compression of the spinal cord at this level. Osteolytic lesions were also shown radiographically at the left elbow (olecranon and radius), the right carpal bones, the distal right fibula, the right calcaneus (Fig. 2), and the right middle and forefoot (the head of the fifth metatarsal and the proximal phalanxes of the fifth, fourth, third and second toes).

What is your diagnosis?

A 57-year-old man was admitted to the intensive care unit (ICU) after initial resuscitation and hemodynamical stabilization in the emergency ward (EW), where he presented in a comatose state with shock (blood pressure 60/40 mmHg, heart rate 140 pulses/min, body temperature 36.5oC, respiratory rate 28 breaths/min, O2 saturation 90% on room air). Family members reported that the patient had developed a rash (not further specified) and fever seven days prior to his admission to the hospital.

The rash gradually extended on large areas of both lower extremities. The patient had a 30-year history of multiple sclerosis and a 2-year history of Waldenström's macroglobulinemia for which he was receiving corticosteroids. He also had a history of fracture of the right hip. He was confined to bed for the last 10 years prior to his admission. The rest of the physical examination on admission showed icteric conjunctivae and decreased respiratory sounds as well as fine crackles in the pulmonary bases. There were extensive, hemorrhagic, necrotic areas of the skin of the lower extremities and the abdomen as well as ulcers and bullae (Figures 1 and 2).

Routine laboratory testing on admission revealed normochromic, normocytic anemia (hematocrit 32.1%), decreased white blood cell count (WBC = 3.38 × 103/ìl of peripheral blood) with 89.9% neutrophils, and thrombocytopenia (20 × 103/ìl of peripheral blood). The prothrombin time (PT) and INR were increased (16.2 sec and 1.35, respectively). Also, blood urea and direct bilirubin were elevated (66 mg/dl and 2.15 mg/dl, respectively). The serum protein electrophoresis revealed increased gamma globulins (25.4%) and detection of monoclonal IgM ê chains. The concentration of IgM was increased (990 mg/dL) while IgG and IgA were decreased (124 mg/dL and < 25 mg/dL, respectively). Chest X-ray films revealed lower lobe atelectasis bilaterally.