Secondary cold agglutinin autoimmune hemolytic anemia (AIHA) occurs most commonly due to infectious causes like Mycoplasma pneumonia and, more rarely, Epstein-Barr virus(EBV). Here we present a case of a 69-year-old female presenting with generalized weakness, who was found to have cold agglutinin hemolytic anemia. She unfortunately experienced some of the most severe complications of the disease including encephalopathy, hypoxia, and dry necrosis of peripheral extremities. Further investigation revealed an EBV infection, the rarest infectious cause of cold AIHA. She was started on steroids, the mainstay of treatment, but continued to worsen over the course of her extensive stay in the intensive care unit (ICU). Given the severity of the disease, the decision was made to use plasmapheresis and rituximab, the monoclonal antibody directed against CD20, as an experimental therapy. After adjunctive therapy was initiated, the patient began to clinically improve and ultimately made a full recovery. Rituximab is historically only effective in primary cold AIHA, but it appeared to elicit significant clinical improvement with our use in secondary cold AIHA. While there have been a handful of studies demonstrating its successful use in secondary cold AIHA, we propose that this medication be further studied to prevent the significant morbidity and mortality associated with the disease.

Neutropenic enterocolitis (NEC), also referred to as typhlitis, is a condition associated with a high mortality risk and primarily manifests in immunocompromised patients. It is characterized by ulceration, edema, and hemorrhage affecting the bowel wall. The underlying cause of NEC is postulated as an immunocompromised condition that facilitates bacterial infiltration through compromised bowel mucosa. The high mortality rate is attributable to bowel necrosis, culminating in perforation and sepsis. This report describes a case involving a patient with metastatic seminoma who exhibited seizure-like activity, fever, Streptococcus gallolyticus bacteremia, and NEC. The patient underwent treatment involving broad-spectrum antibiotics and filgrastim. The patient\'s neutropenia resolved leading to discharge on oral antibiotics. The case reported is unique, as it links NEC to Streptococcus gallolyticus and seminoma. Streptococcus gallolyticus has not been previously associated with NEC.

Obstetrical management of patients with genetic disorders bears its own challenges in the overall care and outcomes of the patient. Hereditary hemorrhagic telangiectasia (HHT), or Osler-Weber-Rendu Syndrome, is an inherited genetic disorder that, due to the nature of the pathophysiology of arteriovenous malformation and dysplasia, has been highly associated with an increased tendency of bleeding. This case presents a patient diagnosed with HHT prior to pregnancy who developed severe postpartum hemorrhage (PPH) after cesarean section delivery. Clinical considerations were made proactively with the knowledge and understanding of the genetic disorder, but due to unforeseen changes in the manifestation of the PPH, clinical decisions were dynamically modified in order to save the patient from exsanguination, ultimately resulting in an emergency hysterectomy and a total of 15 units of transfused packed red blood cells (pRBC). As a result, this case report serves as a preliminary recount for future research and clinical management of similar cases.

Hematohidrosis is an extremely rare condition characterized by the oozing or secretion of blood through intact skin and mucosa, particularly through eccrine glands. Although there is not much literature available on the condition, examples of Hematohidrosis include the crying and sweating of blood. The fluid may have a bloody tinge or may be frank blood. The anomaly has no identifiable etiology, and patients generally present in a good state of health. In this report, we present a 19-year-old female who had weekly occurrences of bloody diaphoresis that had been present consistently for one year. During her presentation at the hematology clinic, she was investigated thoroughly for alternative causes, but none were found. The patient was diagnosed with hematohidrosis and was offered treatment with propranolol, which she declined. She continues to follow up routinely in the hematology clinic with persistent symptoms.

Paroxysmal nocturnal hemoglobinuria is a rare form of intravascular hemolysis caused by an acquired deficiency of complement regulatory glycoproteins. In our case, a 53-year-old male presented with fatigue, discoloration of urine, and reduced urine output. Preliminary investigations showed severe anemia (3.7 g/dl) and hyperkalemia (7.6 mmol/L) in the setting of acute kidney injury, requiring urgent dialysis. Four units of packed cell volumes were transfused for the correction of anaemia. Following initial stabilization, flow cytometry and a fluorescein-labeled proaerolysin (FLAER) study showed a total deficiency of CD59 in 95.92% of granulocytes and a 97.14% deficiency in monocytes. A bone marrow biopsy showed erythroblast hyperplasia confirming the diagnosis of classical paroxysmal nocturnal hemoglobinuria. The patient was treated with steroids, androgens, and iron supplementation and made a complete recovery with a near-total resolution of his acute kidney injury. This paper aims to review the clinical features and investigations in order to focus on acute kidney injury as an outcome of paroxysmal nocturnal hemoglobinuria.

Background and objective Patients suffering from thalassemia major are at higher risk of osteoporosis. Due to their decreased life expectancy, the number of adult patients is low. However, their bone health is rarely checked in developing countries like India. There is no data available in the literature on the bone mineral density (BMD) of adult (aged ≥18 years) thalassemia major patients in eastern India. In this study, we aimed to measure the BMD and serum calcium and vitamin D levels in adult thalassemia major patients and to compare them with healthy controls. Materials and methods We conducted this cross-sectional observational study at a tertiary care hospital in eastern India. We recruited adult thalassemia major patients who were not on calcium or vitamin D supplements. Their BMD was measured by dual-energy X-ray absorptiometry (DXA) on the lumbar spine (L1-L4). Venous blood was tested for serum calcium and vitamin D levels. We compared the parameters between the cases and controls by using the Mann-Whitney U test. Results A total of 31 (male = 19, female = 12) patients with a median age of 28 years comprised the case group. Age- and sex-matched controls showed similar height but higher weight and BMI. The serum calcium level was similar (p = 0.43) in the case and control groups but T-score (p = 0.0003) and vitamin D levels (p: <0.0001) were significantly lower in thalassemia major patients. Conclusion Based on our findings, adult thalassemia major patients have lower BMD and vitamin D levels. Although the serum calcium may be normal in these patients, they should still be screened both for BMD and vitamin D for prompt and early detection of risks and complications so that a proper management strategy can be implemented.

Quinine has been used worldwide to treat malaria; however, it is now used as an agent for night-time muscle cramping. The compound, derived from Cinchona tree bark, is found in antimalaria medication, supplements for leg cramping, and beverages such as tonic water and bitter lemon. Quinine, however, is not without its side effect profile which includes a wide range of ailments ranging from nausea to disseminated intravascular coagulation. The authors present a case of a 35-year-old man diagnosed with disseminated intravascular coagulation due to an excessive intake of tonic water because his friend told him that it would help alleviate nighttime leg cramping. We strive to inform physicians about the side effect profile of quinine and stress that a pertinent history must be elicited in patients with unknown causes of disseminated intravascular coagulation.

Malignant neoplasms may present as paraneoplastic syndromes with mucocutaneous manifestations, which may or may not be chronologically associated. The pathophysiological mechanism is complex and not completely understood; therefore, definitive diagnosis may be achieved with a precise differential diagnosis based on the morphology of skin lesions, clinical picture, and histological pattern. The complexities, and low frequency, make the therapeutic approach quite challenging; consequently, the cornerstone of therapy is the eradication of the underlying neoplasms. Corticosteroids are the therapy of choice for most of these immune-mediated manifestations, but for the most part, the successful resolution requires the eradication of the underlying malignancy.